Dictionary of drugs: P

From WikiMD

Other languages:
English
Medicine.jpg

Dictionary of pharmaceutical drugs/medications sorted alphabetically

Top 50 drugs | Top 200 drugs | Medicare drugs | Canadian drugs | Dictionary of drugs

Drug dictionary P

A fusion DNA vaccine containing the first domain of fragment C (FrC) of tetanus toxin (TT865-1120) (p.DOM) fused to the human Wilms' Tumor gene-1 (WT1)-derived MHC class I-binding epitope WT1.126, with potential antitumor activity. Upon vaccination with p.DOM-WT1-126 DNA and subsequent electroporation, this vaccine may induce a WT1 epitope-specific cytotoxic T-lymphocyte (CTL) response against WT1 expressing cells, resulting in cell lysis and inhibition of cancer cell proliferation in WT1-overexpressing cancer cells. WT1, a tumor associated antigen, is overexpressed in most types of leukemia and in a variety of solid cancers. The FrC of tetanus toxin contains the MHC II-binding sequence, p30, which induces T-helper cell activation for long-lasting immunity.

A fusion DNA vaccine containing the first domain of fragment C (FrC) of tetanus toxin (TT865-1120) (p.DOM) fused to the human Wilms' Tumor gene-1 (WT1)-derived MHC class I-binding epitope WT1.37, with potential antitumor activity. Upon vaccination with p.DOM-WT1-37 DNA and subsequent electroporation, this vaccine may induce a WT1 epitope-specific cytotoxic T-lymphocyte (CTL) response against WT1 expressing cells, resulting in cell lysis and inhibition of cancer cell proliferation in WT1-overexpressing cancer cells. WT1, a tumor associated antigen, is overexpressed in most types of leukemia and in a variety of solid cancers. The FrC of tetanus toxin contains the MHC II-binding sequence, p30, which induces T-helper cell activation for long-lasting immunity.

An inhibitor of the beta and delta isoforms of the 110 kDa catalytic subunit of class IA phosphoinositide-3 kinases (PI3K) with potential immunomodulating and antineoplastic activities. p110beta/delta PI3K inhibitor GS-9820 inhibits the activity of PI3K, thereby preventing the production of the second messenger phosphatidylinositol-3,4,5-trisphosphate (PIP3), which decreases tumor cell proliferation and induces cell death. PI3K-mediated signaling is often dysregulated in cancer cells; the targeted inhibition of PI3K is designed to preserve PI3K signaling in normal, non-neoplastic cells.

The dimesylate salt form of LY2228820, a tri-substituted imidazole derivative and orally available, p38 mitogen-activated protein kinase (MAPK) inhibitor with potential anti-inflammatory and antineoplastic activities. Upon administration, LY2228820 inhibits the activity of p38, particularly the alpha and beta isoforms, thereby inhibiting MAPKAPK2 phosphorylation and preventing p38 MAPK-mediated signaling. This may inhibit the production of a variety of cytokines involved in inflammation, cellular proliferation and angiogenesis such as tumor necrosis factor alpha (TNFa), interleukin (IL)-1, -6 and -8, vascular endothelial growth factor, and macrophage inflammatory protein-1 alpha. Ultimately this induces apoptosis and reduces tumor cell proliferation. In addition, inhibition of the p38 MAPK pathway by LY2228820 increases the antineoplastic activity of certain chemotherapeutic agents. p38 MAPK, a serine/threonine protein kinase that is often upregulated in cancer cells, plays a crucial role in tumor cell proliferation, angiogenesis and metastasis.

An orally active p38 mitogen-activated protein kinase (MAPK) inhibitor with potential immunomodulating, anti-inflammatory, and antineoplastic activity. Upon administration, LY3007113 inhibits the activity of p38, thereby preventing p38 MAPK-mediated signaling. This may result in the inhibition of the production of proinflammatory cytokines and the induction of tumor cell apoptosis. p38 MAPK, a serine/threonine protein kinase often upregulated in cancer cells, plays a crucial part in the production of a variety of cytokines involved in inflammation and cellular proliferation such as tumor necrosis factor (TNF) and interleukin (IL)-1 and -6.

An orally bioavailable small-molecule inhibitor of p38 and Tie2 kinases with potential antineoplastic, anti-inflammatory and antiangiogenic activities. p38/Tie2 kinase inhibitor Arry-614 binds to and inhibits the activities of p38 and Tie2 kinases, which may inhibit the production of proinflammatory cytokines and may decrease tumor angiogenesis and tumor cell growth and survival. p38 is a MAP kinase that is often upregulated in cancer cells, playing a crucial part in the production of a variety of cytokines involved in inflammation and cellular proliferation such as tumor necrosis factor (TNF) and interleukin (IL)-1 and -6. Tie2 is an endothelial cell specific receptor that is activated by angiopoietins, growth factors required for angiogenesis. This agent has also been reported to inhibit other kinases including vascular endothelial growth factor receptor (VEGFR2) and Src tyrosine kinases.

A peptide-based cancer vaccine composed of amino acids 264 to 272 of the wild-type protein encoded by the P53 gene. p53 peptide vaccine may elicit an HLA-A2.1-restricted cytotoxic T lymphocyte immune response against tumor cells that overexpress p53 protein.

A peptide vaccine consisting of 10 synthetic long peptides (SLPs), 25-30 amino acids in size and derived from the middle portion of p53 (amino acids 70-251), mixed with the adjuvant Montanide ISA-51 with potential immunostimulatory and antitumor activities. Upon administration, p53 synthetic long peptide (70-251) vaccine may stimulate the host immune system to mount a cytotoxic T-cell lymphocyte (CTL) response against p53-expressing tumor cells. p53, a tumor associated antigen (TAA), may be overexpressed in variety of cancer cell types.

An orally bioavailable HDM2 (human homolog of double minute 2) antagonist with potential antineoplastic activity. Upon oral administration, p53/HDM2 interaction inhibitor CGM097 inhibits the binding of the HDM2 protein to the transcriptional activation domain of the tumor suppressor protein p53. By preventing this HDM2-p53 interaction, the proteosome-mediated enzymatic degradation of p53 is inhibited, which may result in the restoration of p53 signaling and, thus, the p53-mediated induction of tumor cell apoptosis. HDM2, a zinc finger nuclear phosphoprotein, is a negative regulator of the p53 pathway, often overexpressed in cancer cells and has been implicated in cancer cell proliferation and survival.

An orally available inhibitor of human homologminute 2 (HDM2; mouse double minute 2 homolog; MDM2), with potential antineoplastic activity. Upon oral administration, the p53-HDM2 protein-protein interaction inhibitor APG-115 binds to HDM2, preventing the binding of the HDM2 protein to the transcriptional activation domain of the tumor suppressor protein p53. By preventing this HDM2-p53 interaction, the proteasome-mediated enzymatic degradation of p53 is inhibited and the transcriptional activity of p53 is restored. This may result in the restoration of p53 signaling and lead to the p53-mediated induction of tumor cell apoptosis. HDM2, a zinc finger protein and a negative regulator of the p53 pathway, is often overexpressed in cancer cells. It has been implicated in cancer cell proliferation and survival.

An orally available spiro-oxindole HDM2 (human double minute 2) antagonist with potential antineoplastic activity. Upon oral administration, the p53-HDM2 protein-protein interaction inhibitor MI-773 binds to HDM2, preventing the binding of the HDM2 protein to the transcriptional activation domain of the tumor suppressor protein p53. By preventing this HDM2-p53 interaction, the proteosome-mediated enzymatic degradation of p53 is inhibited and the transcriptional activity of p53 is restored, which may result in the restoration of p53 signaling and lead to the p53-mediated induction of tumor cell apoptosis. HDM2, a zinc finger protein and a negative regulator of the p53 pathway, is often overexpressed in cancer cells. It has been implicated in cancer cell proliferation and survival.

An orally available inhibitor of p70S6K signaling, with potential antineoplastic activity. p70S6K inhibitor LY2584702 inhibits ribosomal protein S6 Kinase (p70S6K), and prevents phosphorylation of the S6 subunit of ribosomes, thereby inhibiting normal ribosomal function within tumor cells leading to a decrease in protein synthesis and in cellular proliferation. P70S6K, a serine/threonine kinase, acts downstream of PIP3 and phosphoinositide-dependent kinase-1 in the PI3 kinase pathway, is often upregulated in a variety of cancer cells, and is involved in the regulation of cell growth, proliferation, motility, and survival.

An orally available inhibitor of the serine/threonine protein kinases ribosomal protein S6 Kinase (p70S6K) and Akt (protein kinase B), with potential antineoplastic activity. Upon administration, p70S6K/Akt inhibitor MSC2363318A binds to and inhibits the activity of p70S6K and Akt. This prevents the activation of the PI3K/Akt/p70S6K signaling pathway and inhibits tumor cell proliferation in cancer cells that have an overactivated PI3K/Akt/p70S6K signaling pathway. Constitutive activation and dysregulated signaling of the PI3K/Akt/p70S6K pathway are frequently associated with tumorigenesis of many tumor types; targeting multiple kinases in this pathway is more efficacious than targeting a single kinase.

An orally bioavailable inhibitor of valosin-containing protein (VCP) p97, with potential antineoplastic activity. Upon oral administration, CB-5083 specifically binds to and inhibits the activity of p97. This prevents ubiquitin-dependent protein degradation and causes cellular accumulation of poly-ubiquitinated proteins. The inhibition of endoplasmic reticulum (ER)-associated protein degradation activates the ER-dependent stress response pathway, and leads to both an induction of apoptosis and inhibition of cell proliferation in susceptible tumor cells. p97, a type II AAA ATPase, plays a key role in cellular protein homeostasis. Its overexpression in many tumor cell types is associated with increased tumor cell proliferation and survival.

A compound extracted from the Pacific yew tree Taxus brevifolia with antineoplastic activity. Paclitaxel binds to tubulin and inhibits the disassembly of microtubules, thereby resulting in the inhibition of cell division. This agent also induces apoptosis by binding to and blocking the function of the apoptosis inhibitor protein Bcl-2 (B-cell Leukemia 2).

A Cremophor EL-free, albumin-stabilized nanoparticle formulation of the natural taxane paclitaxel with antineoplastic activity. Paclitaxel binds to and stabilizes microtubules, preventing their depolymerization and so inhibiting cellular motility, mitosis, and replication. This formulation solubilizes paclitaxel without the use of the solvent Cremophor, thereby permitting the administration of larger doses of paclitaxel while avoiding the toxic effects associated with Cremophor.

A nanoparticle-based injectable concentrate containing the water-insoluble taxane paclitaxel, with potential antineoplastic activity. Upon reconstitution and administration, paclitaxel binds to tubulin and inhibits the disassembly of microtubules, thereby resulting in the inhibition of cell division. Compared to paclitaxel alone, the nanodispersion-based formulation uses less toxic solvents and allows for administration of higher doses resulting in higher concentrations of paclitaxel at the tumor site, and an increased safety profile.

The agent paclitaxel linked to a biodegradable, water-soluble polyglutamate polymer with antineoplastic properties. The polyglutamate residue increases the water solubility of paclitaxel and allows delivery of higher doses than those achievable with paclitaxel alone. Paclitaxel promotes microtubule assembly and prevents microtubule depolymerization, thus interfering with normal mitosis.

A nanoparticle-based formulation consisting of polymeric micelles encapsulating the taxane paclitaxel, with potential antineoplastic activity. Paclitaxel is covalently bound to polyethylene glycol (PEG)-based block copolymers which forms a micellar structure with an outer hydrophilic PEG shell surrounding the hydrophobic paclitaxel. Upon administration of the paclitaxel polymeric micelle formulation NANT-008, the nanoparticles are stable in the bloodstream and specifically accumulate in the tumor tissue. Due to the acidic conditions in the tumor and the pH-responsive nature of the micelles, paclitaxel is released in the tumor environment. Paclitaxel binds to microtubules, promotes microtubule assembly, and prevents depolymerization, thus interfering with normal mitosis. Compared to the administration of paclitaxel alone, this formulation increases the solubility of paclitaxel, enhances its specific retention in cancer tissue, and increases its therapeutic effect, while decreasing its toxicity. In addition, the micellar formulation allows the delivery of higher doses of paclitaxel to target tissues while minimizing systemic toxicity.

A cremophor-free, P-glycoprotein-inhibiting, vitamin E-based emulsion particle formulation of paclitaxel with antineoplastic activity. Paclitaxel binds to tubulin and inhibits the disassembly of microtubules, thereby resulting in the inhibition of cell division. This agent also induces apoptosis by binding to and blocking the function of the apoptosis inhibitor protein Bcl-2 (B-cell Leukemia 2). The vitamin-E based emulsion allows bolus infusion without steroid premedication and may diminish hypersensitivity reactions; tumor tissue may be passively targeted due to preferential deposition of emulsion particles while an emulsion formulation component inhibits the P-glycoprotein drug efflux pump.

An orally bioavailable inhibitor of Janus kinase 2 (JAK2) and the JAK2 mutant JAK2V617F with potential antineoplastic activity. Pacritinib competes with JAK2 for ATP binding, which may result in inhibition of JAK2 activation, inhibition of the JAK-STAT signaling pathway, and so caspase-dependent apoptosis. JAK2 is the most common mutated gene in bcr-abl-negative myeloproliferative disorders; the JAK2V617F gain-of-function mutation involves a valine-to-phenylalanine modification at position 617. The JAK-STAT signaling pathway is a major mediator of cytokine activity.

A chemotherapy regimen containing bortezomib, doxorubicin and dexamethasone regimen used in the treatment of multiple myeloma.

A vascular-acting photosensitizer consisting of a water-soluble, palladium-substituted bacteriochlorophyll derivative with potential antineoplastic activity. Upon administration, paldeliporfin is activated locally when the tumor bed is exposed to low-power laser light; reactive oxygen species (ROS) are formed upon activation and ROS-mediated necrosis may occur at the site of interaction between the photosensitizer, light and oxygen. Vascular-targeted photodynamic therapy (VTP) with padeliporfin may allow tumor-site specific cytotoxicity while sparing adjacent normal tissues.

Pan-DR epitope (PADRE) 965.10 is a helper peptide. PADRE peptides have been shown the capacity to deliver help for antibody responses in vivo. They were also found to be able to provide significant helper T-cell activity in vivo. Acts as an adjuvant.

A peptide-based vaccine containing a pan HLA DR-binding epitope (PADRE) fused to a cytomegalovirus (CMV) peptide epitope, with potential anti-viral and immunomodulating activities. Upon administration, PADRE-CMV fusion peptide may stimulate a cytotoxic T-lymphocyte (CTL) response against CMV in the CMV-infected host. The synthetic peptide PADRE is a universal helper T cell epitope.

An orally bioavailable small-molecule inhibitor of p21-activated kinase 4 (PAK4) with potential antineoplastic activity. PAK4 inhibitor PF-03758309 binds to PAK4, inhibiting PAK4 activity and cancer cell growth. PAK4, a serine/threonine kinase belonging to the p21-activated kinase (PAK) family, is often upregulated in a variety of cancer cell types and plays an important role in cancer cell motility, proliferation, and survival.

An orally bioavailable inhibitor of both the serine/threonine kinase P21-activated kinase 4 (PAK4) and the nicotinamide adenine dinucleotide (NAD)-synthesizing enzyme nicotinamide phosphoribosyltransferase (NAMPT; NAMPRTase), with potential antineoplastic activity. Upon administration, KPT-9274 allosterically binds to, destabilizes and causes degradation of PAK4. This inhibits PAK4-mediated signaling, induces cell death in, and inhibits the proliferation of PAK4-overexpressing tumor cells. In addition, KPT-9274 binds to and inhibits the activity of NAMPT. This depletes cellular NAD and inhibits NAD-dependent enzymes, both of which are needed for rapid cell proliferation; this results in tumor cell death in NAMPT-overexpressing cancer cells. PAK4, a serine/threonine kinase and member of the PAK family of proteins upregulated in various cancer cell types, regulates cell motility, proliferation and survival. NAMPT, an enzyme that is responsible for maintaining the intracellular NAD pool, plays a key role in the regulation of cellular metabolism and has cytokine-like activities. NAMPT is often overexpressed in a variety of cancers and metabolic disorders and tumor cells rely on NAMPT activity for their NAD supply.

An orally available cyclin-dependent kinase (CDK) inhibitor with potential antineoplastic activity. Palbociclib selectively inhibits cyclin-dependent kinase 4 (CDK4) and 6 (CDK6), thereby inhibiting retinoblastoma (Rb) protein phosphorylation early in the G1 phase leading to cell cycle arrest. This suppresses DNA replication and decreases tumor cell proliferation. CDK4 and 6 are serine/threonine kinases that are upregulated in many tumor cell types and play a key role in the regulation of cell cycle progression.

Brand name for diethylstilbestrol

A recombinant form of the endogenous human keratinocyte growth factor. Palifermin binds to epithelial cell surface receptors in the lining of the mouth and gastrointestinal tract, resulting in stimulation of epithelial cell proliferation, differentiation and upregulation of cytoprotective mechanisms.

A synthetic mustard compound with potential antineoplastic activity. An active metabolite of ifosfamide covalently linked to the amino acid lysine for stability, palifosfamide irreversibly alkylates and cross-links DNA through GC base pairs, resulting in irreparable 7-atom inter-strand cross-links; inhibition of DNA replication and cell death follow. Unlike ifosfamide, this agent is not metabolized to acrolein or chloroacetaldehyde, metabolites associated with bladder and CNS toxicities. In addition, because palifosfamide does not require activation by aldehyde dehydrogenase, it may overcome the tumor resistance seen with ifosfamide.

A synthetic mustard compound of the tromethamine (tris) salt of palifosfamide (Isophosphamide mustard), with potential antineoplastic activity. As the stabilized active metabolite of ifosfamide, palifosfamide irreversibly alkylates and crosslinks DNA through GC base pairs, resulting in irreparable 7-atom interstrand crosslinks. This leads to an inhibition of DNA replication and ultimately cell death. Unlike ifosfamide, this agent is not metabolized to acrolein or chloroacetaldehyde, metabolites associated with bladder and CNS toxicities. In addition, because palifosfamide does not require activation by aldehyde dehydrogenase, it may overcome the tumor resistance seen with ifosfamide. Stabilization with tris instead of lysine further increases stability and may further decrease nephrotoxicity.

A radioisotope of the metal palladium used in brachytherapy implants or 'seed'. With a half-life of 17 days, palladium 103 administered with brachytherapy allows continuous, tumor-site specific low-energy irradiation to the tumor cell population while sparing normal adjacent tissues from radiotoxicity.

A novel palladium-substituted bacteriochlorophyll derivative and photosensitizer with potential antitumor activity. Upon administration, inactive palladium-bacteriophephorbide is activated locally when the tumor bed is exposed to photoirradiation; the activated form induces local cytotoxic processes, resulting in local tissue damage, disruption of tumor vasculature, and tumor hypoxia and necrosis.

The hydrochloride salt of palonosetron, a carbazole derivative and a selective serotonin receptor antagonist with antiemetic activity. Palonosetron competitively blocks the action of serotonin at 5-hydroxytryptamine type 3 (5-HT3) receptors located on vagal afferents in the chemoreceptor trigger zone (CTZ), resulting in suppression of chemotherapy-induced nausea and vomiting. The CTZ is located in the area postrema on the dorsal surface of the medulla oblongata at the caudal end of the fourth ventricle and outside the blood-brain barrier (BBB).

The disodium salt of the synthetic bisphosphonate pamidronate. Although its mechanism of action is not completely understood, pamidronate appears to adsorb to calcium phosphate crystals in bone, blocking their dissolution by inhibiting osteoclast-mediated bone resorption. This agent does not inhibit bone mineralization and formation.

Brand name for conjugated linoleic acid

An orally bioavailable inhibitor of the fibroblast growth factor receptor (FGFR) with potential antineoplastic activity. FGFR inhibitor ARQ 087 binds to and potently inhibits the activity of FGFR subtypes 1, 2 and 3. This may result in the inhibition of FGFR-mediated signal transduction pathways, tumor cell proliferation, tumor angiogenesis and tumor cell death in FGFR-overexpressing tumor cells. FGFR, a receptor tyrosine kinase, is upregulated in many tumor cell types and plays a key role in tumor cellular proliferation, differentiation, angiogenesis and survival.

An orally bioavailable pan inhibitor of the serine/threonine protein kinase AKT (protein kinase B) enzyme family with potential antineoplastic activity. Upon oral administration, AKT inhibitor ARQ 751 selectively binds to and inhibits the activity of the AKT isoforms 1, 2 and 3, which may result in the inhibition of the phosphatidylinositol 3-kinase (PI3K)/AKT signaling pathway. This may lead to a reduction in tumor cell proliferation and the induction of tumor cell apoptosis. The AKT signaling pathway is often deregulated in cancer and is associated with tumor cell proliferation, survival and migration.

An aminofurazan-derived inhibitor of Akt kinases with potential antineoplastic activity. Pan-AKT kinase inhibitor GSK-690693 binds to and inhibits Akt kinases 1, 2, and 3, which may result in the inhibition of protein phosphorylation events downstream from Akt kinases in the PI3K/Akt signaling pathway, and, subsequently, the inhibition of tumor cell proliferation and the induction of tumor cell apoptosis. In addition, this agent may inhibit other protein kinases including protein kinase C (PKC) and protein kinase A (PKA). As serine/threonine protein kinases which are involved in a number of biological processes, AKT kinases promote cell survival by inhibiting apoptosis and are required for glucose transport.

Brand name for pancrelipase

A standardized enzyme concentrate containing the pancreatic enzymes, lipase, protease and amylase used in enzyme substitution therapy. Lipase, protease and amylase break down fat, protein, and starches, respectively in the small intestine, thereby promoting digestion. Pancrelipase is used to reduce malabsorption when the pancreas is unable to secrete sufficient amounts of these enzymes.

An orally bioavailable pan-inhibitor of fibroblast growth factor receptor (FGFR) family proteins, with potential antineoplastic activity. Upon oral administration, FGFR inhibitor LY2874455 binds to and inhibits FGFR subtypes 1 (FGFR1), 2 (FGFR2), 3 (FGFR3) and 4 (FGFR4), which results in the inhibition of FGFR-mediated signal transduction pathways. This inhibits both tumor angiogenesis and proliferation of FGFR-overexpressing tumor cells. FGFR, a family of receptor tyrosine kinases upregulated in many tumor cell types, plays a key role in cellular proliferation, cell survival and angiogenesis.

A pan inhibitor of human fibroblast growth factor receptors (FGFRs) with potential antiangiogenic and antineoplastic activities. Pan-FGFR kinase inhibitor BAY1163877 inhibits the activities of FGFRs, which may result in the inhibition of both tumor angiogenesis and tumor cell proliferation, and the induction of tumor cell death. FGFRs are a family of receptor tyrosine kinases, which may be upregulated in various tumor cell types and may be involved in tumor cell differentiation and proliferation, tumor angiogenesis, and tumor cell survival.

Brand name for therapeutic immune globulin

Brand name for therapeutic hemin

An orally bioavailable pan-HER tyrosine kinase inhibitor with potential antineoplastic activity. BMS-599626 inhibits human epidermal growth factor receptors (HER) HER1, HER2 and HER4, thereby inhibiting the proliferation of tumor cells that overexpress these receptors.

A pyrrolotriazine-based compound and a pan inhibitor of receptor tyrosine kinases with potential antineoplastic activity. Pan HER/VEGFR2 receptor tyrosine kinase inhibitor BMS-690514 binds to human epidermal growth factor receptors (EGFR) 1, 2 and 4 (HER1, HER2 and HER4) and vascular endothelial growth factor receptor 1, 2 and 3 (VEGFR-1, -2 and -3), all of which are frequently overexpressed by a variety of tumor types. Binding of this agent to these receptors may result in the inhibition of tumor cell proliferation; the inhibition of endothelial cell migration and proliferation and angiogenesis; and tumor cell death.

A human monoclonal antibody produced in transgenic mice that attaches to the transmembrane epidermal growth factor (EGF) receptor. Panitumumab may inhibit autocrine EGF stimulation of tumor cells that express the EGF receptor, thereby inhibiting tumor cell proliferation.

An imaging agent composed of panitumumab, a humanized anti-epidermal growth factor receptor (EGFR) monoclonal antibody, conjugated to the near-infrared (NIR) fluorescent dye IRDye800, that can potentially be used for the imaging of EGFR-expressing tumors. Upon administration of panitumumab-IRDye800, the panitumumab moiety targets and binds to EGFR expressed on tumor cells. Upon fluorescence imaging of IRDye800, the tumor cells can be detected.

Brand name for gatipotuzumab

An orally available pan-inhibitor of mutant forms of the metabolic enzyme isocitrate dehydrogenase type 1 (IDH1; IDH-1; IDH1 [NADP+] soluble), including forms with mutations of arginine 132 (IDH1(R132)), with potential antineoplastic activity. Upon administration, pan-mutant-IDH-1 inhibitor BAY-1436032 specifically inhibits the activity of IDH1 mutant forms, which prevents the formation of the oncometabolite 2-hydroxyglutarate (2HG) from alpha-ketoglutarate (a-KG). This prevents 2HG-mediated signaling and leads to both an induction of cellular differentiation and an inhibition of cellular proliferation in tumor cells expressing IDH1 mutant forms. IDH1 mutations, including IDH1(R132) mutations, are highly expressed in certain malignancies; they initiate and drive cancer growth by both blocking cell differentiation and catalyzing the formation of 2HG.

A cinnamic hydroxamic acid analogue with potential antineoplastic activity. Panobinostat selectively inhibits histone deacetylase (HDAC), inducing hyperacetylation of core histone proteins, which may result in modulation of cell cycle protein expression, cell cycle arrest in the G2/M phase and apoptosis. In addition, this agent appears to modulate the expression of angiogenesis-related genes, such as hypoxia-inducible factor-1alpha (HIF-1a) and vascular endothelial growth factor (VEGF), thus impairing endothelial cell chemotaxis and invasion. HDAC is an enzyme that deacetylates chromatin histone proteins.

A gold nanoparticle (GNP)-based formulation containing panobinostat, a pan histone deacetylase (HDAC) inhibitor, with potential antineoplastic activity. Upon intra-tumoral injection of MTX110, panobinostat is released from the formulation and selectively targets, binds to and inhibits histone deacetylase (HDAC), which induces hyperacetylation of core histone proteins. The accumulation of highly acetylated histones leads to chromatin remodeling, an altered pattern of gene expression, inhibition of tumor oncogene transcription and the selective transcription of tumor suppressor genes. This results in the inhibition of tumor cell division and the induction of tumor cell apoptosis. HDAC, upregulated in many tumor cell types, is an enzyme family that deacetylates histone proteins. Panobinostat is water insoluble and does not cross the blood-brain barrier (BBB) when administered orally or intravenously. MTX110 solubilizes panobinostat and can be directly injected into the brain, which bypasses the BBB and delivers high concentrations of panobinostat to the tumor, while minimizing systemic toxicity Check for active clinical trials using this agent.

An orally bioavailable pan inhibitor of phosphatidylinositol-3-kinase (PI3K), with potential antineoplastic activity. Upon oral administration, pan-PI3K inhibitor CLR457 inhibits all of the PI3K kinase isoforms, which may result in apoptosis and growth inhibition in tumor cells overexpressing PI3K. Activation of the PI3K pathway promotes cell growth, survival, and resistance to both chemotherapy and radiotherapy.

An orally bioavailable pan inhibitor of phosphoinositide-3-kinases (PI3K) and inhibitor of the mammalian target of rapamycin (mTOR), with potential antineoplastic activity. PI3K/mTOR kinase inhibitor PQR309 inhibits the PI3K kinase isoforms alpha, beta, gamma and delta and, to a lesser extent, mTOR kinase, which may result in tumor cell apoptosis and growth inhibition in cells overexpressing PI3K/mTOR. Activation of the PI3K/mTOR pathway promotes cell growth, survival, and resistance to both chemotherapy and radiotherapy. As mTOR, a serine/threonine kinase downstream of PI3K, may also be activated independent of PI3K, this agent may potentially be more potent than an agent that inhibits either PI3K kinase or mTOR kinase. By inhibiting mTOR to a lesser extent than PI3K, PQR309 does not interfere with the mTOR-mediated negative feedback loop on PI3K signaling. Blocking the negative feedback loop would potentially increase PI3K signaling and decrease therapeutic efficacy.

A water soluble, small-molecule prodrug containing the pan-PI3K/mTOR inhibitor LY294002/SF1101 conjugated to the RGD-containing tetra-peptide SF1174 with potential antineoplastic and antiangiogenic activities. The targeting peptide SF1174 moiety of pan-PI3K/mTOR inhibitor SF1126 selectively binds to cell surface integrins and, upon cell entry, the agent is hydrolyzed to the active drug SF1101; SF1101 selectively inhibits all isoforms of phosphoinositide-3-kinase (PI3K) and other members of the PI3K superfamily, such as the mammalian target of rapamycin (mTOR) and DNA-PK. By inhibiting the PI3K signaling pathway, this agent may inhibit tumor cell and tumor endothelial cell proliferation and survival. Integrins are transmembrane cell adhesion proteins expressed on the surfaces of endothelial and tumor cells.

An orally available, small molecule and selective ATP-competitive pan-inhibitor of proviral integration sites for Moloney murine leukemia virus (PIM) kinases, with potential antineoplastic activity. Upon oral administration, pan-PIM kinase inhibitor INCB053914 binds to and inhibits the activities of the three PIM isoforms, PIM1, PIM2 and PIM3. This prevents phosphorylation of their downstream targets and inhibits proliferation in cells that overexpress PIMs. PIMs, constitutively active proto-oncogenic serine/threonine kinases upregulated in various types of cancers, play key roles in tumor cell proliferation and survival.

An orally available, small molecule inhibitor of PIM kinases with potential antineoplastic activity. Pan-PIM kinase inhibitor AZD1208 inhibits the activities of PIM1, PIM2 and PIM3 serine/threonine kinases, which may result in the interruption of the G1/S phase cell cycle transition, thereby causing cell cycle arrest and inducing apoptosis in cells that overexpress PIMs. The growth inhibition of several leukemia cell lines by this agent is correlated with the expression levels of PIM1, which is the substrate of STAT transcription factors. PIM kinases are downstream effectors of many cytokine and growth factor signaling pathways and are upregulated in various malignancies.

An orally available inhibitor of all members of the serine/threonine protein kinase Raf family, with potential antineoplastic activity. Upon administration, pan-RAF inhibitor LXH254 binds to Raf proteins and inhibits Raf-mediated signal transduction pathways. This inhibits proliferation of Raf-overexpressing tumor cells. Raf protein kinases are critical enzymes in the Ras/Raf/MEK/ERK signaling pathway and are upregulated in a variety of cancer cell types. They play key roles in tumor cell proliferation and survival.

An orally available inhibitor of all members of the serine/threonine protein kinase Raf family, including A-Raf, B-Raf and C-Raf protein kinases, with potential antineoplastic activity. Upon administration, pan-RAF kinase inhibitor LY3009120 inhibits Raf-mediated signal transduction pathways, which may inhibit tumor cell growth. Raf protein kinases play a key role in the RAF/mitogen-activated protein kinase kinase (MEK)/extracellular signal-regulated kinase (ERK) signaling pathway, which is often dysregulated in human cancers and plays a key role in tumor cell proliferation and survival.

An orally available inhibitor of the serine/threonine protein kinase family Raf, including A-Raf, B-Raf and C-Raf, with potential antineoplastic activity. Upon administration, pan-RAF kinase inhibitor CCT3833 inhibits Raf-mediated signal transduction pathways, which may inhibit the proliferation of Raf-overexpressing tumor cells. Raf protein kinases play a key role in the RAF/mitogen-activated protein kinase kinase (MEK)/extracellular signal-regulated kinase (ERK) signaling pathway, which is often dysregulated in human cancers and plays a key role in tumor cell proliferation and survival. Check for active clinical trials using this agent.

An orally available inhibitor of A-Raf, B-Raf and C-Raf protein kinases, with potential antineoplastic activity. Upon administration, pan-RAF kinase inhibitor TAK-580 inhibits Raf-mediated signal transduction pathways, which may inhibit tumor cell growth. Raf protein kinases play a key role in the RAF/MEK/ERK signaling pathway, which is often deregulated in human cancers and plays a key role in tumor cell proliferation and survival.

Brand name for alitretinoin

A synthetic, glycomimetic molecule and pan-selectin antagonist, with potential use in a vaso-occlusive crisis. Upon administration, GMI-1070 prevents the interaction between leukocytes and the endothelium and may prevent cell activation and adhesion. By preventing selectin-mediated cell adhesion in sickle cell anemia, this agent may inhibit red blood cell-white blood cell interactions, normalize blood flow and reduce inflammation and vascular occlusive pain. GMI-1070 has the strongest antagonistic activity towards E-selectin but the incorporation of a sulfate-binding domain allows for interactions with P- and L-selectins. Selectins, containing lectin- and EGF-like domains, are a family of cell adhesion molecules implicated in inflammatory processes and cancer. Check for active clinical trials using this agent.

The sodium salt form of a substituted benzimidazole with proton pump inhibitor activity. Pantoprazole is a lipophilic, weak base that crosses the parietal cell membrane and enters the acidic parietal cell canaliculus where it becomes protonated, producing the active metabolite sulfenamide, which forms an irreversible covalent bond with two sites of the H+/K+-ATPase enzyme located on the gastric parietal cell, thereby inhibiting both basal and stimulated gastric acid production.

An orally bioavailable, selective pan-tropomyosin-related-kinase (tyrosine receptor kinase; TRK) inhibitor, with potential antineoplastic activity. Upon oral administration, ONO-7579 specifically targets and binds to TRK and fusion proteins containing sequences from neurotrophic tyrosine receptor kinase (NTRK) types 1 (NTRK1; TrkA), 2 (NTRK2; TrkB), and 3 (NTRK3; TrkC). This inhibits neurotrophin-TRK interaction and TRK activation, thereby preventing the activation of downstream signaling pathways and resulting in both the induction of cellular apoptosis and the inhibition of cell growth in tumors that overexpress TRK and/or express NTRK fusion proteins. TRK, a family of receptor tyrosine kinases (RTKs) activated by neurotrophins, is encoded by NTRK family genes.The expression of either mutated forms of, or fusion proteins involving, NTRK family members results in uncontrolled TRK signaling, which plays an important role in tumor cell growth, survival, invasion and treatment resistance.

An orally bioavailable, selective pan-tropomyosin-related-kinase (tyrosine receptor kinase; TRK) inhibitor, with potential antineoplastic activity. Upon oral administration, ONO-7579 specifically targets and binds to TRK and fusion proteins containing sequences from neurotrophic tyrosine receptor kinase (NTRK) types 1 (NTRK1; TrkA), 2 (NTRK2; TrkB), and 3 (NTRK3; TrkC). This inhibits neurotrophin-TRK interaction and TRK activation, thereby preventing the activation of downstream signaling pathways and resulting in both the induction of cellular apoptosis and the inhibition of cell growth in tumors that overexpress TRK and/or express NTRK fusion proteins. TRK, a family of receptor tyrosine kinases (RTKs) activated by neurotrophins, is encoded by NTRK family genes. The expression of either mutated forms of, or fusion proteins involving, NTRK family members results in uncontrolled TRK signaling, which plays an important role in tumor cell growth, survival, invasion and treatment resistance.

Brand name for falimarev

Brand name for inalimarev

An orally bioavailable inhibitor of vascular endothelial growth factor receptor (VEGFR) and Tie2 receptor tyrosine kinases with potential antiangiogenic and antineoplastic activities. Pan-VEGFR/Tie2 tyrosine kinase inhibitor CEP-11981 selectively binds to VEGFR and Tie2 receptor tyrosine kinases, which may result the inhibition of endothelial cell migration, proliferation and survival and the inhibition of tumor cell proliferation and tumor cell death. VEGFR and Tie2 are frequently overexpressed by a variety of tumor cell types and play crucial roles in the regulation of angiogenesis and the maintenance of tumor blood vessels. Tie2 (tyrosine kinase with immunoglobulin-like and EGF-like domains) is activated by angiopoietin-1 (Ang-1).

Brand name for warfarin sodium

Brand name for 2-methoxyestradiol

The hydrochloride salt of the opiate alkaloid isolated from the plant Papaver somniferum and produced synthetically. As a direct-acting smooth muscle relaxant, papaverine is not closely related to the other opium alkaloids in structure or pharmacological actions; its mechanism of action may involve the non-selective inhibition of phosphodiesterases and direct inhibition of calcium channels. This agent also exhibits antiviral activity against respiratory syncytial virus, cytomegalovirus, and HIV.

Brand name for chlorzoxazone

A recombinant form of a mature, N-terminal secretory peptide derived from a parathyroid hormone-related protein (PTHrP) preprohormone through posttranslational endoproteolytic processing with vasodilating, myorelaxant, and parathyroid hormone (PTH)-like calciotropic activities. Expressed throughout the cardiovascular system, parathyroid hormone-related protein (1-36) [PTHrP (1-36)] was first identified as the PTH-like hypercalcemic factor of humoral hypercalcemia of malignancy; however, its sequence differs significantly from that of PTH (1-34) although both proteins share the same N-terminal end which accounts for the calciotropic activity. Both PTHrP (1-36) and PTH (1-34) bind to the type 1 parathyroid hormone receptor (PTH1R), a specific seven-transmembrane-helix-containing G protein-coupled receptor mainly located in bone and kidney cells.

A low-molecular-weight organic compound with potential antineoplastic activity. Upon intra-tumoral injection, para-toluenesulfonamide increases lysosomal membrane permeabilization (LMP) and the release of cathepsin B. Cytosolic cathepsin B released from lysosomes cleaves and activates proapoptotic B-cell lymphoma 2 (Bcl-2) family member BH3 interacting-domain death agonist (Bid) and poly [ADP-ribose] polymerase 1 (PARP-1), which may induce tumor cell death.

A water-soluble, injectable sodium salt form of parecoxib, an amide prodrug of the cyclooxygenase II (COX-2) selective, non-steroidal anti-inflammatory drug (NSAID) valdecoxib, with anti-inflammatory, analgesic, and antipyretic activities. Upon intravenous or intramuscular administration, parecoxib is hydrolyzed by hepatic carboxyesterases to its active form, valdecoxib. Valdecoxib selectively binds to and inhibits COX-2. This prevents the conversion of arachidonic acid into prostaglandins, which are involved in the regulation of pain, inflammation, and fever. This NSAID does not inhibit COX-1 at therapeutic concentrations and, therefore, does not interfere with blood coagulation.

A synthetic noncalcemic, nonphosphatemic vitamin D analogue. Paricalcitol binds to the vitamin D receptor and has been shown to reduce parathyroid hormone (PTH) levels. This agent also increases the expression of PTEN ('Phosphatase and Tensin homolog deleted on chromosome Ten'), a tumor-suppressor gene, in leukemic cells and cyclin-dependent kinase inhibitors, resulting in tumor cell apoptosis and tumor cell differentiation into normal phenotypes.

Brand name for bromocriptine mesylate

Brand name for tranylcypromine sulfate

The sulfate salt form of paromomycin, a structural derivative of neomycin, an aminoglycoside antibiotic with amebicidal and bactericidal effects against predominantly aerobic gram-negative bacteria. Paromomycin binds specifically to the RNA oligonucleotide at the A site of bacterial 30S ribosomes, thereby causing misreading and premature termination of translation of mRNA and inhibition of protein synthesis followed by cell death.

The hydrochloride salt form of paroxetine, a phenylpiperidine derivative and a selective serotonin reuptake inhibitor (SSRI) with antidepressant and anxiolytic properties. Paroxetine binds to the pre-synaptic serotonin transporter complex resulting in negative allosteric modulation of the complex thereby blocking reuptake of serotonin by the pre-synaptic transporter. Inhibition of serotonin recycling enhances serotonergic function through serotonin accumulation in the synaptic cleft, resulting in long-term desensitization and downregulation of 5HT1 (serotonin) receptors and leading to symptomatic relief of depressive illness.

An orally available small molecule inhibitor of the nuclear enzymes poly (ADP-ribose) polymerase (PARP) 1 and 2, with potential antineoplastic activity. Upon administration, E7449 selectively binds to PARP 1 and 2, thereby preventing the repair of damaged DNA via the base excision repair (BER) pathway. This agent enhances the accumulation of single and double strand DNA breaks and promotes genomic instability eventually leading to apoptosis. PARP 1/2 inhibitor E7449 may enhance the cytotoxicity of DNA-damaging agents and of radiotherapy. PARP catalyzes post-translational ADP-ribosylation of nuclear proteins that signal and recruit other proteins to repair damaged DNA. Check for active clinical trials using this agent.

An orally available small molecule inhibitor of the nuclear enzymes poly (ADP-ribose) polymerase (PARP) 1 and 2, with potential antineoplastic activity. Upon administration, NOV1401 selectively binds to PARP-1 and -2, thereby preventing PARP-1 and -2-mediated DNA repair. This promotes genetic instability and enhances the accumulation of single and double strand DNA breaks, ultimately leading to apoptosis. The PARP family of proteins catalyzes post-translational ADP-ribosylation of nuclear proteins and is activated by single-strand DNA (ssDNA) breaks.

An orally bioavailable inhibitor of the nuclear enzyme poly(ADP-ribose) polymerase (PARP), with potential antineoplastic activity. PARP inhibitor BGB-290 selectively binds to PARP and prevents PARP-mediated repair of single-strand DNA breaks via the base-excision repair (BER) pathway. This enhances the accumulation of DNA strand breaks, promotes genomic instability, and eventually leads to apoptosis. PARP is activated by single-strand DNA breaks and, subsequently, catalyzes post-translational ADP-ribosylation of nuclear proteins which then transduce signals to recruit other proteins to repair damaged DNA. BGB-290 may both potentiate the cytotoxicity of DNA-damaging agents and reverse tumor cell chemo- and radioresistance.

A small-molecule prodrug of CEP-8983, a novel 4-methoxy-carbazole inhibitor of the nuclear enzymes poly(ADP-ribose) polymerase (PARP) 1 and 2, with potential antineoplastic activity. Upon administration and conversion from CEP-9722, CEP-8983 selectively binds to PARP 1 and 2, preventing repair of damaged DNA via base excision repair (BER). This agent enhances the accumulation of DNA strand breaks and promotes genomic instability and apoptosis. CEP-8983 may potentiate the cytotoxicity of DNA-damaging agents and reverse tumor cell chemo- and radioresistance. PARP catalyzes post-translational ADP-ribosylation of nuclear proteins that signal and recruit other proteins to repair damaged DNA and can be activated by single strand breaks in DNA.

An inhibitor of the nuclear enzyme poly(ADP-ribose) polymerase (PARP) with potential chemo- and/or radiosensitizing activity. PARP inhibitor E7016 selectively binds to PARP and prevents PARP-mediated DNA repair of single strand DNA breaks via the base-excision repair pathway. This enhances the accumulation of DNA strand breaks and promotes genomic instability and eventually leads to apoptosis. In addition, this agent may enhance the cytotoxicity of DNA-damaging agents and reverse tumor cell resistance to chemotherapy and radiation therapy. PARP catalyzes post-translational ADP-ribosylation of nuclear proteins that signal and recruit other proteins to repair damaged DNA and is activated by single-strand DNA breaks.

An orally available inhibitor of the nuclear enzymes poly(ADP-ribose) polymerase (PARP) 1 and 2, with potential antineoplastic activity. Upon administration, ABT-767 selectively binds to PARP 1 and 2, thereby preventing repair of damaged DNA via the base excision repair (BER) pathway. This agent enhances the accumulation of DNA strand breaks and promotes genomic instability eventually leading to apoptosis. ABT-767 may enhance the cytotoxicity of DNA-damaging agents and reverse tumor cell chemo- and radioresistance. PARP catalyzes post-translational ADP-ribosylation of nuclear proteins that signal and recruit other proteins to repair damaged DNA and can be activated by single strand DNA (ssDNA) breaks.

Brand name for etelcalcetide

Partially or closely human leukocyte antigen (HLA)-matched allogeneic cytotoxic T lymphocytes (CTLs), derived from cell lines, specifically reactive to the three human viruses adenovirus (AdV), cytomegalovirus (CMV) and Epstein-Barr virus (EBV), with potential antiviral activity. Upon infusion of the partially HLA-matched AdV/CMV/EBV-specific allogeneic T lymphocytes in immunocompromised patients or upon allogeneic hematopoietic stem cell transplantation (HSCT) in an immunodeficient recipient, these CTLs may kill AdV, CMV, and/or EBV-infected cells, and may prevent or reduce the severity of viral infections by these pathogens.

Brand name for parvovirus H-1

A replication-competent oncolytic parvovirus with potential antineoplastic activity. Upon infection of host cells, parvovirus H-1 preferentially replicates in tumor cells compared to healthy normal cells, thereby potentially resulting in tumor cell lysis and leading to an inhibition of tumor cell proliferation. In addition, H1-infected tumor cells strongly induce the release of the inducible heat shock protein 72 (Hsp72i), which chaperone tumor associated antigens in the H1-mediated tumor lysates and may activate antigen presenting cells (APCs), thereby leading to antitumor immune responses. Parvovirus H-1 does not cause any pathogenic effect in normal, healthy cells and is able to cross the blood brain barrier (BBB).

A synthetic long-acting cyclic peptide with somatostatin-like activity. Pasireotide activates a broad spectrum of somatostatin receptors, exhibiting a much higher binding affinity for somatostatin receptors 1, 3, and 5 than octreotide in vitro, as well as a comparable binding affinity for somatostatin receptor 2. This agent is more potent than somatostatin in inhibiting the release of human growth hormone (HGH), glucagon, and insulin.

A synthetic dye with imaging and food coloring property. It is a sodium or calcium salt of [4-(alpha-(4-diethylaminophenyl)-5-hydroxy- 2,4-disulfophenyl-methylidene)-2,5-cyclohexadien-1-ylidene] diethylammonium hydroxide inner salt. Patent blue V dye is used in sentinel lymph node (SLN) technique to guide nodal dissection or other imaging procedures.

An orally bioavailable, cyclopamine-derived inhibitor of the Hedgehog (Hh) pathway with potential antineoplastic activity. Specifically, patidegib binds to and inhibits the cell membrane-spanning G-protein coupled receptor SMO, which may result in the suppression of Hh pathway signaling and a decrease in tumor cell proliferation and survival. SMO is activated upon binding of Hh ligand to the cell surface receptor Patched (PTCH); inappropriate activation of Hh signaling and uncontrolled cellular proliferation may be associated with SMO mutations. The Hh signaling pathway plays an important role in proliferation of neuronal precursor cells in the developing cerebellum and other tissues.

A patient-specific cancer vaccine directed against the soluble protein idiotype of an individual follicular lymphoma with potential antineoplastic activity. A patient-specific follicular lymphoma-derived anti-idiotype vaccine may be composed of a patient-specific, synthetic idiotype-related peptide (such as one corresponding to a hypervariable region of an IgG heavy chain) conjugated to the immunostimulant carrier protein keyhole limpet hemocyanin (KLH). Upon administration, this vaccine may induce an idiotype-specific cytotoxic T-lymphocyte (CTL) response against follicular lymphoma cells expressing the idiotype, resulting in tumor cell lysis.

Brand name for anti-transthyretin siRNA ALN-TTR02

A fully human monoclonal antibody directed against the membrane-bound receptor HER3 (ERBB3) with potential antineoplastic activity. Patritumab binds to and inhibits HER3 activation, which may result in inhibition of HER3-dependent PI3K/Akt signaling and so inhibition of cellular proliferation and differentiation. HER3, a member of the epidermal growth factor receptor (EGFR) family of receptor tyrosine kinases, is frequently overexpressed in solid tumors, including breast, lung, and colorectal tumors of epithelial origin; it has no active kinase domain itself but is activated through heterodimerization with other members of the EGFR receptor family that do. Check for active clinical trials using this agent.

A compound isolated from the myxobacterium Sorangium cellulosum. Similar to paclitaxel, patupilone induces microtubule polymerization and stabilizes microtubules against depolymerization conditions. In addition to promoting tubulin polymerization and stabilization of microtubules, this agent is cytotoxic for cells overexpressing P-glycoprotein, a characteristic that distinguishes it from the taxanes. Epothilone B may cause complete cell-cycle arrest.

Brand name for papaverine hydrochloride

Brand name for paroxetine hydrochloride

The hydrochloride salt of a small molecule inhibitor of multiple protein tyrosine kinases with potential antineoplastic activity. Pazopanib selectively inhibits vascular endothelial growth factor receptors (VEGFR)-1, -2 and -3, c-kit and platelet derived growth factor receptor (PDGF-R), which may result in inhibition of angiogenesis in tumors in which these receptors are upregulated.

A vaccine composed of a phosphorylated peptide from the tumor-associated antigen breast cancer anti-estrogen resistance-3 (BCAR3) and a tetanus-derived peptide, with potential immunomodulating and antineoplastic activities. Upon administration of pBCAR3 phosphopeptide-tetanus peptide vaccine, the pBCAR3 phosphopeptide may stimulate the immune system to mount a cytotoxic T-lymphocyte (CTL) response against phosphopeptide-containing tumor cells. The tetanus peptide serves as an immunoadjuvant and induces a helper T-cell response, which may help stimulate an immune response against the pBCAR3-expressing melanoma tumor cells. BCAR3 is upregulated in a variety of cancer cells.

A vaccine composed of phosphorylated peptides from the tumor associated antigens breast cancer anti-estrogen resistance-3 (BCAR3) and insulin receptor substrate-2 (IRS2) and a tetanus-derived peptide, with potential immunomodulating and antineoplastic activities. Upon administration of pBCAR3/pIRS2 phosphopeptide-tetanus peptide vaccine, the pBCAR3/pIRS2 phosphopeptide may stimulate the immune system to mount a cytotoxic T-lymphocyte (CTL) response against tumor cells expressing either phosphopeptide. The tetanus peptide serves as an immunoadjuvant and induces a helper T-cell response which may help stimulate an immune response against pBCAR3 and pIRS2-expressing melanoma tumor cells. BCAR3 and IRS2 are upregulated in a variety of cancer cells.

A proprietary RNA interference construct consisting of bifunctional short hairpin RNAs (shRNA) against human stathmin 1 (STMN1) encapsulated in the cationic bilamellar invaginated vesicle lipoplex (LP) with potential antineoplastic activity. pbi-shRNA STMN1 LP contains 2 stem-loop structures encoded by a plasmid vector. Upon intratumoral administration, one shRNA unit with a perfectly matched sequence renders the suppression of STMN1 mRNA translation (mRNA sequestration and cleavage-independent degradation) while the other unit with an imperfectly matched sequence renders STMN1 mRNA degradation via RNase H-like cleavage (cleavage-dependent mRNA silencing). The suppression of STMN1 expression in tumor cells results in a reduction of tumor cell proliferation. STMN1, a ubiquitous cytosolic phosphoprotein and tubulin modulator that plays a key role in mitosis, is overexpressed in a variety of tumors and correlates with poor prognosis.

A disulfonyl derivative of phenyl-tert-butyl nitrone (PBN), with potential anti-glioma activity. Although the exact mechanism(s) of action of OKN007 are still largely unknown, this agent appears to inhibit cancer cell proliferation and migration. This agent appears to inhibit the activity of sulfatase 2 (SULF2), a highly specific endoglucosamine-6-sulfatase that is overexpressed in the extracellular matrix of cancer cells and catalyzes the removal of sulfate from the 6-O-sulfate esters of heparin. In addition, OKN007 may induce changes in tumor metabolism and scavenge free radicals.

Peripheral blood T-lymphocytes (PBTLs) transduced with a retroviral vector expressing a chimeric antigen receptor (CAR) consisting of an anti-CD19 scFv (single chain variable fragment) coupled to the costimulatory signaling domain CD28, the signaling domain of 4-1BB (CD137), and the zeta chain of the T-cell receptor (TCR), with potential immunomodulating and antineoplastic activities. Upon transfusion, PBTL CD19CAR-28/CD137zeta directs the T-lymphocytes to CD19-expressing tumor cells and induces selective toxicity in CD19-expressing tumor cells. CD28, a T-cell surface-associated co-stimulatory molecule, is required for full T-cell activation, proliferation, and survival. The 4-1BB co-stimulatory molecule signaling domain enhances activation and signaling after recognition of CD19. Furthermore, inclusion of the 4-1BB signaling domain may increase the antitumor activity compared to the inclusion of the CD28 costimulatory domain and TCR zeta chain alone. CD19 antigen is a B-cell specific cell surface antigen, which is expressed in all B-cell lineage malignancies.

An agent that inhibits p-cadherin (cdh3), with potential antineoplastic activity. PF-03732010 binds to and inhibits the activity of p-cadherin. Inhibition of the activity of p-cadherin may inhibit tumor cell invasion and proliferation in p-cadherin expressing tumor cells. P-cadherin, a cell-surface protein and member of the cadherin family, is overexpressed in a variety of solid tumors, and plays a role in cell adhesion, motility, invasion and proliferation.

An agent that inhibits p-cadherin, with potential antineoplastic activity. Upon intravenous infusion, PCA062 binds to and inhibits the activity of p-cadherin. Inhibition of the activity of p-cadherin may inhibit both invasion and proliferation of p-cadherin expressing tumor cells. P-cadherin, a cell-surface protein and member of the cadherin family, is overexpressed in a variety of tumors and plays a role in cell adhesion, motility, invasion, and proliferation.

An agent that targets p-cadherin (CDH3), with potential antineoplastic activity. Upon administration, PF-06671008 binds to and inhibits the activity of p-cadherin; this may inhibit both invasion and proliferation of p-cadherin-expressing tumor cells. P-cadherin, a cell-surface protein and member of the cadherin family, is overexpressed in a variety of tumors and plays a role in cell adhesion, motility, invasion, and proliferation.

A regimen consisting of procarbazine, lomustine and vincristine used for the treatment of gliomas.

An orally bioavailable, synthetic organic molecule targeting mitogen-activated protein kinase kinase (MAPK/ERK kinase or MEK) with potential antineoplastic activity. MEK inhibitor PD325901, a derivative of MEK inhibitor CI-1040, selectively binds to and inhibits MEK, which may result in the inhibition of the phosphorylation and activation of MAPK/ERK and the inhibition of tumor cell proliferation. The dual specific threonine/tyrosine kinase MEK is a key component of the RAS/RAF/MEK/ERK signaling pathway that is frequently activated in human tumors.

A population of engineered autologous T lymphocytes in which the gene encoding for the programmed cell death protein 1 (PDCD-1) is deleted, with potential immunomodulating activity. Following collection of peripheral blood lymphocytes and selection of T cells, the PDCD-1 gene was knocked out and the T cells were expanded. Upon reinfusion of the PDCD-1 knockout T lymphocytes, these T cells target and lyse cancer cells. The PDCD-1 protein, found on activated T cells and often overexpressed on T cells in cancer patients, negatively regulates T-cell activity; it plays a key role in immune evasion and prevents tumor cell lysis. PDCD-1 knockout enhances cytotoxicity and T-cell-mediated anti-tumor immune responses.

A preparation of Epstein-Barr virus (EBV) reactive cytotoxic T lymphocytes (CTLs) in which the programmed cell death 1 (PD-1; PDCD1; CD279; programmed death-1) gene is deleted, with potential immunomodulating activity. Upon administration of the PD-1 knockout EBV-specific CTLs, these CTLs target and induce selective toxicity in EBV-positive cancer cells. This results in cell lysis and inhibition of cancer cell proliferation. Expression of PD-1, an inhibitory receptor expressed on activated T cells, plays a key role in CTL suppression, T-cell exhaustion and CTL apoptosis. PD-1 knockout abrogates T-cell exhaustion and increases T-cell activity and cytotoxicity. EBV, a ubiquitous human herpesvirus, is associated with various cancer cell types.

An orally bioavailable, small-molecule, celecoxib-derived inhibitor of phosphoinositide-dependent kinase-1 (PDK1) with potential antineoplastic activity. Devoid of any COX inhibiting activity, PDK1 inhibitor AR-12 binds to and inhibits the phosphorylation of 3-phosphoinositide-dependent kinase-1 (PDK-1).; subsequently, the phosphorylation and activation of the serine/threonine protein kinase Akt (protein kinase B or PKB) is inhibited, which may result in inhibition of the PI3K/Akt signaling pathway, inhibition of tumor cell proliferation, and the induction of tumor cell apoptosis. In addition, this agent appears to induce the activity of protein kinase R-like endoplasmic reticulum kinase (PERK), which plays a key role in the endoplasmic reticulum stress pathway. Activation and dysregulation of the PI3K/Akt signaling pathway is frequently associated with tumorigenesis and dysregulated PI3K/Akt signaling may contribute to tumor resistance to a variety of antineoplastic agents.

A vaccine composed of a peptide derived from the tumor-associated antigen (TAA) and immune checkpoint molecule programmed cell death-1 ligand 1 (PD-L1) combined with the immunoadjuvant montanide ISA-51, with potential immunomodulating and antineoplastic activities. Vaccination with PD-L1 peptide vaccine may activate the immune system to induce an immune response against PD-L1-expressing cells. This may increase and restore the proliferation and activation of various immune cells, including cytotoxic T lymphocytes (CTLs), and may eradicate PD-L1-expressing tumor cells. PD-L1 is overexpressed on many human cancer cell types as well as on antigen presenting cells (APCs) and immunosuppressive cells in the tumor micro-environment (TME), such as regulatory T cells (Tregs). PD-L1 binding to its cognate receptor programmed cell death protein 1 (PD-1; PDCD1; CD279) on T cells suppresses the immune system and results in increased immune evasion and decreased CTL activation. Montanide ISA-51, also known as incomplete Freund's adjuvant or IFA, is a stabilized water-in-oil emulsion adjuvant containing mineral oil with mannide oleate added as a surfactant that non-specifically stimulates cell-mediated immune responses to antigens.

A peptide vaccine composed of IO103, a peptide vaccine derived from the tumor-associated antigen (TAA) programmed cell death-1 ligand 1 (PD-L1), IO102, the 21-mer peptide vaccine derived from the immunomodulatory enzyme indoleamine 2,3-dioxygenase (IDO), and the immunoadjuvant montanide ISA-51, with potential immunomodulating and antineoplastic activities. Vaccination with the PD-L1/IDO peptide vaccine may activate the immune system to induce an immune response against PD-L1 and IDO-expressing cells. This may increase and restore the proliferation and activation of various immune cells, including cytotoxic T lymphocytes (CTLs), and may eradicate PD-L1 and IDO-expressing tumor cells through a CTL-mediated immune response. PD-L1 is overexpressed on many human cancer cell types. PD-L1 binding to its cognate receptor programmed cell death protein 1 (PD-1; PDCD1; CD279) on T-cells suppresses the immune system and results in increased immune evasion and decreased CTL activation. IDO, a cytosolic enzyme responsible for tryptophan catabolism and conversion of tryptophan into kynurenine, is overexpressed by a variety of tumor cell types and antigen presenting cells (APCs) and plays an important role in immunosuppression mainly through suppression of CTL activation; tryptophan depletion inhibits T-lymphocyte proliferation and activation, and suppresses the immune system. Montanide ISA-51, also known as incomplete Freund's adjuvant or IFA, is a stabilized water-in-oil emulsion adjuvant containing mineral oil with mannide oleate added as a surfactant that non-specifically stimulates cell-mediated immune responses to antigens.

A vaccine composed of peptides derived from the immune checkpoint molecules, programmed death ligand 1 (PD-L1) and programmed death ligand 2 (PD-L2), combined with the immunoadjuvant montanide ISA-51, with potential immunomodulating and antineoplastic activities. Vaccination with PD-L1/PD-L2 peptide-montanide vaccine may stimulate an immune response against PD-L1 and PD-L2 expressing cells. This may enhance T-cell proliferation, cytokine production, and T-cell mediated cytolysis. Binding of programmed cell death protein 1 (PD-1; PDCD1; CD279) by its ligands, PD-L1 and PD-L2, results in downregulation of T-cell responses and enhanced immune evasion. Montanide ISA-51, also known as incomplete Freund's adjuvant or IFA, is a stabilized water-in-oil emulsion adjuvant containing mineral oil with mannide oleate added as a surfactant that non-specifically stimulates cell-mediated immune responses to antigens.

An orally bioavailable small molecule inhibitor of the immune checkpoint regulatory proteins programmed cell death ligand-1 (PD-L1; B7-H1; CD274), PD-L2, and V-domain immunoglobulin (Ig) suppressor of T-cell activation (VISTA; programmed death 1 homolog; PD1H; PD-1H), with potential negative immune checkpoint regulatory and antineoplastic activities. Upon oral administration, PD-L1/PD-L2/VISTA antagonist CA-170 targets and binds to PD-L1, PD-L2 and VISTA. This inhibits PD-L1/PD-L2/VISTA-mediated signaling, abrogates the PD-L1-, PD-L2- and VISTA-induced suppression of T-lymphocyte immune responses, enhances cytotoxic T-cell proliferation and activation against tumor cells, increases cytokine production by T-cells, and inhibits tumor cell growth. PD-L1, PD-L2 and VISTA, negative checkpoint molecules of immune activation, play key roles in the suppression of T-cell functions.

A vaccine composed of a peptide derived from the immune checkpoint molecule programmed death ligand 2 (PD-L2) combined with the immunoadjuvant montanide ISA-51, with potential immunomodulating and antineoplastic activities. Vaccination with PD-L2 peptide-montanide vaccine may mount an immune response against PD-L2 expressing cells. This may enhance T-cell proliferation, cytokine production, and T-cell mediated cytolysis. PD-L2 binding to its cognate receptor, programmed cell death protein 1 (PD-1; PDCD1; CD279), downregulates T-cell responses and enhances immune evasion. Montanide ISA-51, also known as incomplete Freund's adjuvant or IFA, is a stabilized water-in-oil emulsion adjuvant containing mineral oil with mannide oleate added as a surfactant that non-specifically stimulates cell-mediated immune responses to antigens.

A whole cell cancer vaccine composed of irradiated autologous whole tumor cells that are transfected, ex vivo, with a plasmid DNA encoding the highly immunogenic Streptococcus pyogenes (S. pyogenes) bacterial antigen Emm55, with potential immunostimulating and antineoplastic activities. Upon intralesional administration of IFx-Hu2.0, the tumor cells expressing the Emm55 bacterial antigen on their cell surface are taken up and processed by antigen-presenting cells (APCs), thereby presenting both the Emm55 and the patient-specific tumor-associated antigens (TAAs) to the immune system. This activates the immune system to elicit a tumor antigen-specific cytotoxic T-lymphocyte (CTL)-mediated immune response against the tumor cells expressing the TAAs.

A fusion protein consisting of a peptide sequence of human papillomavirus (HPV) type 16 E7 nuclear protein and fused to the Pseudomonas aeruginosa exotoxin A (PE) and a endoplasmic reticulum (ER) retention signal (KDEL), with potential antineoplastic activity. Upon administration of PE/HPV16 E7/KDEL fusion protein TVGV-1, the PE moiety binds to CD91 (LRP1) expressed on a variety of cells, including antigen-presenting cells such as dendritic cells (DCs), which facilitates the internalization, through endocytosis, of TVGV-1. Following endocytosis, this agent is proteolytically cleaved by the proteosome and the epitopes from the HPV E7 protein become bound to MHC-I molecules and are presented on the DC-cell surface. This facilitates a cytotoxic T-cell-mediated immune response against HPV16 E7 expressing-tumor cells. KDEL targets the fusion protein to the ER, which increases this agent's potential to be bound by MHC-I molecules; this increases the immune response against HPV16 E7-expressing cancer cells. Check for active clinical trials using this agent.

A chemotherapy regimen consisting of bleomycin, etoposide and cisplatin used for the treatment of pediatric germ cell tumors (GCT). In the PEB regimen, the pediatric patients receive bleomycin once per cycle and do not receive weekly bleomycin during the weeks between cycles (every 21 days); in the adult BEP regimen, patients receive weekly bleomycin.

Brand name for modified citrus pectin supplement

Brand name for diphtheria toxoid/tetanus toxoid/acellular pertussis adsorbed, recombinant hepatitis B/inactivated poliovirus vaccine combined

Brand name for nutritional supplement drink (pediatric)

Brand name for Haemophilus influenzae b vaccine

A preparation containing the nonabsorbable polymer polyethylene glycol (PEG or macrogol) 3350 and sodium sulfate, sodium chloride, potassium chloride, sodium ascorbate and ascorbic acid with laxative activity. Upon oral administration, the PEG-3350, sodium sulfate, sodium chloride, potassium chloride, sodium ascorbate and ascorbic acid-based laxative promotes the retention of water in the bowel. This increases the water content of stool, which results in increased gastrointestinal motility and evacuation of colonic contents. This results in a complete cleansing of the colon. Compared to the 4 liter PEG-3350-based preparations, this PEG-based laxative is a low volume (2 liter) preparation, which improves patients’ tolerance.

A complex of polyethylene glycol conjugated with L-asparaginase. Asparaginase hydrolyzes L-asparagine to L-aspartic acid and ammonia, thereby depleting these cells of asparagine and blocking protein synthesis and tumor cell proliferation, especially in the G1 phase of the cell cycle. The agent also induces apoptosis in tumor cells. Pegylation decreases the enzyme's antigenicity. Asparagine is critical to protein synthesis in leukemic cells, which cannot synthesize this amino acid due to the absence of the enzyme asparagine synthase.

Brand name for PEG-interferon alfa-2a

A preparation containing the nonabsorbable polymer polyethylene glycol (PEG or macrogol) 3350 with laxative activity. Upon oral administration, the PEG-3350-based laxative NER1006 promotes the retention of water in the bowel. This increases both the water content and volume of stool, which results in increased gastrointestinal motility and the evacuation of colonic contents leading to a complete cleansing of the colon. Compared to the 4 liter PEG-3350-based preparations, this PEG-based laxative is a low volume (2 liter) preparation, which may improve tolerance.

A formulation composed of an agonist of toll-like receptor (TLR) type 7 and 8 (TLR7/8) that is attached to polyethylene glycol (PEG) via a hydrolyzable glycine linker, with potential immunostimulating and antitumor activities. Upon intratumoral (IT) administration, TLR7/8 agonist NKTR-262 binds to and activates TLR7 and 8, thereby activating TLR7/8-mediated pathways. This stimulates the maturation and activation of antigen-presenting cells (APCs), including dendritic cells (DCs). Activation of DCs results in the production of pro-inflammatory cytokines, and the activation of cytotoxic T-lymphocyte (CTL)- and B-lymphocyte-mediated immune responses against tumor-associated antigens (TAAs), which lead to tumor cell lysis. TLR7 and 8, members of the TLR family, play fundamental roles in the activation of the innate immune system, myeloid cell responses and tumor antigen presentation. Pegylation of the TLR7/8 agonist enhances retention of this agent in the tumor microenvironment (TME), provides local sustained release of the TLR7/8 agonist, increases efficacy and reduces systemic exposure compared to the administration of the naked TLR7/8 agonist alone.

A highly specific, synthetic peptide vascular endothelial growth factor receptor-2 (VEGFR-2) antagonist with potential antiangiogenic activity. Derived from human fibronectin with a proprietary protein engineering process, pegdinetanib may block the activation of VEGFR-2 by all known activating ligands, thereby inhibiting the growth of new tumor blood vessels.

A long-acting pegylated form of a recombinant therapeutic agent which is chemically identical to or similar to an endogenous human granulocyte colony-stimulating factor (G-CSF). Produced endogenously by monocytes, fibroblasts, and endothelial cells, G-CSF binds to and activates specific cell surface receptors, stimulating neutrophil progenitor proliferation and differentiation and selected neutrophil functions. Conjugation of the cytokine with a branched polyethylene glycol molecule (pegylation) significantly increases its therapeutic half-life.

A long-acting, engineered and pegylated version of human granulocyte-colony stimulating factor (G-CSF), with potential hematopoietic activity. Similar to G-CSF, pegfilgrastim anti-neutropenic factor (ANF) binds to and activates specific cell surface receptors, and stimulates neutrophil progenitor proliferation and differentiation. Therefore, this agent may prevent the duration and incidence of chemotherapy-induced neutropenia. Compared to filgrastim, the conjugation with a branched polyethylene glycol molecule reduces renal clearance and increases its plasma half-life.

A biosimilar of pegfilgrastim, a long-acting pegylated form of recombinant human granulocyte colony-stimulating factor (G-CSF) filgrastim, with hematopoietic activity. In a similar manner to G-CSF, pegfilgrastim biosimilar LA-EP2006 binds to and activates specific cell surface receptors, stimulating neutrophil progenitor proliferation and differentiation and selected neutrophil functions. Therefore, this agent may prevent the incidence and shorten the duration of chemotherapy-induced neutropenia. Conjugation of the cytokine with a branched polyethylene glycol molecule significantly increases this agent's therapeutic half-life compared to filgrastim.

A covalent conjugate of recombinant interferon alfa, subtype 2a, and polyethylene glycol (PEG), used as an antiviral and antineoplastic agent. The biological activity of this agent is derived from its interferon alpha-2a protein moiety. Interferons alfa bind to specific cell-surface receptors, leading to the transcription and translation of genes whose protein products mediate antiviral, antiproliferative, anticancer and immune-modulating effects. The PEG moiety lowers the clearance of interferon alpha-2a, thereby extending the duration of its therapeutic effects, but may also reduce interferon-mediated stimulation of an immune response.

A covalent conjugate of recombinant interferon alpha, subtype 2b, and polyethylene glycol (PEG), used as an antiviral and antineoplastic agent. The biological activity of this agent is derived from its interferon alpha-2b protein moiety. Interferons alfa bind to specific cell-surface receptors, leading to the transcription and translation of genes whose protein products mediate antiviral, antiproliferative, anticancer, and immune-modulating effects. The PEG moiety lowers the clearance of interferon alpha-2b, thereby extending the duration of its therapeutic effects, but may also reduce the interferon-mediated stimulation of an immune response.

A complex of polyethylene glycol conjugated with human recombinant cytokine interleukin-2 (IL-2) with antineoplastic activity. PEG-interleukin-2 induces natural killer (NK) cell activity and the production of interferon-gamma (IFN-gamma), and enhances T cell-mediated cytotoxicity. Pegylation of IL-2 protects the cytokine from degradation.

Brand name for peginterferon alfa-2b

A proprietary 44-nucleotide L-stereoisomer RNA oligonucleotide conjugated to a 40 kDa polyethylene glycol (PEG) that targets hepcidin with potential anti-anemic activity. Upon intravenous or subcutaneous administration, PEG-linked L-RNA oligonucleotide hepcidin targeting agent NOX-H94 binds to hepcidin and prevents it from binding to the iron channel ferroportin, located on the basolateral surface of gastrointestinal enterocytes and the plasma membrane of macrophages. This prevents hepcidin-induced internalization and degradation of ferroportin, thus decreasing macrophage iron retention. In turn, binding of NOX-H94 to hepcidin normalizes plasma iron levels and increases erythropoiesis. This may inhibit anemia caused by inflammation. Hepcidin, a peptide hormone that plays a key role in the homeostasis of systemic iron, is upregulated during acute and chronic inflammation in response to cytokines. The unique mirror-image configuration of this agent renders it resistant to hydrolysis and shows a low antigenicity profile. Pegylation increases the half-life of this agent.

A synthetic peptide derived from erythropoietin (EPO) linked to polyethylene glycol (PEG), with erythropoietic stimulating activity. Upon administration, pegol sihematide binds to and activates EPO receptors on the surface of erythroid progenitor cells in the bone marrow resulting in their differentiation and proliferation. This increases the production of red blood cells and prevents anemia. Pegylation increases this agent's blood circulation time.

A nanoparticle-based formulation composed of a non-viral plasmid DNA vector encoding the human pro-inflammatory cytokine interleukin-12 (IL-12) encapsulated in a biodegradable, biocompatible lipoplex composed of polyethylene glycol (PEG), polyethylenimine (PEI), and cholesterol, with potential immuno-activating and antineoplastic activities. Upon intraperitoneal (IP) delivery of the PEG-PEI-cholesterol lipopolymer-encased IL-12 DNA plasmid vector GEN-1, the lipoplex is endocytosed by nearby cells, and the plasmid DNA is transported into the nucleus, which leads to local expression of IL-12. In turn, the increased IL-12 production at the tumor site activates the immune system by promoting the activation of natural killer cells (NKs), inducing secretion of interferon-gamma (IFN-g) and promoting cytotoxic T-cell responses against tumor cells.

A long-acting formulation of recombinant interferon alpha subtype 2b (IFN-a2b) protein, in which IFN-a2b is coupled, via proline, to polyethylene glycol (PEG), with antiviral, immunomodulating and antineoplastic activities. Upon subcutaneous administration, IFN-a2b binds to specific interferon cell-surface receptors. This activates interferon-mediated signal transduction pathways and induces the transcription and translation of genes with interferon-specific response elements (ISREs); the protein products mediate antiviral, antiproliferative, anticancer, and immune-modulating effects. The PEG moiety inhibits proteolytic breakdown and clearance of IFN-a2b, which prolongs its half-life, extends the duration of its therapeutic effects and allows less frequent dosing. The proline linker facilitates the synthesis of a predominant (90%) positional isomer which allows for further increases in stability and a longer half-life than previous PEG conjugates.

An analogue of pegfilgrastim, a recombinant, pegylated form of endogenous human granulocyte colony-stimulating factor (G-CSF), with hematopoietic activity. Similar to endogenous G-CSF, this agent binds to and activates specific cell surface receptors, and stimulates neutrophil progenitor proliferation, differentiation and selected neutrophil functions. Pegteograstim may prevent and shorten the duration of chemotherapy-induced neutropenia (CIN). Pegylation of teograstim increases the half-life of this agent.

A pegylated, recombinant, human growth hormone (GH) structural analog with GH receptor antagonist activity. As a GH analog, the structure of pegvisomant is similar to that of native GH with the exception of 9 amino acid substitutions. Pegvisomant selectively binds to GH receptors on cell surfaces, interfering with endogenous GH receptor binding and so GH signal transduction. Inhibition of GH signal transduction results in decreased serum concentrations of insulin-like growth factor-I (IGF-I), and other GH-responsive serum proteins, including IGF binding protein-3 (IGFBP-3) and the acid-labile subunit (ALS), and may inhibit the growth of cancers in which IGF-1 is upregulated.

A pegylated, cross-linked, humanized divalent-Fab' antibody fragment directed against vascular endothelial growth factor receptor-2 (VEGFR-2) with potential antiangiogenic and antitumor activities. Pegylated anti-GFR antibody fragment binds to and inhibits VEGFR-2, which may inhibit angiogenesis and tumor cell proliferation. Multivalent Fab' antibody fragments may exhibit improved retention and internalization properties compared to their parent IgGs.

An agent consisting of the arginine-degrading enzyme arginine deiminase combined with polyethylene glycol (20,000 MW) (ADI-PEG 20) with potential antineoplastic activity. Upon administration, arginine deiminase breaks down the amino acid arginine into citrulline. Although arginine is a nonessential amino acid for normal human cells, certain cancer cells are autotrophic for arginine and need arginine in order to survive. Depletion of arginine may lead to an inhibition of cellular proliferation in those cancer cells. ADI is coupled to PEG in order to enhance this agent's half-life.

A long-acting, pegylated recombinant variant of human granulocyte colony-stimulating factor (G-CSF) with immunomodulating activity. Pegylated granulocyte colony stimulating factor MAXY-G34 contains multiple non-naturally occurring lysines that have been introduced into alpha helixes of wild type human G-CSF as pegylation sites; other naturally occurring lysine residues have been removed to prevent pegylation and the variant G-CSF is pegylated with methoxypolyethylene glycol succinimidyl propionate (mPEG SPA) at three amino acid residues. Similar to endogenous G-CSF, this agent binds to and activates specific cell surface receptors, stimulating neutrophil progenitor proliferation and differentiation and selected neutrophil functions. A difference in the degree of pegylation may account for the extended half-life of this agent compared to pegfilgrastim which is pegylated at only one amino acid residue.

A covalent conjugate of recombinant interferon alpha and polyethylene glycol (PEG), used as an antiviral and antineoplastic agent. The biological activity of this agent is derived from its interferon alpha protein moiety. Interferons alfa bind to specific cell-surface receptors, leading to the transcription and translation of genes whose protein products mediate antiviral, antiproliferative, anticancer, and immune-modulating effects. The PEG moiety lowers the clearance of interferon alpha, thereby extending the duration of its therapeutic effects, but may also reduce interferon-mediated stimulation of an immune response.

A formulation of polyethylene glycol (PEG)-modified liposomes encapsulating the semisynthetic derivative of camptothecin irinotecan, with antineoplastic activity. As a prodrug, irinotecan is converted to the biologically active metabolite 7-ethyl-10-hydroxy-camptothecin (SN-38) by a carboxylesterase-converting enzyme. In turn, SN-38 inhibits topoisomerase I activity by stabilizing the cleavable complex of topoisomerase I and DNA, resulting in DNA breaks. This results in an inhibition of DNA replication and an induction of apoptosis. Pegylated liposomal delivery of irinotecan improves drug penetration into tumors and decreases drug clearance, thereby increasing the duration of exposure while lowering systemic toxicity.

A pegylated liposomal formulation comprised of a lipophilic prodrug of the antineoplastic antibiotic mitomycin C containing a cleavable disulfide bond (PL-MLP), with potential antineoplastic activity. Upon administration of the pegylated liposomal mitomycin C lipid-based prodrug, the MLP moiety becomes activated upon thiolysis at the tumor site, thereby releasing mitomycin C. Bioreduced mitomycin C generates oxygen radicals, alkylates DNA, and produces interstrand DNA cross-links, thereby inhibiting DNA synthesis. The thiolytic environment and upregulated expression of thioredoxins at the tumor site allow for the activation and release of mitomycin C. This prodrug formulation allows for greater circulation time, less systemic toxicity and increased accumulation of mitomycin C at the tumor site.

A pegylated liposomal mitoxantrone formulation composed of the hydrochloride salt form of the anthracenedione antibiotic mitoxantrone encapsulated within pegylated small unilamellar vesicles (SUVs), with potential antineoplastic activity. Upon intravenous administration, mitoxantrone intercalates into and forms crosslinks with DNA, thereby disrupting DNA and RNA replication. This agent also binds to topoisomerase II, which both results in DNA strand breaks and prevents DNA synthesis. This leads to the induction of apoptosis in rapidly dividing cancer cells. The pegylated liposomal formulation improves drug penetration into tumors and decreases drug clearance, thereby increasing drug circulation and therapeutic efficacy while lowering toxic effects.

A recombinant human arginase I (liver arginase) covalently attached, via a succinamide propionic acid (SPA) linker, to a polyethylene glycol (PEG) of molecular weight 5,000 [rhArg-peg(5,000mw)] with potential antineoplastic activity. Upon intravenous administration of pegylated recombinant human arginase I BCT-100, arginase metabolizes the amino acid arginine to ornithine and urea, depleting intracellular arginine, which may inhibit proliferation of cells that are auxotrophic for arginine such as hepatocellular carcinoma (HCC) cells. This agent may also work synergistically with various cytotoxic agents.

A pegylated formulation of a recombinant form of human hyaluronidase with potential antitumor activity. Upon intravenous administration, pegylated recombinant human PH20 degrades hyaluronic acid (HA) coating tumor cells, which may result in the inhibition of tumor cell growth. In addition, the degradation of HA may result in a lowering of the interstitial fluid pressure (IFP), allowing better penetration of chemotherapeutic agents into the tumor bed. HA is a glycosaminoglycan found in the extracellular matrix (ECM) that is frequently overproduced by various tumor cell types. The presence of HA in tumors correlates with increased tumor cell growth, metastatic potential, tumor progression, increased resistance to chemotherapeutic agents, and an elevation in tumor IFP.

A covalent conjugate of recombinant human interleukin-10 (IL-10) and polyethylene glycol (PEG), with potential anti-fibrotic, anti-inflammatory, immunomodulating and antineoplastic activities. Upon subcutaneous administration, pegylated recombinant human interleukin-10 AM0010 may activate cell-mediated immunity against cancer cells by stimulating the differentiation and expansion of tumor specific cytotoxic CD8+ T cells. This agent may also lower serum cholesterol levels and reduce atherosclerotic plaques by inhibiting the synthesis of pro-inflammatory cytokines, such as Interferon-gamma, IL-2, IL-3, TNF-alpha, and GM-CSF. The PEG moiety inhibits proteolytic breakdown and clearance of AM0010, which prolongs its half-life, extends the duration of its therapeutic effects and allows less frequent dosing.

A pegylated, recombinant form of L-asparaginase derived from the bacterium Erwinia chrysanthemi (mPEG-R-crisantaspase), with potential antineoplastic activity. Upon intravenous administration of pegylated recombinant L-asparaginase Erwinia chrysanthemi, asparaginase hydrolyzes L-asparagine to L-aspartic acid and ammonia, thereby depleting cancer cells of asparagine thus blocking protein synthesis and tumor cell proliferation. Asparagine is critical to protein synthesis in cancer cells, which cannot synthesize this amino acid due to the absence of the enzyme asparagine synthase. Compared to other available Erwinia chrysanthemi derived L-asparaginase agents, the pegylated form is longer acting and less immunogenic.

A recombinant modified form of the human enzyme arginase 1 (ARG1), in which cobalt is substituted for manganese as a cofactor, covalently attached to polyethylene glycol (PEG), with potential arginine degrading and antineoplastic activities. Upon intravenous administration of pegzilarginase, ARG1 metabolizes the amino acid arginine to ornithine and urea, thereby lowering blood arginine levels. This normalizes blood arginine levels in patients with ARG1 deficiency and prevents hyperargininemia. This also inhibits the proliferation of cancer cells that are dependent on extracellular arginine uptake for their proliferation. In normal, healthy cells, arginine is synthesized intracellularly by the enzymes ornithine transcarbamylase (OTC), argininosuccinate synthase (ASS), and argininosuccinate lyase (ASL); thus they are not dependent on extracellular arginine for survival. In cancer cells these enzymes are disabled; therefore, this agent may inhibit proliferation and survival of these cells by depleting extracellular arginine. Pegylation improves blood circulation times and cobalt substitution increases the catalytic activity of ARG1.

An isolate of the oncolytic, human wild-type serotype 3 Dearing (T3D) strain of the double-stranded RNA virus reovirus (respiratory enteric orphan virus), with potential oncolytic activity. Upon administration, pelareorep is able to replicate specifically in cancer cells bearing an activated Ras pathway. This induces apoptosis in Ras-activated tumor cells and subsequently frees progeny viral particles to infect, replicate in and induce cell death of surrounding cancer cells. In addition, viral replication causes the activation of innate and adaptive immune responses, causing a natural killer (NK)-cell-mediated and a cytotoxic T-cell (CTL)-mediated killing of tumor cells, respectively. Ras-activated tumor cells are deficient in their ability to trigger the antiviral response mediated by the host cellular protein, double-stranded RNA-dependent protein kinase (PKR).

A 3-cyanoquinoline pan-ErbB tyrosine kinase inhibitor with potential antineoplastic activity. Pelitinib irreversibly binds covalently to epidermal growth factor receptors (EGFR) ErbB-1, -2 and -4, thereby inhibiting receptor phosphorylation and signal transduction and resulting in apoptosis and suppression of proliferation in tumor cells that overexpress these receptors.

A water soluble antifolate with anti-proliferative activity. Pelitrexol inhibits activity of glycinamide ribonucleotide formyltransferase (GARFT), the first folate-dependent enzyme of the de novo purine synthesis pathway essential for cell proliferation. Enzyme inhibition reduces the purine nucleotides pool required for DNA replication and RNA transcription. As a result, this agent causes cell cycle arrest in S-phase, and ultimately inhibits tumor cell proliferation.

A humanized monoclonal immunoglobulin (Ig) G4 antibody directed against human cell surface receptor PD-1 (programmed death-1 or programmed cell death-1) with potential immune checkpoint inhibitory and antineoplastic activities. Upon administration, pembrolizumab binds to PD-1, an inhibitory signaling receptor expressed on the surface of activated T cells, and blocks the binding to and activation of PD-1 by its ligands, which results in the activation of T-cell-mediated immune responses against tumor cells. The ligands for PD-1 include programmed cell death ligand 1 (PD-L1), overexpressed on certain cancer cells, and programmed cell death ligand 2 (PD-L2), which is primarily expressed on APCs. Activated PD-1 negatively regulates T-cell activation and plays a key role in in tumor evasion from host immunity.

The disodium salt of a synthetic pyrimidine-based antifolate. Pemetrexed binds to and inhibits the enzyme thymidylate synthase (TS) which catalyses the methylation of 2'-deoxyuridine-5'-monophosphate (dUMP) to 2'-deoxythymidine-5'-monophosphate (dTMP), an essential precursor in DNA synthesis.

An orally bioavailable inhibitor of the fibroblast growth factor receptor (FGFR) types 1, 2, and 3 (FGFR1/2/3), with potential antineoplastic activity. Pemigatinib binds to and inhibits FGFR1/2/3, which may result in the inhibition of FGFR1/2/3-related signal transduction pathways. This inhibits proliferation in FGFR1/2/3-overexpressing tumor cells. FGFR, a family of receptor tyrosine kinases upregulated in many tumor cell types, plays a key role in cellular proliferation, migration, and survival.

A synthetic derivative of pyrimidine with antineoplastic activity. Penclomedine alkylates and crosslinks DNA, resulting in DNA strand breaks and inhibition of DNA and RNA synthesis. This agent is more active against tumor cells that are defective in p53 function.

A beta dimethyl analog of the amino acid cysteine. As a degradation product of penicillin antibiotics, penicillamine chelates with heavy metals and increases their urinary excretion. Possessing antineoplastic properties, penicillamine induces apoptosis by a p53-mediated mechanism and inhibits angiogenesis by chelating with copper, a cofactor for angiogenesis.

The potassium salt of penicillin V, a member of the penicillin antibiotic family with broad-spectrum bactericidal activity. Penicillin V binds to and inactivates penicillin-binding proteins (PBPs), enzymes located on the inner membrane of the bacterial cell wall, resulting in the weakening of the bacterial cell wall and cell lysis. PBPs participate in the terminal stages of assembling the bacterial cell wall, and in reshaping the cell wall during cell division. Inactivation of PBPs interferes with the cross-linkage of peptidoglycan chains necessary for bacterial cell wall strength and rigidity.

Brand name for pentamidine isethionate

A principal metabolite of hexamethylmelamine with antineoplastic activity. Pentamethylmelamine alkylates DNA and other macromolecules and forms DNA intrastrand and DNA-protein crosslinks, thereby preventing DNA replication.

A synthetic derivative of amidine with antiprotozoal and antifungal activities. Although the precise mode of action of pentamidine is unclear, it appears to interact directly with the pathogen genome by binding to AT-rich regions of duplex DNA and the minor groove of DNA, thereby interfering with DNA replication.

A synthetic amidine derivative, Pentamidine Isethionate is an antiprotozoal and antifungal agent that appears to interact with the minor groove of AT-rich DNA regions of the pathogen genome, interfering with DNA replication and function. It is effective in the treatment of trypanosomiasis, leishmaniasis, some fungal infections, and Pneumocystis carinii pneumonia in HIV-infected patients.

Brand name for mesalamine

A pentavalent vaccine comprised of the epitope antigens of the ganglioside lactones GD2L and GD3L, Globo H hexasaccharide 1 (Globo H), fucosyl GM1 and N-propionylated polysialic acid conjugated with the immunostimulant keyhole limpet hemocyanin (KLH), with potential immunostimulating and antineoplastic activity. Vaccination with the pentavalent KLH conjugate vaccine may induce production of IgG and IgM antibodies as well as an antibody-dependent cell-mediated cytotoxicity (ADCC) against tumors expressing any of these antigens. The antigens included in the pentavalent KLH conjugate vaccine are upregulated in a variety of cancer cells. KLH, a natural protein isolated from the marine mollusk keyhole limpet, is an immunostimulant carrier protein.

The calcium salt of pentetic acid, a synthetic chelating agent related to the chelating agent ethylenediaminetetraacetic acid (EDTA). Pentetic acid chelates with the metallic radioisotopic moieties of unbound, extracellular radioimmunotherapeutic agents, resulting in higher specific tumor cell binding of radioimmunotherpeutic agents; this results in improved tumor cell radiocytotoxicity and the sparing of normal cells and tissues from the radiocytotoxic effects of these agents.

The sodium salt of a semisynthetic heparin-like glucosaminoglycan. Although its mechanism of action is unknown, pentosan polysulfate may act as a buffer to control cell permeability by preventing irritating solutes from reaching cells coated with it. Administered orally, excreted pentosan polysulfate adheres to the urinary bladder wall, preventing irritants from entering bladder cells and the development or progression of interstitial cystitis (IC), a complication of some chemotherapies. This agent also exhibits anticoagulant and fibrinolytic properties.

A purine nucleotide analogue antibiotic isolated from the bacterium Streptomyces antibioticus. Also known as 2'-deoxycoformycin, pentostatin binds to and inhibits adenine deaminase (ADA), an enzyme essential to purine metabolism; ADA activity is greatest in cells of the lymphoid system with T-cells having higher activity than B-cells and T-cell malignancies higher ADA activity than B-cell malignancies. Pentostatin inhibition of ADA appears to result in elevated intracellular levels of dATP which may block DNA synthesis through the inhibition of ribonucleotide reductase. This agent may also inhibit RNA synthesis and may selectively deplete CD26+ lymphocytes. Check for active clinical trials using this agent.

A methylxanthine derivative with hemorrheologic and immunomodulating properties. Pentoxifylline inhibits phosphodiesterase, resulting in increased levels of cyclic adenosine monophosphate (cAMP) in erythrocytes, endothelium, and the surrounding tissues. This leads to vasodilation, improves erythrocyte flexibility, and enhances blood flow. In addition, the increased level of cAMP in platelets inhibits platelet aggregation, which may contribute to a reduction in blood viscosity. This agent also inhibits production of tumor necrosis factor-alpha and interferon-gamma, while it induces Th2-like (T-helper 2) cytokine production, thereby inhibiting Th1-mediated (T-helper 1) inflammatory and autoimmune responses.

Brand name for penicillin V potassium

A nanoparticle-based formulation composed of the poorly water-soluble paclitaxel encapsulated within branched polymers composed of polyethyloxazoline (PEOX), with potential antineoplastic activity. Upon injection of the PEOX-based polymer encapsulated paclitaxel FID-007, the nanoparticles accumulate at the tumor site, due to the unique characteristics of the tumor vasculature, while avoiding normal, healthy tissue. Once the paclitaxel is released, it binds to tubulin inside tumor cells and inhibits the disassembly-assembly dynamics of microtubules, resulting in cell cycle arrest and cell death. Compared to the administration of paclitaxel alone, this formulation increases paclitaxel's solubility and enhances its tumor tissue penetration and efficacy, while avoiding systemic exposure, which minimizes its toxicity.

A cancer vaccine consisting of PEP-3, a synthetic peptide encompassing a tumor-specific mutated segment of the epidermal growth factor receptor type vIII (EGFRvIII), conjugated to the naturally-occuring immunoadjuvant keyhole limpet hemocyanin (KLH) with potential immunostimulating and antineoplastic activities. Upon administration, PEP-3-KLH conjugate vaccine may induce a cytotoxic immune response against tumor cells that overexpress EGFRvIII; this antitumoral immune response may involve antibody-dependent cellular cytotoxicity (ADCC).

Brand name for famotidine

Brand name for famotidine

A peptide vaccine derived from cytomegalovirus (CMV) antigens with potential immunostimulating activity. Intradermal administration of the PEP-CMV vaccine may stimulate the immune system to mount a specific helper and cytotoxic T-lymphocyte (CTL) response against CMV-infected tumor cells. Infection with the herpesvirus CMV may play a significant role in tumor cell initiation and progression as well as chemoresistance.

A semisynthetic analog of Bleomycin, a mixture of several basic glycopeptide antineoplastic antibiotics isolated from the fungus Streptomyces verticillus. Peplomycin forms complexes with iron that reduce molecular oxygen to superoxide and hydroxyl radicals that cause single- and double-stranded breaks in DNA. This agent appears to show greater antitumor activity than bleomycin; its use is limited due to pulmonary toxicity.

Brand name for enzymatically hydrolyzed whey protein-based nutritional supplement

Brand name for bismuth subsalicylate

An orally active, non-competitive, and selective alpha-amino-3-hydroxy-5-methyl-4-isoxazolepropionic acid (AMPA) glutamate receptor antagonist, with anti-epileptic activity. Although the mechanism of action through which perampanel exerts its antiepileptic effect has not been fully elucidated, this agent antagonizes the AMPA subtype of the excitatory glutamate receptor found on postsynaptic neurons in the central nervous system (CNS). This antagonistic action prevents AMPA receptor activation by glutamate and results in the inhibition of neuronal excitation, repetitive neuronal firing, and the stabilization of hyper-excited neural membranes. Glutamate, the primary excitatory neurotransmitter in the CNS, plays an important role in various neurological disorders caused by neuronal hyperexcitation.

Brand name for oxycodone/acetaminophen

Brand name for penicillamine

An orally available, acyclic retinoid with potential antineoplastic and chemopreventive activities. Peretinoin binds to and activates nuclear retinoic acid receptors (RAR), which in turn recruit coactivator proteins and promote, with other transcriptional complexes, the transcription of target genes. As a result, this agent may modulate the expression of genes involved in the regulation of cell proliferation, cell differentiation, and apoptosis of both normal and tumor cells.

An oil-in-water nano-emulsion composed of the perfluorocarbon perflenapent, that has oxygen-carrying capacity, can be used as a contrast agent and has potential antihypoxic and radiosensitizing activities. Upon intravenous administration of the perflenapent emulsion, this agent increases the oxygen-carrying capacity of blood, enhances the transport of oxygen to hypoxic and ischemic tissues and increases the oxygen concentration in these tissues. Hypoxic tumors are correlated with increased resistance to radiation treatment; therefore, since perflenapent may increase tumor oxygenation, it may improve the tumor’s sensitivity to radiation therapy.

A synthetic radiopaque liquid form of perfluorooctyl bromide. Used as a contrast agent for magnetic resonance imaging (MRI), perflubron is also used as a liquid ventilation agent to improve pulmonary gas exchange and lung compliance and may be used in surgery to reduce or eliminate the need for a donor blood. Ventilation with perfluorocarbon fluid improves lung function in conditions involving surfactant deficiency and dysfunction, including respiratory distress syndrome and adult respiratory distress syndrome.

A fluorinated hydrocarbon and gaseous substance used as an imaging contrast agent. After administration in microsphere form, perflutren exhibits lower acoustic impedance than blood and improves ultrasound signaling.

An injectable suspension of liposome-encapsuled microspheres containing the fluorocarbon gas perflutren for contrast enhancement in ultrasound procedures. Because the acoustic impedance of perflutren lipid microspheres is much lower than that of blood, impinging ultrasound waves are scattered and reflected at the microsphere-blood interface and may be visualized with ultrasound imaging. Check for active clinical trials using this agent.

A sterile non-pyrogenic suspension of microspheres of human serum albumin with the stable, high-molecular-weight fluorocarbon gas perflutren, used as a contrast enhancement agent for ultrasound procedures. Because the acoustic impedance of perflutren protein-type A microspheres is much lower than that of blood, impinging ultrasound waves are scattered and reflected at the microsphere-blood interface and may be visualized with ultrasound imaging. At the frequencies used in adult echocardiography (2-5 MHZ), the microspheres resonate which further increases the extent of ultrasound scattering and reflection.

The active metabolite of the nitrogen mustard cyclophosphamide with potent antineoplastic and immunosuppressive properties. Perfosfamide alkylates DNA, thereby inhibiting DNA replication and RNA and protein synthesis. Check for active clinical trials using this agent.

Brand name for perfosfamide

Brand name for cyproheptadine hydrochloride

Brand name for chlorhexidine gluconate

perifosine]] An orally active alkyl-phosphocholine compound with potential antineoplastic activity. Targeting cellular membranes, perifosine modulates membrane permeability, membrane lipid composition, phospholipid metabolism, and mitogenic signal transduction, resulting in cell differentiation and inhibition of cell growth. This agent also inhibits the anti-apoptotic mitogen-activated protein kinase (MAPK) pathway and modulates the balance between the MAPK and pro-apoptotic stress-activated protein kinase (SAPK/JNK) pathways, thereby inducing apoptosis. Perifosine has a lower gastrointestinal toxicity profile than the related agent miltefosine.

A naturally occurring monoterpene related to limonene with antineoplastic activity. Perillyl alcohol inhibits farnesyl transferase and geranylgeranyl transferase, thereby preventing post-translational protein farnesylation and isoprenylation and activation of oncoproteins such as p21-ras, and arresting tumor cells in the G1 phase of the cell cycle.

The tert-butylamine salt of perindopril, the ethyl ester of a non-sulfhydryl angiotensin converting enzyme (ACE) inhibitor with antihypertensive activity. Upon hydrolysis, perindopril erbumine is converted to its active form perindoprilat, inhibiting ACE and the conversion of angiotensin I to angiotensin II; consequently, angiotensin II-mediated vasoconstriction and angiotensin II-stimulated aldosterone secretion from the adrenal cortex are inhibited and diuresis and natriuresis ensue.

Brand name for pertuzumab

Brand name for fluphenazine hydrochloride

Brand name for dipyridamole

An mRNA-based individualized, therapeutic cancer vaccine targeting an unspecified amount of tumor-associated antigens (TAAs) that are specifically expressed in the patient's cancer, with potential immunostimulatory and antineoplastic activities. Upon administration, the personalized cancer vaccine RO7198457 is taken up and translated by antigen presenting cells (APCs) and the expressed protein is presented via major histocompatibility complex (MHC) molecules on the surface of the APCs. This leads to an induction of both cytotoxic T-lymphocyte (CTL)- and memory T-cell-dependent immune responses against cancer cells expressing the TAA(s).

A synthetic peptide-based, personalized cancer vaccine consisting of multiple patient-specific tumor peptides, which are immunogenic and unique to the patient's tumor, combined with the immunostimulant polyinosinic-polycytidylic acid stabilized with polylysine and carboxymethylcellulose (poly-ICLC), with potential immunomodulating and antineoplastic activities. Upon vaccination with the personalized genomic vaccine 001 (PGV001), the peptides stimulate the host immune system to mount a specific and potent cytotoxic T-lymphocyte (CTL) response against tumor cells expressing the neoantigens, which results in tumor cell lysis. The adjuvant Poly-ICLC is added to boost the immune response to the peptides and together will expand immune cells to target cancer. The adjuvant poly-ICLC is a ligand for toll-like receptor-3 (TLR3) and induces the release of cytokines which may help to boost the immune response against the selected neoantigens.

A proprietary, personalized live, attenuated, double-deleted (pLADD) strain of the Gram-positive bacterium Listeria monocytogenes encoding multiple, patient-specific neoantigens, with potential immunostimulatory and antineoplastic activities. Upon intravenous administration, the tumor-associated antigens (TAAs) expressed in pLADD are taken up by antigen-presenting cells (APCs), including dendritic cells (DCs), and are processed and presented to the immune system by both major histocompatibility complex (MHC) class I and II molecules. This activates the immune system and leads to both an innate immune response and the recruitment and activation of tumor-specific cytotoxic T lymphocytes (CTLs) against the TAAs specifically expressed by the patient's tumor cells, which eventually results in tumor cell lysis.

A polyepitope DNA vaccine composed of a DNA plasmid encoding multiple, highly immunogenic tumor-associated antigens (TAAs) that are specifically selected after genome profiling of the patient's breast cancer cells, with potential immunostimulatory and antineoplastic activities. Upon intramuscular administration and electroporation of the personalized polyepitope plasmid DNA breast cancer vaccine, the expressed TAAs induce cytotoxic T-lymphocyte (CTL) immune responses against tumor cells expressing the TAAs.

A cancer vaccine consisting of one or more long, synthetic peptides derived from patient-specific breast cancer tumor-associated antigens (TAAs), with potential immunomodulating and antineoplastic activities. Upon intramuscular administration of the personalized synthetic long peptide breast cancer vaccine, the peptides stimulate the host immune system to mount a cytotoxic T-lymphocyte (CTL) response against tumor cells expressing the TAAs, which results in tumor cell lysis.

A personalized peptide vaccine consisting of synthetic long peptides (SLPs), ranging from 20-35 amino acids in size, that are derived from two or more of the patient's tumor-specific mutant antigens (TSMAs), with potential immunostimulatory and antitumor activities. A patient's tumor is isolated, TSMAs are identified, assessed and prioritized, and two or more TSMAs are selected to be further processed into SLPs. Upon administration, personalized SLP vaccine may stimulate the host immune system to mount a cytotoxic T-cell lymphocyte (CTL)-mediated immune response against the TSMAs expressed by the tumor cells.

Brand name for desipramine hydrochloride

A humanized recombinant monoclonal antibody directed against the extracellular dimerization domain of the HER-2 tyrosine kinase receptor. Binding of the antibody to the dimerization domain of the HER-2 tyrosine kinase receptor protein directly inhibits the ability of the HER-2 tyrosine kinase receptor protein (the most common pairing partner) to dimerize with other HER tyrosine kinase receptor proteins; inhibiting receptor protein dimerization prevents the activation of HER signaling pathways, resulting in tumor cell apoptosis.

A petrolatum-based ointment absorbed by dry and moist skin, petrolatum-mineral oil-lanolin-ceresin ointment is non-comedogenic, non-irritating, and non-sensitizing. It can reduce healing time of cracked, dry skin on hands, elbows, and knees, and helps prevent diaper rash. The original ointment also contained mineral oil, ceresin, lanolin alcohol. Its use is indicated in atopic dermatitis, eczema, and psoriasis when extra protection from a heavier base is needed.

A small molecule inhibitor of Nedd8 activating enzyme (NAE) with potential antineoplastic activity. Pevonedistat binds to and inhibits NAE, which may result in the inhibition of tumor cell proliferation and survival. NAE activates Nedd8 (Neural precursor cell expressed, developmentally down-regulated 8), an ubiquitin-like (UBL) protein that modifies cellular targets in a pathway that is parallel to but distinct from the ubiquitin-proteasome pathway (UPP). Functioning in diverse regulatory activities, proteins conjugated to UBLs like Nedd8 typically are not targeted for proteasomal degradation.

A thymidine kinase-deleted vaccinia virus expressing human GM-CSF (hGM-CSF) with oncolytic activity. Upon intratumoral or intravenous administration, pexastimogene-devacirepvec may selectively infect and lyse tumor cells. While vaccinia displays a natural tumor cell tropism, deletion of the thymidine kinase gene increases the tumor selectivity of vaccinia by limiting viral replication to transformed cells. hGM-CSF expression by this agent may help recruit antigen processing cells (APCs), such as denritic cells and macrophages, to virally infected tumor cells, initiating a systemic antitumoral immune response.

A capsule formulation containing a small-molecule receptor tyrosine kinase (RTK) inhibitor of KIT, CSF1R and FLT3 with potential antineoplastic activity. Pexidartinib binds to and inhibits phosphorylation of stem cell factor receptor (KIT), colony-stimulating factor-1 receptor (CSF1R) and FMS-like tyrosine kinase 3 (FLT3), which may result in the inhibition of tumor cell proliferation and down-modulation of macrophages, osteoclasts and mast cells involved in the osteolytic metastatic disease. FLT3, CSF1R and FLT3 are overexpressed or mutated in many cancer cell types and play major roles in tumor cell proliferation and metastasis.

An injectable formulation of the polysaccharide beta 1,3/1,6 glucan derived from the cell wall of the yeast Saccharomyces cerevisiae with potential immunomodulating and antineoplastic activities. PGG beta-glucan binds to an alternate site on the neutrophil complement receptor 3 (CR3), priming the neutrophil to become cytotoxic when binding to complement on tumor cells via CR3. This agent has been reported to selectively activate immune cells without inducing pro-inflammatory cytokines, potentially reducing potential side effects observed with the induction of broad innate immune responses. In addition, PGG beta-glucan may induce hematopoietic progenitor cell (HPC) mobilization.

A controlled-release, intratumoral paclitaxel formulation in which paclitaxel is incorporated into a thermosensitive, biodegradable triblock copolymer consisting of poly(lactide-co-glycolide) (PLGA) and polyethylene glycol (PEG). Upon intratumoral injection, paclitaxel is released slowly and continuously into tumor tissues from the gelled thermosensitive triblock copolymer over a period of 4 to 6 weeks; in tumor cells, paclitaxel binds to tubulin and inhibits the disassembly-assembly dynamics of microtubules, resulting in cell cycle arrest and cell death. The thermosensitive triblock copolymer component of this formulation transforms from a water-soluble polymer at room temperature to a water-insoluble, biodegradable gel depot at body temperature; intratumoral controlled-release of paclitaxel from the gel minimizes systemic exposure to paclitaxel and the paclitaxel toxicity profile.

An inhibitor of the adenosine triphosphate (ATP)-binding cassette (ABC) transporter P-glycoprotein (P-gp), with adjuvant activity. Upon oral administration, P-gp inhibitor HM30181AK selectively binds to and inhibits the multidrug resistance (MDR) efflux pump P-gp, which prevents the efflux of various chemotherapeutic agents from intestinal epithelial cells to the gastrointestinal tract. This leads to an increase in both oral bioavailability and therapeutic efficacy. P-gp prevents the intestinal uptake and intracellular accumulation of various cytotoxic agents. HM30181AK is not systemically absorbed.

An oncolytic, replication-competent adenovirus encoding the human glycosylphosphatidylinositol-anchored enzyme PH20 hyaluronidase with potential antitumor activity. After intratumoral administration, PH20 hyaluronidase-expressing adenovirus VCN-01 selectively replicates in tumor cells, which may both cause oncolytic virus-induced cell death and induce the infection of adjacent tumor cells. In addition, the virus expresses hyaluronidase, which hydrolyzes and degrades the hyaluronic acid (HA) that coats tumor cells. The degradation of HA may result in a decrease for both the viscosity of the interstitial space and the tumor's interstitial fluid pressure (IFP). This increases viral spread and may result in the inhibition of tumor cell growth. In addition, HA degradation facilitates the penetration of chemotherapeutic agents into the tumor. HA is a glycosaminoglycan found in the extracellular matrix (ECM) and is frequently overproduced by various tumor cell types. The presence of HA in tumors correlates with increases in tumor cell growth, metastatic potential, tumor progression and resistance to chemotherapeutic agents.

An extract of the flesh from the fruit of Phaleria macrocarpa, an Indonesian herbal medicine, with potential antineoplastic activity. Although the active ingredients and exact components are unclear, gallic acid and its derivatives in DLBS-1425 appear to inhibit the phosphoinositide-3 kinase (PI3K)/protein kinase B (AKT) signaling pathway by reducing PI3K transcription followed by a reduction in AKT phosphorylation. This extract also appears to induce apoptosis through induction of pro-apoptotic genes such as BAX, BAD and PUMA and inhibition of the apoptosis suppressor Bcl-2. Check for active clinical trials using this agent.

A high dose (HD) of ascorbic acid, a pro-oxidant agent, with potential antineoplastic and radio-chemo-sensitizing activities. Upon intravenous (IV) administration, pharmacological ascorbate is able to generate reactive oxygen species (ROS) by donating an electron to oxygen (O2) and forming hydrogen peroxide (H2O2), thereby causing oxidative stress and overwhelming the cell’s anti-oxidant defense mechanisms. This induces DNA double-stranded breaks (DSBs) and cell death. Tumor cells are highly susceptible to ascorbate-mediated oxidative stress and cytotoxicity while normal, healthy cells are mostly unaffected. This induces the cell death of susceptible tumor cells and decreases tumor cell growth. Higher plasma ascorbate concentrations are achieved upon higher intravenous doses of ascorbate; oral administration of ascorbate is limited and uptake does not increase after a certain amount is administered. Only IV ascorbate produces plasma concentrations high enough to induce ascorbate-mediated cytotoxicity to susceptible tumor cells. In addition, HD parenteral ascorbate enhances radio- and chemo-sensitivity of susceptible cancer cells.

Brand name for cholecalciferol/d-alpha tocopherol/L-selenomethionine/green tea extract/saw palmetto berry extract/daidzein/genistein/lycopene prostate health supplement

A proprietary formulation consisting of a Phellodendron amurense (Amur cork tree) bark extract, often used in traditional Chinese medicine, with anti-inflammatory, anti-oxidant and potential chemopreventive and antineoplastic activities. Phellodendron amurense bark extract contains certain isoquinoline alkaloids, flavone glycosides and phenolic compounds. Upon administration of Phellodendron amurense bark extract, the various phytochemicals in this formulation modulate multiple signal transduction pathways. This agent appears to block the activation of the transcription factor cAMP response binding protein (CREB) and inhibits Akt signaling, thereby inhibiting tumor cell growth and inducing apoptosis in Akt- and CREB-overexpressing cancer cells. In addition, this agent inhibits cyclooxygenase type 2 (COX-2), nuclear factor kappa b (NF-kB) and tumor necrosis factor alpha (TNF-a)-mediated signaling; COX-2, NF-kB and TNF-a are upregulated in certain types of cancer and during inflammation.

A hydrazine derivative and a potent non-selective monoamine oxidase (MAO) inhibitor with anxiolytic and antidepressant properties. Phenelzine sulfate irreversibly binds to MAO, thereby blocking the oxidative deamination of monoamines resulting in an increased concentration of biogenic amines and a concurrent decrease in catabolism of monoamine neurotransmitters, norepinephrine and serotonin, in the brain. In addition, through its primary metabolite phenylethylidenehyrazine (PEH), phenelzine causes elevated GABA levels in the caudate-putamen and nucleus accumbens thereby exerting its anxiolytic effects.

Brand name for promethazine hydrochloride

An isothiocyanate found in cruciferous vegetables with chemopreventive and potential antitumor activities. Although the mechanism of action is unclear, phenethyl Isothiocyanate (PEITC) was shown to induce apoptosis in tumor cells, possibly mediated through its metabolic intermediates, reactive oxygen species (ROS). PEITC also is able to activate ERK and JNK signal transduction, which in turn induces expression of stress-responsive genes. Specifically, this agent has been shown to reactivate gene expression of a detoxification enzyme, glutathione S-transferase that is silenced in prostate carcinoma.

A juice extracted from watercress containing high amounts of phenethyl isothiocyanate (PEITC), with potential chemopreventive and antitumor activities. Although the mechanism(s) of action through which PEITC exerts its effect(s) has yet to be fully elucidated, PEITC is able to induce apoptosis in tumor cells through the induction of reactive oxygen species (ROS). Additionally, PEITC is able to modulate extracellular signal-regulated kinases (ERK), c-Jun N-terminal kinase (JNK) and mitogen-activated protein kinase (MAPK) signal transduction pathways, activating the expression of stress-responsive genes and eventually inducing apoptosis. PEITC also inhibits the expression of genes involved in tumor progression such as HIF, STAT-3, HER2, BCL-XL, and XIAP and induces the expression of genes involved in tumor suppression such as p53, ATF-2, and p57. Furthermore, this agent has been shown to reactivate the gene expression of certain detoxification enzymes.

The hydrochloride salt form of phenformin, an agent belonging to the biguanide class of antidiabetics with antihyperglycemic activity. Phenformin is not used clinically due to the high risk of lactic acidosis that is associated with its use.

A long-acting barbituric acid derivative with antipsychotic property. Phenobarbital binds to and activates the gamma-aminobutyric acid (GABA)-A receptor, thereby mimicking the inhibitory actions of GABA in the brain. The activation effects of the phenobarbital-receptor-ionophore complex include increased frequency of chloride channel openings, membrane hyperpolarization and ultimately synaptic inhibition and decreased neuronal excitability. In addition, this agent inhibits glutamate induced depolarization.

The hydrochloride salt form of phenoxybenzamine, a synthetic, dibenzamine alpha-adrenergic antagonist with antihypertensive and vasodilatory properties. Phenoxybenzamine non-selectively and irreversibly blocks the postsynaptic alpha-adrenergic receptor in smooth muscle, thereby preventing vasoconstriction, relieving vasospasms, and decreasing peripheral resistance. Reflex tachycardia may occur and may be enhanced by blockade of alpha-2 receptors which enhances norepinephrine release. Phenoxybenzamine is reasonably anticipated to be a human carcinogen.

An orally available, long-acting derivative of coumarin with anticoagulant activity. Upon administration, phenprocoumon inhibits the vitamin K epoxide reductase enzyme; inhibition of this enzyme prevents the formation of the reduced, active form of vitamin K (vitamin KH2), which is essential for the carboxylation of glutamate residues of vitamin K-dependent proteins. This prevents the activation of vitamin K-dependent coagulation factors II, VII, IX, and X and the anticoagulant proteins C and S, which abrogates both thrombin production and thrombus formation.

The mesylate salt of a synthetic imidazoline with alpha-adrenergic antagonist activity. As a competitive alpha-adrenergic antagonist, phentolamine binds to alpha-1 and alpha-2 receptors, resulting in a decrease in peripheral vascular resistance and vasodilatation. This agent also may block 5-hydroxytryptamine (5-HT) receptors and stimulate release of histamine from mast cells.

A platinum (Pt)-based agent belonging to the phosphaplatin family comprised of Pt complexed to a pyrophosphate ligand, with potential antineoplastic activity. Although the exact mechanisms through which PT-112 exerts its effect have yet to be fully elucidated, this agent, upon intravenous administration, binds to certain transmembrane proteins and activates several genes involved in tumor suppression and apoptosis. This leads to the activation of various signal transduction pathways, induces S/G2 phase cell cycle, and causes tumor cell apoptosis. In addition, PT-112 may inhibit angiogenesis. Unlike conventional Pt-based chemotherapeutics, PT-112 does not bind to DNA and is able to overcome drug resistance, which occurs with conventional Pt-based chemotherapeutics; it also has a more favorable side effect profile and is more stable in plasma.

An oral preparation of the flavonoid silybin with potential antioxidant and chemopreventive activities. Silybin, also known as silibinin, is a mixture of two stereoisomers, denoted silybin A and silybin B, and is the major active constituent of silymarin, a mixture of flavonolignans extracted from blessed milk thistle (Silybum marianum). Silybin modulates P-glycoprotein (P-gp)-mediated cellular efflux; has oxygen radical-scavenging effects; inhibits the arachidonic acid pathway; and inhibits various cytochrome P450 enzymes. This agent may also exhibit anti-angiogenic activity, possibly by inducing endothelial cell apoptosis via modulation of the transcription factor NF-kB, the Bcl-2 family of proteins, and caspases. Complexing silybin with phosphatidylcholine increases its bioavailability.

A radiopharmaceutical composed of a mixture of proprietary phospholipid ethers (CLR 1404) that are covalently linked to the cytotoxic radioisotope iodine I 131 (iodine-131), with potential antineoplastic activity. Upon administration of CLR 131, the phospholipid ether (PLE) moiety is selectively taken up by lipid raft microdomains expressed on tumor cells and accumulates in the cytoplasm of tumor cells;. CLR 131 is not taken up by normal, healthy cells. This delivers cytotoxic iodine I 131 directly to and induces cell death in tumor cells. PLEs allows for targeted delivery of the radioisotope. Check for active clinical trials using this agent.

Brand name for sodium phosphate

A c-Myc antisense phosphorodiamidate morpholino oligomer (PMO) with potential antineoplastic activity. Phosphorodiamidate morpholino oligomer AVI-4126 binds to c-Myc mRNA and blocks its translation, which may result in the death of tumor cells overexpressing c-Myc. Differing from traditional antisense oligodeoxynucleotides (ODNs), neutrally charged PMOs are composed of subunits of nucleic acid bases linked to a synthetic backbone and, so, are less prone to enzymatic degradation. c-Myc, a proto-oncogene overexpressed in a variety of cancers, is involved in cellular proliferation, differentiation, and apoptosis.

A radioactive isotope of phosphorus with beta particle-emitting radiocytotoxic activity. Emitted by phosphorus P32, beta particles directly damage cellular DNA and, by ionizing intracellular water to produce several types of cytotoxic free radicals and superoxides, indirectly damage intracellular biological macromolecules, resulting in tumor cell death.

Brand name for HPPH

A metal complex compound of phthalocyanide with photosensitizing activity. Upon injection with photocyanide and subsequent introduction to photodynamic therapy (PDT), photocyanide becomes activated and forms reactive oxygen species that induce apoptosis.

Brand name for phytochlorin sodium-polyvinylpyrrolidone complex

A bacteriochlorin-based photosensitizer, with antineoplastic activity upon photodynamic therapy (PDT). Following intravenous administration, the photosensitizer LUZ 11 preferentially accumulates in hyperproliferative tissues, such as tumors. Local application of laser light at the tumor site results in the absorption of light by this agent and a photodynamic reaction between LUZ 11 and oxygen. This results in the production of reactive oxygen species (ROS), which includes singlet oxygen molecules, the superoxide ion, and other cytotoxic free radicals. The formation of ROS induces free radical-mediated DNA damage and cell death.

Brand name for aminophylline

The term 'phyto' originated from a Greek word meaning plant. Phytonutrients are certain organic components of plants, and these components are thought to promote human health. Fruits, vegetables, grains, legumes, nuts and teas are rich sources of phytonutrients. Unlike the traditional nutrients (protein, fat, vitamins, minerals), phytonutrients are not 'essential' for life, so some people prefer the term 'phytochemical'. (USDA Agricultural Research Service]]

A photosensitizer composed of the sodium salt form of chlorin e6 and its derivatives complexed with a low-molecular weight polyvinylpyrrolidone (PVP) polymer component, with diagnostic and antineoplastic activities upon photodynamic therapy (PDT). Upon intravenous administration, the photosensitizer phytochlorin-PVP sodium complex preferentially accumulates in hyperproliferative tissues, such as tumors. Local application of light with a certain wavelength to the tumor site results in the absorption of light by this agent, leading to its photoactivation. This results in a photodynamic reaction between phytochlorin and oxygen, which causes the production of reactive oxygen species (ROS), including singlet oxygen molecules, the superoxide ion, and other cytotoxic free radicals. The formation of ROS induces free radical-mediated oxidative DNA damage followed by apoptosis of tumor cells. Chlorin e6-PVP is able to penetrate deeply into tissues and is therefore able to treat hard-to-reach tumors.

An analogue of the naphthoquinone vitamin K found in plants. The vitamins K are essential for blood coagulation as it is necessary for the hepatic synthesis of the coagulation factors II, VII, IX, and X; deficiency results in a bleeding diathesis. These vitamins are lipo-soluble; absorption via intestinal lymphatics requires the presence of bile salts.

An orally bioavailable inhibitor of the class I phosphoinositide 3-kinase (PI3K) alpha isoform with potential antineoplastic activity. PI3K alpha inhibitor MLN1117 selectively inhibits PI3K alpha kinase, including mutations of PIK3CA, in the PI3K/Akt/mTOR pathway, which may result in tumor cell apoptosis and growth inhibition in PI3K alpha-expressing tumor cells. By specifically targeting class I PI3K alpha, this agent may be more efficacious and less toxic than pan PI3K inhibitors. Dysregulation of the PI3K/Akt/mTOR pathway is frequently found in solid tumors and results in promoting tumor cell growth, survival, and resistance to chemotherapy and radiotherapy; PIK3CA, one of the most highly mutated oncogenes, encodes the p110-alpha catalytic subunit of the class I PI3K.

An orally bioavailable inhibitor of the class I phosphoinositide 3-kinase (PI3K) alpha and beta isoforms with potential antineoplastic activity. PI3K alpha/beta inhibitor BAY1082439 selectively inhibits both PI3K alpha, including mutated forms of PIK3CA, and PI3K beta in the PI3K/Akt/mTOR pathway, which may result in tumor cell apoptosis and growth inhibition in PI3K-expressing and/or PTEN-driven tumor cells. By specifically targeting class I PI3K alpha and beta, this agent may be more efficacious and less toxic than pan PI3K inhibitors. Dysregulation of the PI3K/Akt/mTOR pathway is frequently found in solid tumors and results in increased tumor cell growth, survival, and resistance to chemotherapy and radiotherapy. PIK3CA, one of the most highly mutated oncogenes, encodes the p110-alpha catalytic subunit of the class I PI3K. PTEN, a tumor suppressor protein and negative regulator of PI3K activity, is often mutated in a variety of cancer cells.

The mesylate salt form of PWT33597, an orally bioavailable dual inhibitor of phosphatidylinositide 3-kinase (PI3K) alpha and mammalian target of rapamycin (mTOR) kinase with potential antineoplastic activity. PI3K alpha/mTOR dual inhibitor PWT33597 selectively inhibits both PI3K alpha kinase and mTOR kinase, which may result in tumor cell apoptosis and growth inhibition in PI3K/mTOR-overexpressing tumor cells. Activation of the PI3K/mTOR pathway promotes cell growth, survival, and resistance to chemotherapy and radiotherapy; mTOR, a serine/threonine kinase downstream of PI3K, may also be activated independent of PI3K.

An orally bioavailable selective inhibitor of the delta isoform of phosphatidylinositide 3-kinase (phosphoinositide 3'-kinase delta; PI3Kd; PI3K-d), with potential antineoplastic activity. Upon oral administration, PI3K-delta inhibitor HMPL 689 selectively binds to and inhibits PI3Kd, and prevents the activation of the PI3Kd/AKT signaling pathway, and B-cell activation. This both decreases proliferation and induces cell death in PI3Kd-overexpressing tumor cells. PI3Kd plays a key role in the B-cell receptor (BCR) signaling pathway and the proliferation of hematologic cancer cells. The targeted inhibition of PI3Kd is designed to preserve PI3K signaling in normal, non-neoplastic cells and thereby to minimize serious side effects. PI3Kd, an enzyme often overexpressed in cancer cells, plays a crucial role in tumor cell regulation and survival.

An orally bioavailable inhibitor of the delta isoform of phosphatidylinositide 3-kinase (PI3K), with potential antineoplastic activity. Upon oral administration, PI3K-delta inhibitor ME-401 selectively inhibits the delta isoform of PI3K and prevents the activation of the PI3K/AKT signaling pathway. This both decreases proliferation and induces cell death in PI3K-delta-overexpressing tumor cells. PI3K-delta plays a key role in the proliferation and survival of hematologic cancer cells. The targeted inhibition of PI3K-delta is designed to preserve PI3K signaling in normal, non-neoplastic cells. PI3K, an enzyme often overexpressed in cancer cells, plays a crucial role in tumor cell regulation and survival.

An orally available inhibitor of phosphatidylinositol 3-kinase (PI3K), with potential antineoplastic activity. PI3K inhibitor ACP-319 inhibits PI3K, which prevents the activation of the PI3K/AKT (protein kinase B)-mediated signaling pathway. This results in the inhibition of growth and survival of PI3K-overexpressing tumor cells. Activation of the PI3K signaling pathway is frequently associated with tumorigenesis.

A phosphatidylinositol 3-kinase (PI3K) inhibitor with potential antineoplastic activity. PI3K inhibitor BGT226 specifically inhibits PIK3 in the PI3K/AKT kinase (or protein kinase B) signaling pathway, which may trigger the translocation of cytosolic Bax to the mitochondrial outer membrane, increasing mitochondrial membrane permeability; apoptotic cell death may ensue. Bax is a member of the proapoptotic Bcl2 family of proteins.

An orally available inhibitor of phosphatidylinositol 3-kinase (PI3K), with potential antineoplastic activity. PI3K inhibitor GDC0077 binds to and inhibits various members of the PI3K family, including activating mutations in the catalytic alpha isoform PIK3CA. PI3K inhibition prevents the activation of the PI3K-mediated signaling pathway and results in the inhibition of growth and survival of PI3K-overexpressing tumor cells. Dysregulation of the PI3K signaling pathway is frequently associated with tumorigenesis and tumor resistance to a variety of antineoplastic agents and radiotherapy. PIK3CA, which encodes the p110-alpha catalytic subunit of the class I PI3K, is frequently mutated in a variety of cancer cell types and plays a key role in cancer cell growth and invasion.

A phosphatidylinositol 3-kinase (PI3K) inhibitor with potential antineoplastic activity. PI3K inhibitor GDC-0084 specifically inhibits PI3K in the PI3K/AKT kinase (or protein kinase B) signaling pathway, thereby inhibiting the activation of the PI3K signaling pathway. This may result in the inhibition of both cell growth and survival in susceptible tumor cell populations. Activation of the PI3K signaling pathway is frequently associated with tumorigenesis. Dysregulated PI3K signaling may contribute to tumor resistance to a variety of antineoplastic agents.

The orally bioavailable bismesylate salt of a potent small-molecule thieno[3,2-d]pyrimidine inhibitor of the class I phosphatidylinositol 3 kinase (PI3K) isoforms p100alpha and p100delta with potential antineoplastic activity. PI3K inhibitor GDC-0941 selectively binds to PI3K isoforms in an ATP-competitive manner, inhibiting the production of the secondary messenger phosphatidylinositol-3,4,5-trisphosphate (PIP3) and activation of the PI3K/Akt signaling pathway; inhibition of tumor cell growth, motility and survival in susceptible tumor cell populations may result. Activation of the PI3K/Akt signaling pathway is frequently associated with tumorigenesis; dysregulated PI3K/Akt signaling may contribute to tumor resistance to a variety of antineoplastic agents. Check for active clinical trials using this agent.

A phosphoinositide 3-kinase (PI3K) inhibitor with potential antineoplastic activity. PI3K inhibitor GSK1059615 inhibits PI3K in the PI3K/AKT kinase signaling pathway, which may trigger the translocation of cytosolic Bax to the mitochondrial outer membrane and an increase in mitochondrial membrane permeability, followed by apoptosis. Bax is a member of the proapoptotic Bcl-2 family of proteins. PIK3, an enzyme often overexpressed in cancer cells, plays a crucial role in tumor cell regulation and survival. Check for active clinical trials using this agent.

A small-molecule pyridylsulfonamide inhibitor of phosphatidylinositol 3-kinase (PI3K) with potential antineoplastic activity. PI3K inhibitor GSK2126458 binds to and inhibits PI3K in the PI3K/mTOR signaling pathway, which may trigger the translocation of cytosolic Bax to the mitochondrial outer membrane, increasing mitochondrial membrane permeability and inducing apoptotic cell death. Bax is a member of the proapoptotic Bcl2 family of proteins. PI3K, often overexpressed in cancer cells, plays a crucial role in tumor cell regulation and survival.

A small-molecule wortmannin analogue inhibitor of the alpha, gamma, and delta isoforms of phosphoinositide 3-kinase (PI3K) with potential antineoplastic activity. PI3K inhibitor PX-866 inhibits the production of the secondary messenger phosphatidylinositol-3,4,5-trisphosphate (PIP3) and activation of the PI3K/Akt signaling pathway, which may result in inhibition of tumor cell growth and survival in susceptible tumor cell populations. Activation of the PI3K/Akt signaling pathway is frequently associated with tumorigenesis and dysregulated PI3K/Akt signaling may contribute to tumor resistance to a variety of antineoplastic agents.

A phosphatidylinositol 3-kinase (PI3K) inhibitor with potential antineoplastic activity. PI3K inhibitor WX-037 specifically inhibits PI3K, which prevents the activation of the PI3K/protein kinase B-mediated signaling pathway. This may result in the inhibition of both tumor cell growth and survival in PI3K-overexpressing tumor cells. Activation of the PI3K signaling pathway is frequently associated with tumorigenesis. Dysregulated PI3K signaling may contribute to tumor resistance to a variety of antineoplastic agents.

An orally available, s-triazine derivative, ATP-competitive phosphatidylinositol 3-kinase (PI3K) inhibitor with potential antineoplastic activity. PI3K inhibitor ZSTK474 inhibits all four PI3K isoforms. Inhibiting the activation of the PI3K/AKT kinase (or protein kinase B) signaling pathway results in inhibition of tumor cell growth and survival in susceptible tumor cell populations. Dysregulated PI3K signaling may contribute to tumor resistance to a variety of antineoplastic agents. This agent does not induce apoptosis but rather induces strong G(0)/G(1) arrest, which might contribute to its favorable efficacy in tumor cells.

A dual selective inhibitor of the beta and delta isoforms of the 110 kDa catalytic subunit of class I phosphoinositide-3 kinase (PI3K)-beta/delta, with potential antineoplastic activity. PI3K-beta/delta inhibitor KA2237 selectively inhibits the PI3K-beta and -delta isoforms and prevents their activation, which inhibits PI3K-beta/delta-mediated signal transduction pathways. This decreases proliferation and induces cell death in susceptible tumor cells. Unlike other isoforms of PI3K, PI3K-beta and -delta are overexpressed primarily in solid and hematological tumor cells and play crucial roles in tumor cell survival, and immunoregulation. The targeted inhibition of these PI3Ks allows this agent to potentially be more efficacious and less toxic than pan-PI3K inhibitors, which also affect normal, healthy cells.

An orally bioavailable inhibitor of both phosphoinositide 3-kinase (PI3K) class I and pan histone deacetylase (HDAC) enzymes, with potential antineoplastic activity. Upon oral administration, CUDC-907 inhibits the activity of both PI3K class I isoforms and HDAC, thereby preventing the activation of the PI3K-AKT-mTOR signal transduction pathway that is often overactivated in many cancer cell types. This may prevent growth of PI3K and/or HDAC-expressing tumor cells. CUDC-907 shows an increased inhibition of tumor cell growth and induction of apoptosis when compared to inhibitors that target either PI3K or HDAC.

An orally bioavailable small molecule targeting the phosphatidylinositol 3 kinase (PI3K) and mammalian target of rapamycin (mTOR) kinases in the PI3K/mTOR signaling pathway, with potential antineoplastic activity. PI3K/mTOR dual kinase inhibitor XL765 inhibits both PI3K kinase and mTOR kinase, which may result in tumor cell apoptosis and growth inhibition in susceptible tumor cell populations. Activation of the PI3K/mTOR pathway promotes cell growth, survival, and resistance to chemotherapy and radiotherapy; mTOR, a serine/threonine kinase downstream of PI3K, may also be activated in a PI3K-independent fashion in response to nutrient and energy deprivation. Accordingly, this agent maybe more potent compared to an agent that inhibits either PI3K kinase or mTOR kinase alone.

An orally bioavailable, small molecule inhibitor of certain class I phosphoinositide 3-kinase (PI3K) isoforms and mammalian target of rapamycin kinase (mTOR) in the PI3K/mTOR signaling pathway, with potential antineoplastic activity. PI3K/mTOR inhibitor LY3023414 inhibits both certain PI3K isoforms and mTOR in an ATP-competitive manner which may inhibit both the PI3K/mTOR signaling pathway in and proliferation of tumor cells overexpressing PI3K and/or mTOR. The PI3K/mTOR pathway is upregulated in a variety of tumor cells and plays a key role in promoting cancer cell proliferation, and survival, motility and resistance to chemotherapy and radiotherapy. mTOR, a serine/threonine kinase downstream of PI3K, may also be activated in a PI3K-independent fashion; therefore, this agent may be more potent than an agent that inhibits either PI3K or mTOR alone. In addition, LY3023414 may inhibit DNA-dependent protein kinase (DNA-PK), thereby inhibiting the ability of tumor cells to repair damaged DNA. DNA-PK is activated upon DNA damage and plays a key role in repairing double-stranded DNA breaks.

An orally bioavailable imidazoquinoline targeting the phosphatidylinositol 3 kinase (PI3K) and the mammalian target of rapamycin (mTOR), with potential antineoplastic activity. PI3K/mTOR inhibitor BEZ235 inhibits PI3K kinase and mTOR kinase in the PI3K/AKT/mTOR kinase signaling pathway, which may result in tumor cell apoptosis and growth inhibition in PI3K/mTOR-overexpressing tumor cells. Activation of the PI3K/mTOR pathway promotes cell growth, survival, and resistance to chemotherapy and radiotherapy; mTOR, a serine/threonine kinase downstream of PI3K, may also be activated independent of PI3K.

An orally bioavailable inhibitor of phosphatidylinositol 3 kinase (PI3K) and mammalian target of rapamycin (mTOR) kinase in the PI3K/mTOR signaling pathway, with potential antineoplastic activity. PI3K/mTOR kinase inhibitor DS-7423 inhibits both PI3K kinase and mTOR kinase, which may result in tumor cell apoptosis and growth inhibition in susceptible tumor cells. Activation of the PI3K/mTOR pathway promotes cell growth, survival, and resistance to chemotherapy and radiotherapy; mTOR, a serine/threonine kinase downstream of PI3K, may also be activated independent of PI3K. Consequently, this agent may potentially be more potent than an agent that inhibits either PI3K kinase or mTOR kinase.

An agent targeting the phosphatidylinositol 3 kinase (PI3K) and mammalian target of rapamycin (mTOR) in the PI3K/mTOR signaling pathway, with potential antineoplastic activity. PI3K/mTOR kinase inhibitor PF-04691502 inhibits both PI3K and mTOR kinases, which may result in apoptosis and growth inhibition of cancer cells overexpressing PI3K/mTOR. Activation of the PI3K/mTOR pathway promotes cell growth, survival, and resistance to chemotherapy and radiotherapy; mTOR, a serine/threonine kinase downstream of PI3K, may also be activated independent of PI3K.

A potent and selective inhibitor of both phosphatidylinositol 3 kinase (PI3K) and mammalian target of rapamycin (mTOR) kinase in the PI3K/mTOR signaling pathway, with potential antineoplastic activity. PI3K/mTOR kinase inhibitor VS-5584 inhibits mTOR kinase and all class I PI3K isoforms. Consequently, this disrupts phosphorylation of substrates downstream of PI3K and mTOR and may result in apoptosis and growth inhibition in susceptible tumor cells. Activation of the PI3K/mTOR pathway promotes cell growth, survival, and resistance to chemotherapy and radiotherapy. mTOR is a serine/threonine kinase downstream of PI3K, which also has PI3K-independent activity. Consequently, this agent may potentially be more potent than an agent that inhibits either PI3K kinase or mTOR kinase.

An orally bioavailable inhibitor of phosphoinositide 3-kinase (PI3K), mammalian target of rapamycin (mTOR), activin receptor-like kinase 1 (ALK-1) and DNA-dependent protein kinase (DNA-PK), with potential anti-angiogenic and antineoplastic activities. Upon oral administration, PI3K/mTOR/ALK-1/DNA-PK inhibitor P7170 inhibits the activity of all four kinases. This prevents PI3K/mTOR and ALK-1-mediated signaling pathways and may lead to the inhibition of cancer cell growth in PI3K/mTOR-overexpressing tumor cells and angiogenesis in ALK-1-overexpressing endothelial cells. Also, by inhibiting DNA-PK, this agent inhibits the ability of tumor cells to repair damaged DNA. The PI3K/mTOR pathway is upregulated in a variety of tumors and plays an important role in regulating cancer cell proliferation, growth, and survival. ALK-1, a member of the transforming growth factor beta (TGF-b) type I receptor family, is overexpressed on endothelial cells in a variety of tumor types and increases endothelial cell proliferation and migration. DNA-PK is activated upon DNA damage and plays a key role in repairing double-stranded DNA breaks.

An inhibitor of phosphatidylinositide 3-kinase (PI3K), raptor-mTOR (mTOR complex 1 or mTORC1) and rictor-mTOR (mTOR complex 2 or mTORC2) with potential antineoplastic activity. Upon intravenous infusion, PI3K/mTORC1/mTORC2 inhibitor DCBCI0901 binds to and inhibits PI3K as well as both mTORC1 and mTORC2, which may result in both apoptosis and a decrease in cell proliferation in tumor cells overexpressing PI3K, mTORC1, and mTORC2. Activation of the PI3K/mTOR signaling pathway promotes cell growth, survival, and resistance to chemotherapy and radiotherapy; mTOR, a serine/threonine kinase downstream of PI3K, may also be activated independently of PI3K.

A second generation, small-molecule mimetic of ATP that targets the mammalian target of rapamycin (mTOR) with potential antineoplastic activity. PKI-179 selectively inhibits mTOR and phosphoinositide-3-kinase (PI3K) alpha. By inhibiting the PI3K/mTOR signaling pathway, this agent may inhibit tumor cell proliferation and survival.

An orally bioavailable inhibitor of the class I phosphatidylinositol-4,5-bisphosphate 3-kinase (PI3K) catalytic subunit alpha (PIK3CA), with potential antineoplastic activity. PI3K alpha inhibitor AZD8835 selectively binds to and inhibits PIK3CA and its mutated forms, in the PI3K/Akt (protein kinase B)/mammalian target of rapamycin (mTOR) pathway. This results in both apoptosis and growth inhibition in PIK3CA-expressing tumor cells. By specifically targeting PIK3CA, this agent may be more efficacious and less toxic than pan-PI3K inhibitors. Dysregulation of the PI3K/Akt/mTOR pathway is often found in solid tumors and results in the promotion of tumor cell growth, survival, and resistance to chemo- and radio-therapy. PIK3CA, one of the most frequently mutated oncogenes, encodes the p110-alpha catalytic subunit of the class I PI3K.

An inhibitor of the beta isoform of phosphoinositide-3 kinase (PI3K), with potential antineoplastic activity. Upon administration, PI3Kbeta inhibitor AZD8186 selectively inhibits the activity of PI3Kbeta in the PI3K/Akt/mTOR signaling pathway, which may result in a decrease of tumor cell proliferation. It also induces cell death in PI3K-expressing cancer cells. By specifically targeting class I PI3K beta, this agent may be more efficacious and less toxic than pan PI3K inhibitors. PI3K-mediated signaling is often dysregulated in cancer cells and contributes to increased tumor cell growth, survival, and tumor resistance to a variety of antineoplastic agents.

An orally bioavailable, substituted benzimidazole inhibitor of the class I phosphoinositide 3-kinase (PI3K) beta isoform with potential antineoplastic activity. PI3K beta inhibitor GSK2636771 selectively inhibits PI3K beta kinase activity in the PI3K/Akt/mTOR pathway, which may result in tumor cell apoptosis and growth inhibition in PI3K beta-expressing and/or PTEN-driven tumor cells. Dysregulation of the PI3K/Akt/mTOR pathway is frequently found in solid tumors and results in the promotion of tumor cell growth, survival, and resistance to both chemotherapy and radiotherapy. PI3K beta is the p110-beta catalytic subunit of the class I PI3K. PTEN, a tumor suppressor protein and negative regulator of PI3K activity, is often mutated in a variety of cancer cells.

An orally bioavailable inhibitor of the class I phosphatidylinositol 3-kinase (PI3K) beta isoform with potential antineoplastic activity. PI3K beta inhibitor SAR260301 selectively inhibits PI3K beta kinase activity in the PI3K/Akt/mTOR pathway, which may result in apoptosis and growth inhibition in PI3K beta-expressing and/or phosphatase and tensin homolog (PTEN)-deficient tumor cells. Dysregulation of the PI3K/Akt/mTOR pathway is frequently found in solid tumors and contributes to increased tumor cell growth, tumor cell survival, and resistance to both chemotherapy and radiotherapy. PI3K beta is the p110-beta catalytic subunit of the class I PI3K. PTEN, a tumor suppressor protein and negative regulator of PI3K activity, is often mutated in a variety of cancer cells. By specifically targeting class I PI3K beta, this agent may be more efficacious and less toxic than pan-PI3K inhibitors.

A highly selective, potent, and orally bioavailable small molecule inhibitor of the delta isoform of the 110 kDa catalytic subunit of class IA phosphoinositide-3 kinases (PI3K) with potential immunomodulating and antineoplastic activities. PI3K-delta inhibitor AMG 319 prevents the activation of the PI3K signaling pathway through inhibition of the production of the second messenger phosphatidylinositol-3,4,5-trisphosphate (PIP3), thus decreasing proliferation and inducing cell death. Unlike other isoforms of PI3K, PI3K-delta is expressed primarily in hematopoietic lineages. The targeted inhibition of PI3K-delta is designed to preserve PI3K signaling in normal, non-neoplastic cells.

An orally bioavailable, selective inhibitor of the delta isoform of the 110 kDa catalytic subunit of class I phosphoinositide-3 kinases (PI3K) with potential antineoplastic activity. PI3Kdelta inhibitor INCB040093 specifically inhibits PI3Kdelta, which prevents both the production of the second messenger phosphatidylinositol-3,4,5-trisphosphate (PIP3) and the activation of the PI3K/AKT kinase signaling pathway. This decreases proliferation and induces cell death in PI3K-overexpressing tumor cells. Unlike other isoforms of PI3K, PI3Kdelta is often overexpressed in tumor cells, especially those of hematologic origin, and plays a crucial role in tumor cell regulation and survival. The targeted inhibition of PI3Kdelta allows for PI3K signaling in normal, non-neoplastic cells.

An inhibitor of the delta isoform of phosphoinositide-3 kinase (PI3K) with potential antineoplastic activity. PI3K-delta inhibitor INCB050465 inhibits the delta isoform of PI3K and prevents the activation of the PI3K/AKT signaling pathway. This both decreases proliferation and induces cell death in PI3K-delta-overexpressing tumor cells. Unlike other isoforms of PI3K, PI3K-delta is expressed primarily in hematopoietic disease and cell lineages. The targeted inhibition of PI3K-delta is designed to preserve PI3K signaling in normal, non-neoplastic cells. PI3K, an enzyme often overexpressed in cancer cells, plays a crucial role in tumor cell regulation and survival.

An orally bioavailable, highly selective small molecule inhibitor of the gamma isoform of phosphoinositide-3 kinase (PI3K-gamma) with potential immunomodulating and antineoplastic activities. Upon administration, IPI-549 prevents the activation of the PI3K-gamma-mediated signaling pathways, which may lead to a reduction in cellular proliferation in PI3K-gamma-expressing tumor cells. In addition, this agent is able to modulate anti-tumor immune responses and inhibit tumor-mediated immunosuppression. Unlike other isoforms of PI3K, the gamma isoform is overexpressed in certain tumor cell types and immune cells; its expression increases tumor cell proliferation and survival. By selectively targeting the gamma isoform, PI3K signaling in normal, non-neoplastic cells is minimally or not affected, which results in a reduced side effect profile.

A mixture of highly sulfated, monophosphorylated mannose oligosaccharides, derived from the extracellular phosphomannan of the yeast Pichia (Hansenula) holstii, with potential antiangiogenic activity. Heparanase inhibitor PI-88 inhibits the endo-beta-D-glucuronidase heparanase, which may interfere with the heparanase-mediated degradation of heparan-sulfate proteoglycans in extracellular matrices, an important step in the metastatic process. This agent may also bind with high affinity to the heparan sulfate-binding domains of vascular endothelial growth factor (VEGF) and fibroblast growth factors 1 and 2, thereby reducing their functional activities and inhibiting VEGF and FGF stimulation of tumor angiogenesis. Increased heparanase activity has been implicated in tumor angiogenesis and metastasis.

A fluorescent dye of benzimidazole derivative. Pibenzimol binds to AT-specific sites in the minor groove of duplex DNA and inhibits topoisomerase I, and DNA polymerase, thereby preventing DNA replication. This agent prolongs the G2 phase of the cell cycle and initiates apoptosis in tumor cells.

A semisynthetic water-soluble derivative of the antineoplastic antibiotic duocarmycin B2. Activated by carboxyl esterase, pibrozelesin alkylates DNA by binding to adenine-thymine (A-T)-rich sequences in the minor groove of DNA, thereby inhibiting DNA replication and inducing apoptosis.

Brand name for ingenol mebutate

Brand name for ingenol mebutate gel

A lyophilized formulation containing cultures of a low-virulent strain of Streptococcus pyogenes, treated and killed with pencillin G, with potential sclerosing, immunostimulating and antineoplastic activities. Besides its activity as a sclerosing agent, picibanil appears to have multiple effects on the immune system as a non-specific immunostimulant. This agent activates the host immune system by stimulating the activity of natural killer (NK) cells, macrophages and lymphocytes, and by enhancing the production of several key immune mediators, including interleukins (ILs) and tumor necrosis factor (TNF).

A new generation organic platinum analog with an extended spectrum of antineoplastic activity. Designed to overcome platinum drug resistance, picoplatin alkylates DNA, forming both inter- and intra-strand cross-linkages, resulting in inhibition of DNA replication and transcription, and the induction of apoptosis.

A cyclolignan alkaloid found in the mayapple plant family (Podophyllum peltatum), and a small molecule inhibitor of the insulin-like growth factor 1 receptor (IGF1R) with potential antineoplastic activity. Picropodophyllin specifically inhibits the activity and downregulates the cellular expression of IGF1R without interfering with activities of other growth factor receptors, such as receptors for insulin, epidermal growth factor, platelet-derived growth factor, fibroblast growth factor and mast/stem cell growth factor (KIT). This agent shows potent activity in the suppression o f tumor cell proliferation and the induction of tumor cell apoptosis. IGF1R, a receptor tyrosine kinase overexpressed in a variety of human cancers, plays a critical role in the growth and survival of many types of cancer cells.

A humanized, immunoglobulin (Ig) G1 monoclonal antibody directed against human inhibitory receptor programmed cell death 1 (PD-1; PDCD1), with potential immune checkpoint inhibitory and antineoplastic activities. Pidilizumab binds to PD-1 and blocks the interaction between PD-1 and its ligands, PD-1 ligand 1 (PD-L1) and PD-1 ligand 2 (PD-L2). This prevents the activation of PD-1 and its downstream signaling pathways. This may restore immune function through the activation of natural killer (NK) cells and cytotoxic T-lymphocytes (CTLs) against tumor cells. PD-1, an inhibitory receptor belonging to the B7-receptor family expressed on activated T-lymphocytes, B-cells and NK cells, negatively regulates T-cell activation and effector function when activated by its ligands; it plays an important role in tumor evasion from host immunity.

The hydrochloride salt of a natural alkaloid extracted from plants of the genus Pilocarpus with cholinergic agonist activity. As a cholinergic parasympathomimetic agent, pilocarpine predominantly binds to muscarinic receptors, thereby inducing exocrine gland secretion and stimulating smooth muscle in the bronchi, urinary tract, biliary tract, and intestinal tract. When applied topically to the eye, this agent stimulates the sphincter pupillae to contract, resulting in miosis; stimulates the ciliary muscle to contract, resulting in spasm of accomodation; and may cause a transitory rise in intraocular pressure followed by a more persistent fall due to opening of the trabecular meshwork and an increase in the outflow of aqueous humor.

An orally available pan-PIM protein kinase inhibitor with potential antineoplastic activity. PIM kinase inhibitor LGH447 binds to and inhibits the activities of PIM-1, -2 and -3 serine/threonine kinases, which may result in the interruption of the G1/S phase cell cycle transition, the expression of the pro-apoptotic Bcl2 protein, and tumor cell apoptosis in cells that overexpress PIMs. PIM kinases, downstream effectors of many cytokine and growth factor signaling pathways, play key roles in cell cycle progression and apoptosis inhibition and may be overexpressed in various malignancies. Check for active clinical trials using this agent.

A small-molecule pan-Pim protein kinase inhibitor with potential antineoplastic activity. Pim kinase inhibitor SGI-1776 binds to and inhibits the activities of Pim-1, -2 and -3, serine-threonine kinases, which may result in the interruption of the G1/S phase cell cycle transition, the expression of pro-apoptotic Bcl2 proteins and tumor cell apoptosis. PIM kinases play key roles in cell cycle progression and apoptosis inhibition and may be overexpressed in various malignancies.

An orally available inhibitor of PIM family serine/threonine protein kinases and mutant forms of FMS-related tyrosine kinase 3 (FLT3; STK1) with potential antineoplastic activity. PIM/FLT3 kinase inhibitor SEL24 binds to and inhibits the kinase activities of PIM-1, -2 and -3, and mutant forms of FLT3, which may result in the interruption of the G1/S phase cell cycle transition, an inhibition of cell proliferation, and an induction of apoptosis in tumor cells that overexpress PIMs or express mutant forms of FLT3. FLT3, a tyrosine kinase receptor that is overexpressed or mutated in various cancers, plays a role in signaling pathways that regulate hematopoietic progenitor cell proliferation, and in leukemic cell proliferation and survival. PIM kinases, downstream effectors of many cytokine and growth factor signaling pathways, including the FLT3 signaling pathway, play key roles in cell cycle progression and apoptosis inhibition and may be overexpressed in various malignancies.

An orally bioavailable small-molecule inhibitor of MEK1 and MEK2 (MEK1/2) with potential antineoplastic activity. Pimasertib selectively binds to and inhibits the activity of MEK1/2, preventing the activation of MEK1/2-dependent effector proteins and transcription factors, which may result in the inhibition of growth factor-mediated cell signaling and tumor cell proliferation. MEK1/2 (MAP2K1/K2) are dual-specificity threonine/tyrosine kinases that play key roles in the activation of the RAS/RAF/MEK/ERK pathway and are often upregulated in a variety of tumor cell types.

A 33-epi-chloro-derivative of the ascomycin macrolactam with immunosuppressant properties. Pimecrolimus binds to the receptor macrophilin-12 (FKBP-12) forming a complex that blocks the calcium-dependent signal transduction cascade mediated by calcineurin. Via dephosphorylation, calcineurin is the enzyme responsible for activating nuclear factor of activated T-cells (NF-AT), a T cell transcriptional regulatory factor. As a consequence, the synthesis and release of Th1- (T helper 1) and Th2- (T helper 2) type cytokines, and other inflammatory mediators from T-cells and mast cells are blocked and the expression of signals essential for the activation of inflammatory T-lymphocytes is inhibited. However, pimecrolimus mode of action is cell-selective and does not affect Langerhans' cells/dendritic cells and primary fibroblasts. Check for active clinical trials using this agent.

A nitroimidazole with hypoxic selectivity and radiosensitizing property. Pimonidazole is reduced in hypoxic environments as in tumor cells, thereby it can be used as an hypoxia marker. In hypoxic cells, reduced pimonidazole binds to -SH-containing molecules such as glutathione and proteins, and the resulting complexes accumulated in tissues, thereby sensitizing cells to be more susceptible for radiation treatment.

A substituted nitroimidazole salt. Hypoxic cells bioreductively activate and bind pimonidazole. This agent may be used as a hypoxia marker for detecting oxygen gradients in living tissues. Pimonidazole also exhibits radiosensitizing properties.

An orally available bromide salt form of pinaverium, a calcium channel blocker (CCB) with antispasmodic activity. Upon oral administration, pinaverium blocks the voltage-dependent calcium channels and inhibits calcium ion influx into the smooth muscle cells located in the gastrointestinal (GI) tract. This prevents smooth muscle contraction and relaxes the GI tract. In addition, pinaverium may both reduce bowel uptake of and facilitate the function of locally active, co-administered drugs.

AA small molecule inhibitor of histone methyltransferase with potential antineoplastic activity. Upon intravenous administration, pinometostat specifically blocks the activity of the histone lysine-methyltransferase DOT1L, thereby inhibiting the methylation of nucleosomal histone H3 on lysine 79 (H3K79) that is bound to the mixed lineage leukemia (MLL) fusion protein which targets genes and blocks the expression of leukemogenic genes. This eventually leads to an induction of apoptosis in the leukemic cells bearing the MLL gene translocations. DOT1L, a non-SET domain-containing histone methyltransferase, specifically methylates H3K79 and plays a key role in normal cell differentiation and in the development of leukemia with MLL gene rearrangement on chromosome 11 and promotes the expression of leukemia-causing genes.

The hydrochloride salt of an orally-active thiazolidinedione with antidiabetic properties and potential antineoplastic activity. Pioglitazone activates peroxisome proliferator-activated receptor gamma (PPAR-gamma), a ligand-activated transcription factor, thereby inducing cell differentiation and inhibiting cell growth and angiogenesis. This agent also modulates the transcription of insulin-responsive genes, inhibits macrophage and monocyte activation, and stimulates adipocyte differentiation.

The sodium salt of piperacillin, a broad-spectrum semisynthetic, ampicillin-derived ureidopenicillin antibiotic with bactericidal activity. Piperacillin binds to and inactivates penicillin-binding proteins (PBPs), enzymes located on the inner membrane of the bacterial cell wall, resulting in the weakening of the bacterial cell wall and cell lysis. PBPs participate in the terminal stages of assembling the bacterial cell wall, and in reshaping the cell wall during cell division. Inactivation of PBPs interferes with the cross-linkage of peptidoglycan chains necessary for bacterial cell wall strength and rigidity. Check for active clinical trials using this agent.

A crystalline antibiotic fermentation product isolated from the bacterium Streptomyces griseoluteus with antineoplastic activity. Piperazinedione alkylates DNA at the N-7 position of guanine, inhibiting DNA replication and inducing cell cycle arrest.

A standardized extract containing the active alkaloid piperine, derived from the fruit of the plant Piper nigrum (black pepper) and/or the plant Piper longum L. (long pepper), with thermogenic properties. Co-ingestion of piperidine enhances the bioavailability of various nutrients, including beta-carotene, curcumin, selenium, pyridoxine and coenzyme Q10. In addition, this agent may exert anti-inflammatory and anti-tumor activities and may enhance the production of serotonin.

Brand name for piperacillin sodium

An analogue of the anthracycline antineoplastic antibiotic doxorubicin. Pirarubicin intercalates into DNA and interacts with topoisomerase II, thereby inhibiting DNA replication and repair and RNA and protein synthesis. This agent is less cardiotoxic than doxorubicin and exhibits activity against some doxorubicin-resistant cell lines.

An orally active synthetic antifibrotic agent structurally similar to pyridine 2,4-dicarboxylate. Pirfenidone inhibits fibroblast, epidermal, platelet-derived, and transforming beta-1 growth factors, thereby slowing tumor cell proliferation. This agent also inhibits DNA synthesis and the production of mRNA for collagen types I and III, resulting in a reduction in radiation-induced fibrosis.

A diphenylpropylamine and opioid receptor agonist, with analgesic activity. Upon administration, piritramide binds to and activates mu-opioid receptors in the central nervous system (CNS), thereby mimicking the effects of endogenous opioids and producing analgesic relief.

A synthetic antifolate agent with antiparasitic, antipsoriatic and antitumor properties. Piritrexim inhibits the enzyme dihydrofolate reductase enzyme, thereby disrupting folate metabolism and DNA synthesis and cell division.

An orally bioavailable inhibitor of the receptor tyrosine kinase (RTK) epidermal growth factor receptor (ErbB; EGFR) family, with potential antineoplastic activity. Upon administration, pirotinib selectively and irreversibly binds to and inhibits the epidermal growth factor receptors 1 (ErbB1; EGFR), 2 (ErbB2; HER2), and 4 (ErbB4; HER4). This may result in the inhibition of cell growth and angiogenesis in tumors overexpressing these RTKs. EGFRs play major roles in both tumor cell proliferation and tumor vascularization, and are overexpressed in many cancer cell types.

An anthrapyrazole antineoplastic antibiotic. Piroxantrone intercalates into DNA and interacts with topoisomerase II, thereby inhibiting DNA replication and repair and RNA and protein synthesis. Although less cardiotoxic than doxorubicin, this agent exhibits a narrow spectrum of antineoplastic activity.

A nonsteroidal oxicam derivative with anti-inflammatory, antipyretic and analgesic properties. As a non-selective, nonsteroidal anti-inflammatory drug (NSAID), piroxicam binds and chelates both isoforms of cyclooxygenases (COX1 and COX2), thereby stalling phospholipase A2 activity and conversion of arachidonic acid into prostaglandin precursors at the rate limiting cyclooxygenase enzyme step. This results in inhibition of prostaglandin biosynthesis. As a second, independent effect, piroxicam inhibits the activation of neutrophils thereby contributing to its overall anti-inflammatory effects.

A vaccine composed of a phosphorylated peptide from the tumor associated antigen insulin receptor substrate-2 (IRS2) and a tetanus-derived peptide, with potential immunomodulating and antineoplastic activities. Upon administration of pIRS2 phosphopeptide-tetanus peptide vaccine, the pIRS2 phosphopeptide may stimulate the immune system to mount a cytotoxic T-lymphocyte (CTL) response against phosphopeptide-containing tumor cells. The tetanus peptide serves as an immunoadjuvant and induces a helper T-cell response which may help stimulate an immune response against the pIRS2-expressing melanoma tumor cells. IRS2 is upregulated in a variety of cancer cells.

Brand name for recombinant oxytocin

The dimaleate salt of a synthetic, noncardiotoxic aza-anthracenedione analogue with potential antineoplastic activity. Pixantrone intercalates into DNA and induces topoisomerase II-mediated DNA strand crosslinks, resulting in inhibition of DNA replication and tumor cell cytotoxicity.

An orally available inhibitor of the beta-isoform of protein kinase C (PKC), with potential immunosuppressive and antineoplastic activities. Upon oral administration, PKC-beta inhibitor MS-553 selectively binds to and inhibits PKC-beta, which prevents the activation of PKC-beta-mediated signaling pathways. This may lead to the induction of cell cycle arrest and apoptosis in susceptible tumor cells. PKC-beta, a serine/threonine protein kinase overexpressed in certain types of cancer cells, is involved in tumor cell differentiation, proliferation, invasion and survival.

An orally available, small-molecule, allosteric activator of the red cell isoform of pyruvate kinase (PK-R), with potential to improve hemolytic anemia in patients with pyruvate kinase deficiency (PKD). Upon oral administration, AG-348 binds to and activates PK-R, thereby enhancing glycolytic pathway activity, improving adenosine triphosphate (ATP) levels and reducing 2,3-diphosphoglycerate (2,3-DPG) levels. Mutations in PK-R cause deficiency in PK-R which prevents adequate red blood cell (RBC) glycolysis, leading to a buildup of the upstream glycolytic intermediate 2,3-DPG and deficiency in the PK-R product ATP.

An inactive substance, treatment or procedure that is intended to provide baseline measurements for the experimental protocol of a clinical trial. Check for active clinical trials using this agent.

A synthetic urethane derivative of pladienolide D with potential antineoplastic activity. Pladienolide derivative E7107 is generated from the 12-membered macrolide pladienolide D, one of several macrolides derived from the bacterium Streptomyces platensis Mer-11107. This agent appears to bind to the 130-kDa subunit 3 (spliceosome-associated protein 130; SAP130) of the splicing factor 3b (SF3b), resulting in inhibition of pre-messenger RNA splicing and the arrest of cell-cycle progression. The splicing factor SF3b is a multiprotein complex integral to the accurate excision of introns from pre-messenger RNA; the subunit SAP130 associates with U2 snRNP and is recruited to prespliceosomal complexes.

Brand name for levonorgestrel

A proprietary botanical formulation derived from a traditional Chinese medicinal (TCM) plant with hematopoietic activity. Although the mechanism of action has yet to be fully elucidated, plant-derived hematopoiesis enhancer PG2 appears to stimulate multi-lineage progenitor cells that may be closely related to the hematopoietic stem cell. In both chemotherapy- and radiation therapy-induced animal models of myelosuppression, this agent has been shown to restore granulocyte, erythrocyte, and platelet counts to normal levels. Plant-derived hematopoiesis enhancer PG2 stimulates the production of numerous cytokines such as granulocyte-colony stimulating factor (G-CSF) and may stimulate the production of neuroendocrine hormones.

A whole cell vaccine derived from a distinct subset of dendritic cells (DCs) with a plasma cell-like morphology that exhibits immunomodulating activity. Plasmacytoid dendritic cells (pDCs) express a characteristic set of surface markers, such as CD123 (interleukin-3 receptor alpha chain), BDCA-2 (blood dendritic cell antigen 2; CD303) and BDCA-4 (CD304), as well as intracellular toll-like receptors 7 and 9. Upon stimulation, the activated pDCs produce substantial amounts of interferon (IFN) alpha, and to a lesser degree IFN-beta, as well as other cytokines and chemokines, such as tumor necrosis factor alpha and interleukins 1, 6 and 8. In addition, these pDCs, directly or indirectly stimulate T-cells, B-cells and natural killer cells. This may potentially lead to increased immunity against tumor cells.

A plasmid encoding the protein antiangiogenic metargidin plasmid (AMEP), the disintegrin domain of ADAM-15 (metargidin), with potential antiangiogenic and antimetastatic activities. Upon intratumoral electrotransfer of plasmid encoding AMEP, AMEP binds to cellular integrin receptors alpha-v-beta-3 (avb3) and alpha-5-beta-1 (a5b1), which are upregulated on activated endothelial cells and a variety of tumor cells. Binding to the integrin receptors may inhibit angiogenesis and may inhibit tumor cell proliferation.

A preparation of red blood cells (RBCs) that have been infected with the malaria parasite Plasmodium vivax (P. vivax), with potential immunomodulating and antineoplastic activities. Upon administration of the P. vivax-infected RBCs, the P. vivax infection stimulates host immune responses against the P. vivax-infected RBCs. This also stimulates both innate and adaptive anti-tumor immune responses. This leads to the production of cytokines, including interferon-gamma (IFN-g) and tumor-necrosis factor alpha (TNF-a), the proliferation and activation of natural killer (NK) cells, dendritic cells (DCs), CD4-positive T lymphocytes, and cytotoxic T lymphocytes (CTLs). This results in the inhibition of tumor cell proliferation, induction of tumor cell apoptosis, and prevents angiogenesis.

A preparation of platinum acetylacetonate supported by sol-gel technology functionalized titania, with potential antineoplastic activity. Upon intravenous administration, the platinum moiety forms complexes with nucleophilic groups such as GC-rich sites in DNA, inducing intrastrand and interstrand DNA cross-links, as well as DNA-protein cross-links, resulting in apoptosis and cell growth inhibition. Compared to platinum alone, the nanoparticle formulation allows increased delivery of platinum to the tumor site, thereby increasing efficacy while reducing systemic toxicity.

Brand name for clopidogrel bisulfate

A derivative of pyridoxyl ethyldiamine (PLED) and mimetic of the human mitochondrial manganese superoxide dismutase (MnSOD), with antioxidant, metal chelating and potential chemoprotective activities. Upon administration, PLED-based MnSOD mimetic mimics MnSOD and scavenges oxygen free radicals such as superoxide anion, hydrogen peroxide, and hydroxyl radical, thereby preventing oxygen free radical damage to macromolecules such as DNA and minimizing oxygen free radical-related chemotoxicity in normal tissues. In addition, this agent is able to strongly bind to iron.

The hydrochloride salt form of CC-122, an orally available pleiotropic pathway modulator with potential antineoplastic activity.

A bicyclam with hematopoietic stem cell-mobilizing activity. Plerixafor blocks the binding of stromal cell-derived factor (SDF-1alpha) to the cellular receptor CXCR4, resulting in hematopoietic stem cell (HSC) release from bone marrow and HSC movement into the peripheral circulation.

An orally bioavailable, small molecule, non-polyglutamatable, antifolate quinazoline derivative thymidine synthetase inhibitor with potential antineoplastic activity. Plevitrexed is transported into the cell via the physiological reduced folate carrier (RFC) system. Intracellularly, this agent selectively binds to the folate binding site of thymidylate synthase and inhibits thymidine synthesis, which may result in DNA synthesis inhibition and apoptosis.

An antibiotic isolated from the bacterium Streptomyces plicatus with antineoplastic activity. Plicamycin, also known as mithramycin, binds to the minor groove of DNA at GC-rich sites, resulting in inhibition of RNA synthesis; this agent also inhibits mRNA expression, resulting in a reduction in protein synthesis. In addition, plicamycin may inhibit bone resorption by down regulating transcription of c-src, an oncogene involved in bone metabolism and resorption.

An orally active diketopiperazine derivative with potential antineoplastic activity. Plinabulin selectively binds to the colchicine-binding site of tubulin, thereby interrupting equilibrium of microtubule dynamics; mitotic spindle assembly is disrupted, resulting in cell cycle arrest at the M phase and blockage of cell division in tumor cells. In addition, this agent induces tubulin depolymerization in vascular endothelial cells, resulting in the disruption of tumor blood vessel architecture and a selective collapse of tumor vasculature.

A cyclic depsipeptide isolated from the marine tunicate Aplidium albicans. Plitidepsin displays a broad spectrum of antitumor activities, inducing apoptosis by triggering mitochondrial cytochrome c release, initiating the Fas/DC95, JNK pathway and activating caspase 3 activation. This agent also inhibits elongation factor 1-a, thereby interfering with protein synthesis, and induces G1 arrest and G2 blockade, thereby inhibiting tumor cell growth.

An orally available, Polo-like kinase 1 (PLK1) inhibitor with potential antineoplastic activity. Polo-like kinase 1 inhibitor TAK-960 selectively inhibits PLK1, inducing selective G2/M cell-cycle arrest followed by apoptosis in a variety of tumor cells while causing reversible cell-cycle arrest at the G1 and G2 stages without apoptosis in normal cells. PLK1 inhibition may result in the inhibition of proliferation in PLK1-overexpressed tumor cells. PLK1, named after the polo gene of Drosophila melanogaster, is a serine/threonine kinase crucial in the regulation of mitosis.

A humanized monoclonal antibody directed against the human chemokine receptor 2 (CCR2), with potential antiangiogenic, immunomodulating, antimetastatic, and antineoplastic activities. Plozalizumab binds to CCR2 and prevents binding of the endothelium-derived CLL2 (monocyte chemoattractant protein-1 or MCP1) to its receptor CCR2, which may result in inhibition of CCR2 activation and so inhibition of angiogenesis, tumor cell migration, and tumor cell proliferation. In addition, this agent may reduce levels of C-reactive protein (CRP). The G-protein coupled receptor CCR2 is expressed on the surface of monocytes and macrophages, stimulates the migration and infiltration of these cell types, and plays an important role in inflammation, angiogenesis, and tumor cell migration and proliferation.

A synthetic tetrahydroisoquinoline alkaloid related to the marine natural compounds Jorumycin and the family of Renieramycins, obtained from molluscs and sponges, respectively, with potential antineoplastic activity. PM00104 reversibly binds to DNA and interferes with DNA replication, transcription, and translation. DNA binding by this agent does not trigger DNA damage checkpoint responses, hence PM00104 exhibits a reversible cytotoxicity.

A pneumococcal conjugate vaccine containing 13 different strains of the bacterium Streptococcus pneumoniae, used in children and studied in immunocompromised patients for the prevention of pneumococcal disease. The pneumococcal 13-valent conjugate vaccine contains capsular antigen polysaccharides derived from the S. pneumoniae serotypes 1, 3, 4, 5, 6A, 6B, 7F, 9V, 14, 18C, 19A, 19F and 23F that are individually conjugated to a nontoxic diphtheria cross-reactive material (CRM) carrier protein (CRM197). Upon vaccination, pneumococcal 13-valent conjugate vaccine induces active immunization against 13 different serotypes of S. pneumoniae and protects against pneumococcal disease.

An active immunizing agent used to prevent infection by the bacterium Streptococcus pneumoniae. Pneumococcal 7-valent conjugate vaccine consists of a solution of saccharides of the capsular antigens of Streptococcus serotypes 4, 6B, 9V, 14, 18C, 19F, and 23F individually conjugated to diphtheria CRM 197 protein. Check for active clinical trials using this agent.

An polyvalent vaccine used to prevent infection by the bacterium Streptococcus pneumoniae. Pneumococcal polyvalent vaccine contains higly purified capsular antigens from the 23 most prevalent or invasive pneumococcal types of Streptococcus pneumoniae to ensure cross-protection. Following vaccination, protective capsular type-specific antibody levels typically develop by the third week; serotype-specific antibody levels generally decline after 5-10 years.

Brand name for pneumococcal polyvalent vaccine

A plasmid DNA cancer vaccine encoding the intracellular domain (ICD) of the HER-2/neu proto-oncogene. Upon administration and after cellular uptake by skin or muscle cells, the pNGVL3-hICD vaccine plasmid expresses the HER-2/neu protein, which, after intracellular processing, may elicit both antigen-specific cytotoxic T-lymphocyte (CTL) and humoral immune responses against tumor cells expressing HER-2. The HER-2/neu ICD protein is highly immunogenic and, as a subdominant epitope, may be associated with decreased immune tolerance.

A cancer vaccine consisting of the DNA plasmid pNGVL4a-A encoding calreticulin (CRT) linked to a detox form of human papillomavirus (HPV) type 16 E7 antigen, with potential immunomodulating and antineoplastic activities. Upon administration, this vaccine may generate a potent cytotoxic T-lymphocyte (CTL) response against E7-expressing tumor cells, resulting in tumor cell death. For E7(detox), the amino acids in E7 at positions 24 (cysteine to glycine) and 26 (glutamic acid to glycine) were substituted. CRT, a 46 kDa protein located in the lumen of the cell's endoplasmic reticulum (ER), may potentiate MHC class I presentation of HPV-16 E7 to E7-specific CD8-positive T cells. In addition, pNGVL4a-A contains two short immunostimulatory DNA sequences (ISS) in the noncoding region, which may elicit the production of IFN- and IL-12 in transfected keratinocytes and dermal antigen presenting cells (APCs), resulting in a potent T helper cell type 1 response.

An antigen-specific DNA cancer vaccine consisting of the coding sequences of a signal peptide (pNGVL4a-Sig), a detox form of the human papillomavirus type 16 (HPV-16) antigen E7, and the heat shock protein 70 (HSP70). Upon administration, this vaccine may generate potent cytotoxic CD8(+) T-cell responses against E7-expressing tumor cells, resulting in tumor cell death.

An ovine atadenovirus encoding E. coli purine nucleoside phosphorylase (PNP) with prodrug activating activity. Under the control of a prostate-directed promoter, PNP-expressing atadenovirus vaccine FP253 expresses PNP in prostate tissue only after intraprostatic administration; this enzyme catalyzes systemically administered fludarabine prodrug into the active agent, 2-fluoroadenine. Localized prodrug activation provides prostate-targeted chemotherapy, potentially reducing systemic side effects.

Brand name for pneumococcal polyvalent vaccine

An orally bioavailable inhibitor of RNA polymerase I (Pol I), with potential antineoplastic activity. Upon oral administration, CX-5461 selectively binds to and inhibits Pol I, prevents Pol I-mediated ribosomal RNA (rRNA) synthesis, induces apoptosis, and inhibits tumor cell growth. Pol I, the multiprotein complex that synthesizes rRNA, is upregulated in cancer cells and plays a key role in cell proliferation and survival. Hyperactivated rRNA transcription is associated with uncontrolled cancer cell proliferation.

An orally bioavailable chelate composed of zinc and L-carnosine, with potential gastroprotective, anti-oxidant, anti-ulcer and anti-inflammatory activities. Upon administration, polaprezinc increases the expression of various anti-oxidant enzymes, such as superoxide dismutase 1 (SOD-1), SOD-2, heme oxygenase-1 (HO-1), glutathione S-transferase (GST), glutathione peroxidase (GSH-px), peroxidredoxin-1 (PRDX1; PRXI) and PRXD5 (PRXV) in the gastric mucosa, which protect cells against reactive oxygen species (ROS). In addition, this agent inhibits the activity of the transcription factor nuclear factor-kappaB (NF-kB) and reduces the expression of several pro-inflammatory cytokines, such as interleukin (IL) 1beta, IL-6, IL-8, and tumor necrosis factor alpha (TNF-a). Polaprezinc also increases the expression of various growth factors, such as platelet-derived growth factor-B (PDGF-B), vascular endothelial growth factor (VEGF), and nerve growth factor (NGF), and various heat shock proteins (HSPs), including HSP90, HSP70, HSP60, HSP47, HSP27, and HSP10. This protects against damages to, and accelerates healing of the gastric mucosa.

An antibody-drug conjugate (ADC) composed of a monoclonal antibody directed against B-cell antigen receptor complex-associated protein beta chain (CD79B) conjugated, via a protease-cleavable peptide linker, to monomethyl auristatin E (MMAE), an auristatin derivative and a potent microtubule inhibitor, with potential antineoplastic activity. Upon administration, polatuzumab vedotin selectively binds to CD79B, a protein which is abundantly expressed on the surface of B-cells. Upon internalization and proteolytic cleavage, MMAE binds to tubulin and inhibits its polymerization, resulting in G2/M phase arrest and tumor cell apoptosis. CD79B, a component of the B-cell receptor (BCR), plays a key role in B-cell receptor signaling and is expressed on the surface of almost all types of malignant B-cells.

A naturally occurring polysaccharide composed of beta-1,4-linked glucosamine residues with potential antineoplastic activity. Upon administration, poliglusam may, through a not yet fully elucidated mechanism, reduce advanced glycation end product (AGE) levels. This may reduce the interaction between AGEs and the receptor for advanced glycation end products (RAGE, AGER), which is overexpressed in some tumor types and is associated with poor patient outcomes. AGE-RAGE interaction may induce the phosphorylation and subsequent degradation of retinoblastoma protein (Rb), a key cell cycle inhibitor and tumor suppressor, through the phosphoinositide 3-kinase (PI3K)/protein kinase B (PKB, Akt) signaling pathway. Hyperphosphorylation of Rb leads to the dissociation of the Rb-E2F complex, which triggers the activation of genes required for G1/S transition and tumorigenesis. Reducing AGE levels may limit AGE-RAGE interaction and normalize the G1 to S-phase transition, potentially reducing the development and progression of certain cancers. AGEs are non-enzymatic protein modifications produced during the normal aging process that have been shown to play a role in the development and progression of some cancers.

A solution containing the polymer polihexanide, with potential antimicrobial, disinfectant and wound healing activities. Upon application to a wound, polihexanide strongly binds to the wound surface and exerts an antiseptic effect through the binding of the positively charged guanidine groups of polihexanide with the negatively charged phospholipids of the bacterial cell membrane. This compromises the stability of the bacterial cell membrane, which results in the leakage of cytoplasmic components and leads to bacterial cell death. In addition, polihexanide accelerates wound healing by promoting epithelial cell migration and proliferation.

Brand name for mepivacaine hydrochloride

A small molecule Polo-like kinase 1 (PLK1) inhibitor with potential antineoplastic activity. Polo-like kinase 1 inhibitor GSK461364 selectively inhibits Plk1, inducing selective G2/M arrest followed by apoptosis in a variety of tumor cells while causing reversible cell arrest at the G1 and G2 stage without apoptosis in normal cells. Plk1, named after the polo gene of Drosophila melanogaster, is a serine/threonine protein kinase involved in regulating mitotic spindle function in a non-ATP competitive manner. Check for active clinical trials using this agent.

An orally bioavailable Polo-like kinase 1 (Plk1) inhibitor with potential antineoplastic activity. Polo-like kinase 1 inhibitor MK1496 selectively inhibits Plk1, inducing selective G2/M arrest followed by apoptosis in a variety of tumor cells while causing reversible cell arrest at the G1 and G2 stage without apoptosis in normal cells. Plk1, named after the polo gene of Drosophila melanogaster, is a serine/threonine protein kinase involved in regulating mitotic spindle function in a non-ATP competitive manner.

An orally bioavailable, small-molecule Polo-like kinase 1 (PLK1) inhibitor with potential antineoplastic activity. Polo-like kinase 1 inhibitor NMS-1286937 selectively inhibits PLK1, inducing selective G2/M cell-cycle arrest followed by apoptosis in a variety of tumor cells while causing reversible cell-cycle arrest at the G1 and G2 stages without apoptosis in normal cells. PLK1 inhibition may result in the inhibition of proliferation in PLK1-overexpressing tumor cells. PLK1 is a serine/threonine protein kinase crucial in the regulation of mitosis.

An orally available fumarate salt form of CFI-400945, a polo-like kinase 4 (PLK4) inhibitor with potential antineoplastic activity. Upon oral administration, polo-like kinase 4 inhibitor CFI-400945 selectively inhibits PLK4, which results in the disruption of mitosis and the induction of apoptosis. PLK4 inhibition also prevents cell division and inhibits proliferation of PLK4-overexpressing tumor cells. PLK4, a member of the polo family of serine/threonine kinases overexpressed in a variety of cancer cell types, plays a crucial role in the regulation of centriole duplication during the cell cycle.

A synthetic polyadenylic-polyuridylic acid double-stranded RNA. Poly AU may stimulate the release of cytotoxic cytokines and, by inducing the production of interferon, may increase the number and tumoricidal activities of various immunohematopoietic cells.

A synthetic polyinosinic-polycytidylic acid double-stranded RNA. Poly IC may stimulate the release of cytotoxic cytokines and, by inducing interferon-gamma production, may increase the number and tumoricidal activities of various immunohematopoietic cells.

A synthetic complex of carboxymethylcellulose, polyinosinic-polycytidylic acid, and poly-L-lysine double-stranded RNA. Poly ICLC may stimulate the release of cytotoxic cytokines and, by inducing interferon-gamma production, may increase the tumoricidal activities of various immunohematopoietic cells.

A transparent, biocompatible, non-resorbable, homogenous hydrogel containing 97.5% apyrogenic water and 2.5% of the cross-linked, synthetic polyacrylamide. Upon injection into the urethral submucosal tissue, the polyacrylamide hydrogel serves as a bulk forming agent and may possibly increase the strength of the urethral sphincter and thereby prevent or decrease stress-induced urinary incontinence. Check for active clinical trials using this agent.

A polybisphosphonate dextran-guanidine conjugate with potential anti-resorptive and antineoplastic activities. Alendronic acid and aminoguanidine were conjugated sequentially to oxidized dextran resulting in an average of 8 alendronate and 50 guanidine groups coupled to the dextran backbone. Upon administration, the poly-alendronate dextran-guanidine conjugate inhibits the mevalonate pathway by inhibiting farnesyl diphosphate synthase (FDPS) which leads to a reduction in protein prenylation and to the loss of downstream metabolites essential for osteoclast function. This eventually leads to the induction of apoptosis in osteoclasts. Also, by preventing osteoclast-mediated bone resorption, this agent decreases bone turnover and stabilizes the bone matrix. The guanidine moiety increases the nitrogen content and possibly the activity of the bisphosphonate and its ability to inhibit FDPS. In addition, the guanidine moiety facilitates cell internalization and may contribute to this agent’s cytotoxicity.

A second generation polyamine analogue, synthesized through the restriction of molecular conformations of parent polyamine compounds, with potential antineoplastic activity. Polyamine analogue PG11047 may displace endogenous polyamines from DNA binding sites, thereby interfering with cell cycle processes dependent upon polyamine binding and function, and resulting in cell-cycle arrest, induction of apoptosis, depletion of polyamines, and interference with gene and ligand-receptor activities involved with cell growth. This agent may exhibit decreased toxicity and enhanced cytotoxicity profiles compared to first-generation polyamine compounds. In tumor cells, there is an increase dependence on polyamines as well as a dysregulated polyamine metabolic pathway resulting in abnormal or sustained tumor growth.

An analogue of naturally occurring polyamine (PA), with potential antineoplastic activity. Upon subcutaneous administration, SBP-101 displaces endogenous PAs from PA-binding sites on the cell surface, which prevents internalization of PA. This inhibits PA-dependent cell cycle processes and results in cell cycle arrest, the induction of apoptosis, and inhibition of tumor cell proliferation. PA uptake is upregulated in various tumor types and increased levels of PA leads to enhanced tumor cell growth. Check for active clinical trials using this agent.

The dicaprate salt form of AMXT-1501, an orally bioavailable polyamine transport inhibitor, with immunostimulating and antineoplastic activities. Upon administration, AMXT-1501 targets, binds to and blocks polyamine transport from the bloodstream into the tumor microenvironment (TME), thereby preventing cancer cell uptake. This decreases polyamine concentrations inside the TME and tumor cell, inhibits tumor cell proliferation and induces apoptosis. In addition, AMXT-1501 may abrogate polyamine-mediated immune suppression in the TME. Polyamines, naturally found in normal, heathy cells, are required for normal cell growth and division. In cancer cells, polyamines play key roles in tumor cell proliferation and tumor-induced suppression of the patient's immune system.

A commercial combination preparation that contains an adhesive polycarbophil polymer, which is used for vaginal lubrication. Polycarbophil is an insoluble compound that absorbs water and, after topical administration, adheres to vaginal epithelial cells. As a result, it helps both moisturize vaginal tissue and relieve the discomfort that is associated with vaginal dryness.

A cream containing a non-ionic surfactant belonging to the polyethylene glycol (PEG) family. Polyethylene glycol 1000 cetyl ether is used as an ointment base, but can also be used as an emulsifier and solubilizer.

An enema containing the osmotic agent polyethylene glycol (PEG) 3350, also called macrogol 3350, with laxative activity. Upon rectal administration of the PEG3350-containing enema NER1008, PEG creates an osmotic gradient, which promotes the retention of water in the bowel. This increases the water content of stool, which results in increased gastrointestinal (GI) motility, decreased stool transit time and evacuation of colonic contents.

A 2- or 3-dimensional hydrophilic, cross-linked polymer of polyethylene glycol (PEG). These hydrogels can be used as scaffolds for tissue engineering or as drug delivery carriers.

A formulation containing recombinant endostatin attached to polyethylene glycol (PEG), with potential anti-angiogenic and antineoplastic activities. Endostatin, a 20 kDa C-terminal proteolytic fragment of collagen XVIII, induces microvascular endothelial cell apoptosis and inhibits endothelial proliferation and angiogenesis, which may result in a reduction of tumor cell growth. Modification with PEG extends the circulation half-life of endostatin, improves stability and increases solubility in organic solvents. Check for active clinical trials using this agent.

A polyethylene glycol (PEG) conjugate of 7-ethyl-10-hydroxycamptothecin with potential antineoplastic activity. After hydrolysis in vivo, 7-ethyl-10-hydroxycamptothecin (SN38), an active metabolite of irinotecan, is released from polyethyleneglycol-7-ethyl-10-hydroxycamptothecin (PEG-SN38); 7-ethyl-10-hydroxycamptothecin selectively stabilizes topoisomerase I-DNA covalent complexes, resulting in single-stranded and double-stranded DNA breaks, the inhibition of DNA replication, and the induction of apoptosis. This agent is designed to deliver the active metabolite to tumor cells without the need for conversion as is the case with irinotecan. Compared to unPEGylated 7-ethyl-10-hydroxycamptothecin, PEGylation improves solubility and allows for parental delivery, and may result in a longer half-life and higher exposure for tumor cells.

A long-acting formulation composed of 7-ethyl-10-hydroxycamptothecin (SN38), a camptothecin derivative and active metabolite of irinotecan conjugated to polyethylene glycol (PEG), via a proprietary, cleavable linker, with potential antineoplastic activity. Upon administration, the proprietary linkage system allows for very slow release of SN38 from the formulation. Upon release, SN38 selectively stabilizes covalent topoisomerase I-DNA complexes, and results in single-stranded and double-stranded DNA breaks, the inhibition of DNA replication, and the induction of apoptosis. This agent is designed to deliver the active metabolite to tumor cells without the need for conversion as is the case with irinotecan. Compared to other PEG-SN38-based formulations, the linker system in DFP-13318 increases its half-life and the exposure time for tumor cells, while decreasing both blood plasma concentrations and exposure to off-target organs; this results in increased efficacy.

Brand name for therapeutic immune globulin

A water-soluble and biodegradable polymer naturally synthesized by various strains of Bacillus and composed of D- and L-glutamic acid polymerized via gamma-amide linkages, with potential antineoplastic activity. Upon administration, poly-gamma glutamic acid may augment the immune response by increasing the production of interferon-gamma (IFN-gamma) and tumor necrosis factor-alpha (TNF-alpha) and inducing the activation of macrophage and natural killer (NK) cells. In addition to its tumor control properties, IFN-gamma is a major mediator of innate and adaptive immunity against viral and intracellular bacterial infections. TNF-alpha is a cytokine involved in systemic inflammation, which is capable of inducing apoptotic cell death and exhibits anti-tumoral effects.

A therapeutic formulation consisting of camptothecin, an alkaloid isolated from the Chinese tree Camptotheca acuminata, conjugated with polyglutamate. During the S phase of the cell cycle, camptothecin selectively stabilizes topoisomerase I-DNA covalent complexes, thereby inhibiting religation of topoisomerase I-mediated single-strand DNA breaks and producing potentially lethal double-strand DNA breaks when encountered by the DNA replication machinery. Conjugation with polyglutamate renders this agent more water soluble and less toxic than the parent molecule.

A cancer vaccine composed of inactivated rabies vaccine (RV-V) and polyinosinic-polycytidylic acid (poly IC; poly I-C), an immunostimulant and Toll-like receptor 3 (TLR3) agonist, with potential immunostimulating and antineoplastic activities. Upon administration of the poly IC/inactivated RV-V YS-ON-001, the RV-V stimulates the immune system in various ways, such as promoting the activation and proliferation of T helper type 1 (Th1) cells, dendritic cells (DCs), B cells and natural killer cells (NKs), promoting macrophage M1 polarization, downregulating regulatory T cells (Tregs), and inducing the production of anti-tumor cytokines. This re-activates immune responses in the suppressed tumor microenvironment (TME), leading to an induction of cytotoxic T-lymphocyte (CTL)-mediated immune response against the tumor cells, which cause tumor cell apoptosis and a reduction of tumor cell proliferation. Poly IC, a synthetic double-stranded RNA with one strand composed of a inosinic acid polymer and the other strand a cytidylic acid polymer, binds to TLR3 and stimulates the release of cytotoxic cytokines, such as interferon-gamma (IFNg). This may boost the immune response against the tumor cells.

A nanoparticle formulation containing the poorly water-soluble naturally-occurring flavonoid luteolin encapsulated within a water-soluble polymer, with potential anti-oxidant, anti-inflammatory, apoptosis-inducing and chemopreventive activities. Upon administration of the polymer-encapsulated luteolin nanoparticle, luteolin scavenges free radicals, protects cells from reactive oxygen species (ROS)-induced damage and induces direct tumor cell cycle arrest and apoptosis in tumor cells. This inhibits tumor cell proliferation and suppresses metastasis. Compared to luteolin alone, encapsulation increases the delivery of luteolin to the tumor cells by protecting the drug against clearance and degradation, increases blood circulation time and enhances delivery into the tumor through the leaky vasculature.

A polymeric prodrug of camptothecin (CPT) with potential antineoplastic activity. Polymeric camptothecin prodrug XMT-1001 consists of CPT conjugated to the 60-70 kDa, inert, bio-degradable, hydrophilic copolymer poly[1-hydroxymethylene hydroxymethyl formal] (PHF). Through a dual-phase, non-enzymatic release mechanism, CPT is first released in plasma from XMT-1001 as the lipophilic prodrugs CPT-SI (a succinimidoglycinate derivative) and CPT-SA (a succinamidoyl glycinate derivative), which are then hydrolyzed within tissues to release the lactone form of CPT. CPT inhibits the catalytic activity of DNA topoisomerase I, thereby inhibiting DNA replication and inducing apoptosis. This agent may exhibit a more favorable pharmacokinetic profile than other agents in the same class.

Brand name for amoxicillin

Brand name for alpha-lipoic acid/vitamin/mineral supplement PolyMVA

A mixture of the polypeptides polymyxins B1 and B2, both obtained from Bacillus polymyxa strains, with antimicrobial activity. Polymyxin B exerts its antimicrobial effect through its cationic detergent action on cell membranes. Specifically, this antibiotic binds to the negatively charged site in the lipopolysaccharide layer of the bacterial cell membrane via electrostatic affinity with the positively charged amino groups in the cyclic peptide portion. Subsequently, the fatty acid portion of polymyxin B dissolves in the hydrophobic region of the bacterial cell membrane. This results in an alteration in cell membrane structure, disruption of cell wall integrity and an increase in permeability for water and molecules. This will eventually lead to bacterial cell death.

A cartridge containing a polystyrene-based composite woven fiber that is covalently attached to the anti-microbial cyclic cationic polypeptide antibiotic polymyxin-B (PMX) and can potentially be used for hemoperfusion purposes. Upon extracorporeal treatment, a patient's blood flows through the fibers in the polymyxin-B immobilized fiber PMX-20R cartridge and the circulating endotoxins from the blood are selectively adsorbed by PMX, which has positively charged amino groups that bind to the negatively charged site in the lipid A portion of the lipopolysaccharide (LPS) layer of the bacterial cell membrane. This removes endotoxins from the blood and, upon administration of the blood back into the patient, helps treat or reduce the incidence of endotoxemia and sepsis.

Brand name for kunecatechins ointment

A nutritional supplement composed of an aqueous extract derived from the leaves of the tropical fern belonging to the Polypodiaceae family, Polypodium leucotomos (PL; Phlebodium aureum), with potential photoprotective, skin protective, anti-inflammatory, immunomodulating and antioxidant activities. This extract contains many phenolic compounds, such as ferulic, caffeic, coumaric and vanillic acid, which are mainly responsible for this extract's effects. Upon administration, Polypodium leucotomos extract (PLE) exerts antioxidant activity by scavenging free radicals and inhibiting the generation and release of reactive oxygen species (ROS), thereby preventing ultraviolet (UV)-induced as well as ROS-induced DNA damage. In addition, the chemicals in this extract protect antioxidant enzymes and modulate expression of cancer and inflammation-related genes, including the induction of the expression of tumor suppressor genes and the inhibition of the expression of pro-inflammatory cytokines and inflammatory enzymes, thereby inhibiting the activation of signal transduction pathways involved in carcinogenesis and inflammation, respectively. PLE also stimulates tissue inhibitors of metalloproteinases (TIMPs) and inhibits matrix metalloproteinases (MMPs).

A protein-bound polysaccharide derived from the mushroom Trametes versicolor (Turkey Tail) with immunoadjuvant and potential antitumor activities. Although its mechanism of action has yet to be fully elucidated, in vitro and in vivo studies indicate that polysaccharide-K induces peripheral blood monocyte secretion of IL-8 and TNF-alpha, induces T cell proliferation, and prevents cyclophosphamide-induced immunosuppression. This agent has also been reported to stimulate macrophages to produce reactive nitrogen intermediates and superoxide anions and to promote apoptosis in the promyelocytic leukemia cell line HL-60.

A nanoparticle formulation composed of a polysiloxane-based inorganic matrix bound to cyclic chelates composed of the chelating agent DOTA (1,4,7,10-tetra-azacyclododecane-1-glutaric anhydride-4,7,10-triacetic acid) covalently bound to the paramagnetic contrast enhancer gadolinium (Gd), a high-Z material, with potential use in enhancing diagnostic images upon magnetic resonance imaging (MRI) and potential radiosensitizing activity. Upon intravenous administration of polysiloxane matrix-gadolinium chelates-based nanoparticles, the nanoparticles extravasate to tumor sites due to the unique, hyperpermeable environment of the tumor vasculature. In addition, the small nanoparticles allow for deep penetration into the tumor, where they subsequently accumulate. Upon placement in a magnetic field, this agent produces a large magnetic moment and creates a large local magnetic field, which can enhance the relaxation rate of nearby protons. This change in proton relaxation dynamics increases the MRI signal intensity of tissues in which this agent has accumulated; therefore, contrast and visualization of those tissues are enhanced compared to unenhanced MRI. The ultra-small nanoparticles, less than 5 nm in diameter, allow for rapid renal clearance and reduced toxicity. Due to their magnetic properties, these nanoparticles make tumor cells more sensitive to radiation therapy.

A poly-Toll-like receptor (TLR) agonist polyantigenic vaccine containing heat killed Mycobacterium indicus pranii (Mycobacterium w or Mw) with potential immunostimulating and antineoplastic activities. Upon administration, poly-TLR agonist polyantigenic vaccine activates a number of TLRs, which may result in macrophage and plasmacytoid dendritic cell (pDC) stimulation; secretion of interferon alpha; production of pro-inflammatory cytokines; upregulation of co-stimulatory molecules, enhanced T and B-cell stimulatory responses; T cell proliferation, and a Th1 immune response. TLRs are transmembrane receptors that recognize structurally conserved microbial molecules such as bacterial cell-surface lipopolysaccharides (LPS), lipoproteins, lipopeptides, lipoarabinomannan and flagellin, among others; immune responses stimulated by TLR activation may result in antineoplastic effects.

A fatty acid containing more than one double bond (C=C). The essential fatty acids omega-3 and omega-6 are polyunsaturated fatty acids (PUFAs) that contain 2 or more cis double bonds. Dietary intake of some PUFAs may have beneficial effects on blood pressure, serum lipds, and inflammation. Some PUFAs, such as omega-3 PUFAs, may have antineoplastic or chemopreventive activities.

A multivalent cancer vaccine comprised of the five tumor-associated antigens (TAAs) globo H, GM2 ganglioside, Tn-MUC1, TF, and sTn conjugated with the immunoadjuvant keyhole limpet hemocyanin (KLH), with potential antineoplastic activity. Upon administration, polyvalent antigen-KLH conjugate vaccine may induce production of IgG and IgM antibodies and antibody-dependent cell-mediated cytotoxicity (ADCC) against tumor cells expressing these TAAs, resulting in tumor cell death and tumor growth inhibition. Globo H (globo H hexasaccharide 1); GM2 ganglioside; Tn-MUC1 (human tumor-associated epithelial mucin 1 carrying the tumor-specific glycan Tn); TF (Thompson-Friedreich); and sTn (sialyl-Tn) are overexpressed in a variety of cancer cells. KLH is a hapten carrier and serves as an immunostimulant to improve immune recognition of antigens.

A cancer vaccine consisting of whole irradiated heterologous melanoma cells which express multiple melanoma-related antigens. Polyvalent melanoma vaccine may stimulate an antitumoral cytotoxic T-cell immune response in the host, resulting in inhibition of tumor cell proliferation and tumor cell death.

An oral bioadherent gel containing polyvinylpyrrolidone (PVP) and sodium hyaluronate with muco-protective activity. Upon oral application, this gel adheres to the mucosal surface of the mouth and throat, forming a thin layer that acts as a barrier to protect exposed and sensitized nerve endings from the painful stimuli associated with eating, drinking, and talking.

An orally bioavailable derivative of thalidomide with potential immunomodulating, antiangiogenic and antineoplastic activities. Although its exact mechanism of action has yet to be fully elucidated, pomalidomide appears to inhibit TNF-alpha production, enhance the activity of T cells and natural killer (NK) cells and enhance antibody-dependent cellular cytotoxicity (ADCC). In addition, pomalidomide may inhibit tumor angiogenesis, promote cell cycle arrest in susceptible tumor cell populations, and stimulate erythropoeisis.

Brand name for pomalidomide

A natural juice isolated from the fruit of the plant Punica granatum with antioxidant, potential antineoplastic, and chemopreventive activities. Pomegranate juice contains flavonoids which promote differentiation and apoptosis in tumor cells by down-regulating vascular endothelial growth factor (VEGF) and stimulating migration inhibitory factor (MIF), thereby inhibiting angiogenesis. The flavanoids in pomegranate juice also scavenge reactive oxygen species (ROS) and, in some cell types, may prevent ROS-mediated cell injury and death.

A liquid extract preparation derived from pomegranate (Punica granatum) seeds with antioxidant, and potential antineoplastic and chemopreventive activities. Pomegranate liquid extract contains flavonoids which may promote differentiation and apoptosis in tumor cells by down-regulating vascular endothelial growth factor (VEGF) and stimulating migration inhibitory factor (MIF), thus inhibiting angiogenesis.Pomegranate liquid extract flavanoids also scavenge reactive oxygen species (ROS) and, in some cell types, may prevent ROS-mediated cell injury and death.

A pill formulation of polyphenol extracts derived from the fruit of the deciduous shrub Punica granatum with antioxidant and potential chemopreventive activities. By binding and neutralizing free-radical compounds, the polyphenol extracts contained in pomegranate-extract pill may prevent their genotoxic and carcinogenic effects.

Brand name for pomegranate-extract pill

An orally bioavailable multitargeted receptor tyrosine kinase (RTK) inhibitor with potential antiangiogenic and antineoplastic activities. Ponatinib hydrochloride inhibits unmutated and all mutated forms of Bcr-Abl, including T315I, the highly drug therapy-resistant missense mutation of Bcr-Abl. This agent also inhibits other tyrosine kinases including those associated with vascular endothelial growth factor receptors (VEGFRs) and fibroblast growth factor receptors (FGFRs); in addition, it inhibits the tyrosine kinase receptor TIE2 and FMS-related tyrosine kinase receptor-3 (Flt3). RTK inhibition by ponatinib hydrochloride may result in the inhibition of cellular proliferation and angiogenesis and may induce cell death. Bcr-Abl is a fusion tyrosine kinase encoded by the Philadelphia chromosome.

An orally available sphingosine-1-phosphate receptor 1 (S1PR1, S1P1) agonist that acts as a functional antagonist, with potential immunomodulating activity. Upon oral administration, ponesimod selectively binds to S1PR1 on lymphocytes and causes transient receptor activation followed by S1PR1 internalization and degradation. This results in the sequestration of lymphocytes in lymph nodes. By preventing egress of lymphocytes, ponesimod reduces both the number of circulating peripheral lymphocytes and the infiltration of lymphocytes into target tissues. This prevents a lymphocyte-mediated immune response. S1PR1, a G-protein coupled receptor, plays a key role in lymphocyte migration from lymphoid tissues.

An orally bioavailable inhibitor of the membrane-bound O-acyltransferase (MBOAT) porcupine (PORCN), with potential antineoplastic, protective and regenerative activities. Upon oral administration, PORCN inhibitor CGX1321 specifically targets and binds to PORCN in the endoplasmic reticulum (ER), thereby inhibiting the post-translational palmitoylation and secretion of Wnt ligands, thus preventing the activation of Wnt-mediated signaling, and inhibiting cell growth in Wnt-driven tumors. In addition, by inhibiting the secretion of Wnt ligands and preventing Wnt-mediated signaling, CGX1321 may also limit fibrosis and promote regeneration of certain tissues upon cell injury. PORCN catalyzes the palmitoylation of Wnt ligands, and plays a key role in Wnt ligand secretion. Wnt signaling is dysregulated in a variety of cancers and plays a key role in tumor cell proliferation. It also plays a key role in tissue regeneration. Check for active clinical trials using this agent.

porcupine inhibitor ETC-1922159]] An orally bioavailable inhibitor of the membrane-bound O-acyltransferase (MBOAT) porcupine (PORCN), with potential antineoplastic activity. Upon oral administration, ETC-1922159 binds to and inhibits PORCN in the endoplasmic reticulum (ER), which blocks post-translational palmitoylation of Wnt ligands and inhibits their secretion. This prevents the activation of Wnt ligands, interferes with Wnt-mediated signaling, and inhibits cell growth in Wnt-driven tumors. Porcupine catalyzes the palmitoylation of Wnt ligands, and plays a key role in Wnt ligand secretion. Wnt signaling is dysregulated in a variety of cancers.

An orally available inhibitor of porcupine (PORCN), with potential antineoplastic activity. Upon oral administration, RXC004 binds to and inhibits PORCN in the endoplasmic reticulum (ER), which blocks post-translational acylation of Wnt ligands and inhibits their secretion. This prevents the activation of Wnt ligands, interferes with Wnt-mediated signaling, and inhibits cell growth in Wnt-driven tumors. Porcupine, a membrane-bound O-acyltransferase (MBOAT), is required for the palmitoylation of Wnt ligands, and plays a key role in Wnt ligand secretion and activity. Wnt signaling is dysregulated in a variety of cancers.

An orally available inhibitor of porcupine (PORCN), with potential antineoplastic activity. Upon oral administration, WNT974 binds to and inhibits PORCN in the endoplasmic reticulum (ER), which blocks post-translational acylation of Wnt ligands and inhibits their secretion. This prevents the activation of Wnt ligands, interferes with Wnt-mediated signaling, and inhibits cell growth in Wnt-driven tumors. Porcupine, a membrane-bound O-acyltransferase (MBOAT), is required for the palmitoylation of Wnt ligands, and plays a key role in Wnt ligand secretion and activity. Wnt signaling is dysregulated in a variety of cancers.

The sodium salt of a mixture of oligomers formed by ether and ester linkages of up to eight porphyrin units with photodynamic activity. Absorbed selectively by tumor cells, porfimer produces oxygen radicals after activation by 630 nm wavelength laser light, resulting in tumor cell cytotoxicity. In addition, tumor cell death may occur due to ischemic necrosis secondary to vascular occlusion that appears to be partly mediated by the release of thromboxane A2.

An N-methyl derivative of the antineoplastic antibiotic mitomycin C isolated from the bacterium Streptomyces ardus and other Streptomyces bacterial species. Bioreduced porfiromycin generates oxygen radicals and alkylates DNA, producing interstrand cross-links and single-strand breaks, thereby inhibiting DNA synthesis. Porfiromycin is preferentially toxic to hypoxic cells.

Brand name for ethinyl estradiol/levonorgestrel

Brand name for necitumumab

A broad-spectrum, second generation, triazole compound with antifungal activity. Posaconazole strongly inhibits 14-alpha demethylase, a cytochrome P450-dependent enzyme. Inhibition of 14-alpha-demethylase prevents the conversion of lanosterol to ergosterol, an important component of the fungal cell wall. Inhibition of ergosterol synthesis changes the fungal cell membrane composition and integrity, alters membrane permeability and eventually leads to fungal cell lysis. Compared to other azole antifungals, posaconazole is a significantly more potent inhibitor of sterol 14-alpha demethylase.

Brand name for extended release bupivacaine hydrochloride resorbable matrix formulation

Brand name for mogamulizumab-kpkc

An iodophor solution containing a water-soluble complex of iodine and polyvinylpyrrolidone (PVP) with broad microbicidal activity. Free iodine, slowly liberated from the povoiodine-iodine (PVPI) complex in solution, kills eukaryotic or prokaryotic cells through iodination of lipids and oxidation of cytosplasmic and membrane compounds. This agent exhbits a broad range of microbicidal activity against bacteria, fungi, protozoa, and viruses. Slow release of iodine from the PVPI complex in solution minimizes iodine toxicity towards mammalian cells.

An orally bioavailable, quinazoline-based, mall-molecular and irreversible pan-epidermal growth factor receptor (EGFR or HER) inhibitor with potential antineoplastic activity. Poziotinib inhibits EGFR (HER1 or ErbB1), HER2, HER4 and EGFR mutants, thereby inhibiting the proliferation of tumor cells that overexpress these receptors. EGFRs, cell surface receptor tyrosine kinases, are often upregulated in a variety of cancer cell types and play key roles in cellular proliferation and survival.

A preparation of allogeneic HLA-matched leukocytes treated with a derivative of placental protein 14 (PP14) with potential immunomodulating activity. PP14 derivative-treated HLA-matched donor mononuclear cell-enriched leukocytes contain at least fifty-five percent early-apoptotic T cells; after infusion and when processed by recipient dendritic cells, early-apoptotic T cells may help induce a decrease in the donor effector T-cell responses against the recipient of an allogeneic hematopoietic stem cell (HSC) transplant, thereby minimizing allogeneic HSC transplant-related graft-versus-host disease (GVHD). PP14, a 162 amino acid glycosylated protein secreted by the late secretory phase endometrium, binds to T cells in a carbohydrate fashion and has been shown to induce T-cell apoptosis; maternal immune tolerance to the fetus and pregnancy-related remissions of autoimmune disease may involve PP14-induced T cell apoptosis.

An orally bioavailable small molecule inhibitor of phosphorylated-p68 RNA helicase (P-p68), with potential anti-proliferative and antineoplastic activity. Upon oral administration, P-p68 inhibitor RX-5902 may both inhibit the activity of the anti-apoptotic B-cell lymphoma 2 (Bcl-2) protein and facilitate the induction of cyclin-dependent kinase inhibitor 1 (p21). This may prevent G2/M cell cycle progression and lead to growth inhibition in tumor cells. P-p68 is overexpressed in various types of solid tumors but absent in normal tissues, and plays a role in tumor progression and metastasis. p21 is a potent cyclin-dependent kinase inhibitor which regulates cell cycle progression and mediates both growth arrest and cellular senescence.

A replication-defective (ICP4-deleted) herpes simplex virus type 1 (HSV-1) viral vector expressing the human preproenkephalin A (PPE) gene with potential antinociceptive activity. Upon intradermal administration, PPE-expressing replication-defective HSV-1 vector NP2 is transported by retrograde axonal transport to the dorsal root ganglion (DRG) and becomes dormant. In the DRG, the vector transduces sensory neurons with high efficiency, delivering the engineered PPE gene; transduced neurons then express the protein proenkephalin A, the precursor for Met- and Leu-enkephalin. After proteolytic cleavage from proenkephalin A in the DRG neuronal cytosol, transgene-mediated Met- and Leu-enkephalin bind to mu and gamma- opioid receptors, which may result in the inhibition of nociceptive neurotransmission.

A synthetic derivative of fumagillin with antineoplastic and cytotoxic properties. PPI-2458 irreversibly inhibits the enzyme methionine aminopeptidase type 2 (MetAP2), thereby preventing abnormal cell growth and angiogenesis. PPI-2458 is reported to have a better toxicity profile compared to other agents of its class.

A cancer vaccine containing PR1, a 9 amino-acid human leukocyte antigen (HLA)-A2 restricted peptide derived from proteinase 3, with potential immunotherapeutic activity. Vaccination with PR1 leukemia peptide vaccine may stimulate the host immune system to mount a cytotoxic T lymphocyte (CTL) response against tumor cells expressing proteinase 3, resulting in tumor cell lysis. Often overexpressed in leukemic cells, proteinase 3 is a serine proteinase that activates progelatinase A and is involved in angiogenesis and metastasis.

A non-toxic, small-molecule, hypoxia-activated, 3,5-dinitrobenzamide nitrogen mustard pre-prodrug with potential antitumor activity. Upon intravenous administration, PR-104 is converted by systemic phosphatases to the alcohol intermediate PR-104A, which is reduced to form the active DNA-crosslinking mustard species hydroxylamine PR-104H intracellularly under hypoxic conditions. PR-104H specifically crosslinks hypoxic tumor cell DNA, resulting in the inhibition of DNA repair and synthesis, cell-cycle arrest, and apoptosis in susceptible hypoxic tumor cell populations while sparing normoxic tissues.

An orally bioavailable, small-molecule histone deacetylase (HDAC) inhibitor with potential antineoplastic activity. Pracinostat inhibits HDACs, which may result in the accumulation of highly acetylated histones, followed by the induction of chromatin remodeling; the selective transcription of tumor suppressor genes; the tumor suppressor protein-mediated inhibition of tumor cell division; and, finally, the induction of tumor cell apoptosis. This agent may possess improved metabolic, pharmacokinetic and pharmacological properties compared to other HDAC inhibitors.

Brand name for dabigatran etexilate mesylate

A folate analogue inhibitor of dihydrofolate reductase (DHFR) exhibiting high affinity for reduced folate carrier-1 (RFC-1) with antineoplastic and immunosuppressive activities. Pralatrexate selectively enters cells expressing RFC-1; intracellularly, this agent is highly polyglutamylated and competes for the folate binding site of DHFR, blocking tetrahydrofolate synthesis, which may result in depletion of nucleotide precursors; inhibition of DNA, RNA and protein synthesis; and apoptotic tumor cell death. Efficient intracellular polyglutamylation of pralatrexate results in higher intracellular concentrations compared to non-polyglutamylated pralatrexate, which is more readily effuxed by the MRP (multidrug resistance protein) drug efflux pump. RFC-1, an oncofetal protein expressed at highest levels during embryonic development, may be overexpressed on the cell surfaces of various cancer cell types.

Human allogeneic T lymphocytes transduced with a retroviral vector encoding a high-affinity T-cell receptor (TCR) specific for human leukocyte antigen (HLA)-A2-01-restricted, preferentially-expressed antigen in melanoma (PRAME) and containing the chemical induction of dimerization (CID) suicide/safety switch, composed of a drug binding domain coupled to the signaling domain of the suicide enzyme caspase-9, with potential antineoplastic activity. Peripheral blood mononuclear cells (PBMCs) are isolated from a patient, transduced with an anti-PRAME-HLA-A2 restricted TCR, expanded ex vivo, and reintroduced into the HLA-A2-positive patient. Upon reintroduction, PRAME-targeting T-cell receptor-based therapy BPX-701 binds to tumor cells expressing PRAME, which may induce cell death in and halt the growth of PRAME-expressing cancer cells. The tumor-associated antigen PRAME is overexpressed by a variety of cancer cell types. If potential T-cell toxicity due to graft-versus-host disease (GvHD) occurs, the chemical dimerizer rimiducid (AP1903) can be adminstered. Rimiducid binds to the drug binding domain expressed by the BPX-701 T cells, and triggers activation of the caspase-9 domain, which leads to caspase 9-mediated signaling, the induction of apoptosis and to selective and complete elimination of BPX-701 cells.

The hydrochloride salt of pramipexole, a benzothiazole derivative. As a nonergot dopamine agonist, pramipexole binds to D2 and D3 dopamine receptors in the striatum and substantia nigra of the brain. Compared to other dopamine agonists, the use of this agent may be associated with fewer dyskinetic side effects in treated subjects.

Brand name for repaglinide

A synthetic form of dehydroepiandrosterone with potential chemopreventive activity. Produced endogenously, dehydroepiandrosterone (DHEA) is an intermediate in the conversion of cholesterol to androgens and estrogens. Although the mechanisms of action of exogenously administered DHEA have not been fully illuminated, they may result in both direct and indirect physiologic effects. Direct effects include GABA-a receptor complex and NMDA receptor modulation, and enhanced pancreatic beta cell insulin secretion and antiglucocorticoid activities.

Brand name for pravastatin sodium

The sodium salt of pravastatin with cholesterol-lowering and potential antineoplastic activities. Pravastatin competitively inhibits hepatic hydroxymethyl-glutaryl coenzyme A (HMG-CoA) reductase, the enzyme which catalyzes the conversion of HMG-CoA to mevalonate, a key step in cholesterol synthesis. This agent lowers plasma cholesterol and lipoprotein levels, and modulates immune responses by suppressing MHC II (major histocompatibility complex II) on interferon gamma-stimulated, antigen-presenting cells such as human vascular endothelial cells. In addition, pravastatin, like other statins, exhibits pro-apoptotic, growth inhibitory, and pro-differentiation activities in a variety of tumor cells; these antineoplastic activities may be due, in part, to inhibition of the isoprenylation of Ras and Rho GTPases and related signaling cascades.

Brand name for dexmedetomidine hydrochloride

Brand name for acarbose

A synthetic glucocorticoid with anti-inflammatory and immunomodulating properties. After cell surface receptor attachment and cell entry, prednisolone enters the nucleus where it binds to and activates specific nuclear receptors, resulting in an altered gene expression and inhibition of proinflammatory cytokine production. This agent also decreases the number of circulating lymphocytes, induces cell differentiation, and stimulates apoptosis in sensitive tumor cells populations.

A synthetic glucocorticoid with anti-inflammatory and immunomodulating properties. After cell surface receptor attachment and cell entry, prednisone enters the nucleus where it binds to and activates specific nuclear receptors, resulting in an altered gene expression and inhibition of proinflammatory cytokine production. This agent also decreases the number of circulating lymphocytes, induces cell differentiation, and stimulates apoptosis in sensitive tumor cell populations.

A 3-isobutyl derivative of gamma-amino butyric acid (GABA) with anti-convulsant, anti-epileptic, anxiolytic, and analgesic activities. Although the exact mechanism of action is unknown, pregabalin selectively binds to alpha2delta (A2D) subunits of presynaptic voltage-dependent calcium channels (VDCCs) located in the central nervous system (CNS). Binding of pregabalin to VDCC A2D subunits prevents calcium influx and the subsequent calcium-dependent release of various neurotransmitters, including glutamate, norepinephrine, serotonin, dopamine, and substance P, from the presynaptic nerve terminals of hyperexcited neurons; synaptic transmission is inhibited and neuronal excitability is diminished. Pregabalin does not bind directly to GABA-A or GABA-B receptors and does not alter GABA uptake or degradation.

Brand name for recombinant human chorionic gonadotropin

A synthetic version, known as PIF-1, of the peptide preimplantation factor (PIF), an embryo-secreted peptide, with potential activity against graft-versus-host disease (GVHD). PIF-1 is believed to have wide-ranging activity on the immunologic system, including a whole host of immunologic changes that resemble pregnancy, in which there is neither graft-versus-host or host-versus-graft disease between the mother and the embryo. Replication of the immunologic profile of pregnancy through the administration of PIF-1 may thus benefit patients undergoing bone marrow transplant (BMT) who experience graft-versus-host disease (GVHD). Native embryonic PIF has been found to have a multi-targeted effect on various aspects of the immune system, coordinated so that there is a successful embryonic implantation and a successful pregnancy.

An orally bioavailable antagonist of the adenosine A2A receptor (A2AR; ADORA2A), with potential immunomodulating and antineoplastic activities. Upon administration, preladenant selectively binds to and inhibits A2AR expressed on T lymphocytes. This blocks tumor-released adenosine from interacting with A2AR and prevents the adenosine/A2AR-mediated inhibition of T lymphocytes. This results in the proliferation and activation of T lymphocytes, and stimulates a T-cell-mediated immune response against tumor cells. A2AR, a G protein-coupled receptor, is highly expressed on the cell surfaces of T cells and, upon activation by adenosine, inhibits T-cell proliferation and activation. Adenosine is often overproduced by cancer cells and plays a key role in immunosuppression.

Brand name for troglitazone

Brand name for prednisolone

Brand name for conjugated estrogens

Brand name for pneumococcal 7-valent conjugate vaccine

Brand name for pneumococcal 13-valent conjugate vaccine

An inhibitor of checkpoint kinase 1 (chk1) with potential antineoplastic activity. Upon administration, prexasertib selectively binds to chk1, thereby preventing activity of chk1 and abrogating the repair of damaged DNA. This may lead to an accumulation of damaged DNA and may promote genomic instability and apoptosis. Prexasertib may potentiate the cytotoxicity of DNA-damaging agents and reverse tumor cell resistance to chemotherapeutic agents. Chk1, a serine/threonine kinase, mediates cell cycle checkpoint control and is essential for DNA repair and plays a key role in resistance to chemotherapeutic agents.

Brand name for ziconotide

The hydrochloride salt form of prilocaine, an intermediate-acting local anesthetic of the amide type chemically related to lidocaine. Prilocaine hydrochloride binds to voltage-gated sodium ion channels in the neuronal membrane, thereby preventing the permeability of sodium ions. This leads to a stabilization of the neuronal membrane and inhibits depolarization and results in a reversible blockage of nerve impulse generation and propagation along nerve fibres and subsequent reversible loss of sensation.

Brand name for omeprazole

A methylated derivative and structural analog of PRIMA-1 (p53 re-activation and induction of massive apoptosis), with potential antineoplastic activity. Upon administration, PRIMA-1 analog APR-246 covalently modifies the core domain of mutated forms of cellular tumor antigen p53 (p53) through the alkylation of thiol groups. These modifications restore both the wild-type conformation and function to mutant p53, which reconstitutes endogenous p53 activity, leading to cell cycle arrest and apoptosis in tumor cells. This agent may work synergistically with other antineoplastic agents. p53, a tumor suppressor and transcription factor normally activated upon DNA damage, is frequently mutated and overexpressed in cancer cells; it plays a key role in both DNA repair and the induction of apoptosis.

An autologous dendritic cell (DCs) vaccine targeting prostate cancer with immunostimulating activity. The autologous DC vaccine is prepared via transfecting DCs with mRNAs extracted from primary prostate cancer tissue, and mRNAs of human telomerase reverse transcriptase (hTERT) and survivin. Upon administration, this DC vaccine may elicit a potent cytotoxic T-cell (CTL) response against prostate cancer cells, resulting in tumor cell death. Both hTERT and survivin are essential in neoplastic growth, and are considered to be universal tumor antigens.

A cancer priming vaccine consisting of a proprietary version of the recombinant vaccinia viral vector, modified vaccinia Ankara-Bavarian Nordic (MVA-BN), encoding both the two human tumor-associated antigens (TAAs) carcinoembryonic antigen (CEA) and mucin-1 (MUC-1), and TRICOM, which is comprised of the three human immune-enhancing co-stimulatory molecules B7-1, ICAM-1 and LFA-3, with potential immunostimulatory and antineoplastic activities. Upon subcutaneous administration of MVA-BN-CV301, followed by multiple boosting doses of the fowlpox virus (FPV) vaccine CV301, a cytotoxic T-lymphocyte (CTL) response against CEA- and MUC-1-expressing tumor cells is activated. In addition, the CV301-dependent anti-tumor CTL response upregulates the expression of programmed cell death ligand 1 (PD-L1); therefore, when CV301 is combined with a programmed cell death 1 (PD-1) immune checkpoint inhibitor, the antitumor effect may be increased. CEA and MUC-1 are overexpressed in a variety of cancers.

Brand name for adenoviral tumor-specific neoantigen priming vaccine GRT-C901

Brand name for testosterone enanthate

Brand name for lisinopril

A synthetic hydroxamic acid derivative with potential antineoplastic activity. Prinomastat inhibits matrix metalloproteinases (MMPs) (specifically, MMP-2, 9, 13, and 14), thereby inducing extracellular matrix degradation, and inhibiting angiogenesis, tumor growth and invasion, and metastasis. As a lipophilic agent, prinomastat crosses the blood-brain barrier.

Brand name for desvenlafaxine succinate

A thiazolylamide and helicase-primase enzyme inhibitor that is active against herpes simplex virus types 1 and 2 (HSV-1 and HSV-2). Pritelivir inhibits the helicase-primase complex and prevents helicase or primase catalytic cycling of viral DNA, which interferes with DNA replication and growth. This agent does not require activation by HSV thymidine kinase and has a longer plasma half-life than nucleoside analogues.

An orally available inhibitor of protein arginine N-methyltransferase 1 (PRMT1; Histone-arginine N-methyltransferase PRMT1; Interferon receptor 1-bound protein 4) with potential antineoplastic activity. Upon administration, GSK3368715 inhibits monomethylation and asymmetric dimethylation of arginine-bearing substrates, including histones, estrogen receptors, RNA-binding proteins, and numerous non-histone substrates catalyzed by PRMT1. This may inhibit tumor cell proliferation, migration, and invasion that is potentially driven by PRMT1 overexpression or dysregulation. PRMT1-mediated methylation plays a key role in the modulation of protein function, gene expression and cellular signaling. Dysregulation and overexpression of PRMT1 has been associated with a number of solid and hematopoietic cancers.

An orally bioavailable second-generation selective apoptotic antineoplastic drug (SAAND) and analog of the nonsteroidal anti-inflammatory drug (NSAID) sulindac, with potential pro-apoptotic and antineoplastic activities. Upon administration, CP-461 specifically binds to and blocks the activity of cyclic guanosine monophosphate-phosphodiesterase (cGMP-PDE), an enzyme that inhibits the normal apoptosis signal pathway. Inhibition of cGMP-PDE permits the apoptotic signal pathway to proceed unopposed, resulting in apoptotic cell death. cGMP-PDE is overexpressed in a variety of cancer cell types; therefore, CP-461 selectively induces apoptosis in cancer cells, with minimal or no effect in healthy cells.

A benzoic acid derivative with antihyperuricemic property. Probenecid competitively inhibits the active reabsorption of urate at the proximal tubule in the kidney thereby increasing urinary excretion of uric acid and lowering serum urate concentrations. This prevents urate deposition and promotes resolution of existing urate deposits. In addition, probenecid modulates the transport of organic acids and acidic drugs at the proximal and distal renal tubule, thereby increasing the drug serum concentration.

A probiotic containing the bacterium Lactobacillus acidophilus with potential antimicrobial and immunomodulatory activities. As a dietary supplement, Lactobacillus acidophilus (L. acidophilus), a naturally-occurring bacteria, may improve digestion and help maintain adequate colonization of the gastrointestinal (GI) tract by modulating the composition of the normal microflora. Because it produces lactic acid and hydrogen peroxide and other substances during fermentation, this bacterium creates an acidic environment unfavorable to pathogens such as Candida albicans. In addition, during colonization of the GI tract, L. acidophilus may form a protective barrier, preventing attachment of pathogens. Dietary supplementation with this bacterium has been shown to enhance natural and acquired immunity in mice.

The hydrochloride salt of a methylhydrazine derivative with antineoplastic and mutagenic activities. Although the exact mode of cytotoxicity has not been elucidated, procarbazine, after metabolic activation, appears to inhibit the trans-methylation of methionine into transfer RNA (t-RNA), thereby preventing protein synthesis and consequently DNA and RNA synthesis. This agent may also undergo auto-oxidation, resulting in the formation of cytotoxic free radicals which damage DNA through an alkylation reaction.

An orally bioavailable procaspase activating compound-1 (PAC-1), with potential proapoptotic and antineoplastic activities. Upon administration, VO-100 binds to and forms a chelating complex with zinc (Zn) ions inside cells, which prevents the binding of Zn ions to procaspase-3 (PC3) and abrogates the Zn-mediated inhibition of PC3. This allows for the proteolytic autoactivation of PC3 into the active form caspase-3. This results in the selective caspase-3-mediated induction of apoptosis and cell death in cancer cells. In addition, VO-100 is able to cross the blood-brain-barrier (BBB). PC3, a Zn-inhibited proenzyme, is upregulated in a variety of cancer cell types, while its expression is minimal in normal healthy cells.

The maleate salt form of prochlorperazine, a synthetic, piperazine phenothiazine derivative with antiemetic, antipsychotic, antihistaminic, and anticholinergic activities. Prochlorperazine binds to and blocks the postsynaptic dopamine D2-receptor in the chemoreceptor trigger zone (CTZ) of the brain and may prevent chemotherapy-induced emesis. Prochlorperazine maleate also blocks anticholinergic and alpha-adrenergic receptors. Its antagonistic actions on the alpha-1 adrenergic receptors results in sedation, muscle relaxation, and hypotension.

Brand name for remestemcel-L

Brand name for epoetin alfa

Brand name for therapeutic hydrocortisone

Brand name for chlorpropamide

Brand name for telapristone acetate

Brand name for recombinant human chorionic gonadotropin

The hemisulfate salt form of proflavine, an acridine-derived fluorescent contrast and disinfectant agent that can potentially be used for cellular imaging and antiseptic purposes. Upon topical application of proflavine hemisulfate, proflavine diffuses into cells and intercalates into DNA, thereby accumulating in and staining the nucleus. During fluorescence imaging, the cell nuclei can be visualized. This allows nuclear morphometry and the identification of cancer cells. In addition, proflavine exerts its antibacterial effect by binding to bacterial DNA, thereby disrupting DNA synthesis and halting bacterial cell growth.

A recombinant, chimeric, dual-receptor agonist fusion protein with immunohematopoietic activity. Progenipoietin (ProGP) consists of portions of the ligands for granulocyte colony-stimulating factor (G-CSF) and human fetal liver tyrosine kinase-3 (FLT3); variants progenipoietin-1, 2 and 3 differ in the orientation of the two receptor agonists. ProGP binds simultaneously to G-CSF and FLT3 receptors with receptor affinities approximately two- to three-fold higher than the respective native ligands. When administered in vivo, this agent may augment the number of circulating granulocytes and dendritic cells (DCs). ProGP may promote the proliferation of and prevent apoptosis in several human hematopoietic cell lineages, exhibiting the additive activities of a combination of C-GSF and FLT3.

Brand name for telapristone acetate

A tablet preparation formulated for vaginal administration containing a micronized synthetic form of the endogenous steroid hormone progesterone with progesterone activity. Upon vaginal insertion, progesterone binds to the progesterone receptor, resulting in dissociation of heat shock proteins, receptor phosphorylation, and transcription activation through direct or indirect interaction with transcription factors. This agent exerts inhibitory effects on estrogen by decreasing the number of estrogen receptors and increasing its metabolism to inactive metabolites. Progesterone induces secretory changes in the endometrium, decreases uterine contractility during pregnancy, and maintains pregnancy.

Brand name for therapeutic progesterone

Brand name for diazoxide

Brand name for tacrolimus

A chimeric, 25-mer peptide that targets prohibitin, with potential antineoplastic activity. Prohibitin-targeting peptide 1 (prohibitin-TP01) consists of a fat-targeting motif (CKGGRAKDC), two repeats of a proapoptotic peptide motif (KLAKLAK) and a GG linker. This peptide binds specifically to prohibitin in the white adipose vasculature; upon receptor-mediated cell internalization, the ligand/receptor complex triggers apoptosis and results in ablation of white fat. Destruction of white fat may potentially have positive consequences for men with prostate cancer since a high level of white fat has been implicated as a critical contributing factor in poor prostate cancer outcome. Prohibitin, a multifunctional membrane-associated protein that is thought to regulate cell survival and growth, has been shown by immunohistochemical analysis to be expressed in the membrane of endothelial cells in white adipose tissue.

Brand name for sargramostim

Brand name for caricotamide/tretazicar

Brand name for alpha-1-proteinase inhibitor human

Brand name for aldesleukin

Brand name for denosumab

Brand name for fluphenazine hydrochloride

Brand name for therapeutic progesterone

Brand name for eltrombopag olamine

The hydrochloride salt form of promethazine, a phenothiazine derivative with antihistaminic, sedative and antiemetic properties. Promethazine hydrochloride selectively blocks peripheral H1 receptors thereby diminishing the effects of histamine on effector cells. Promethazine hydrochloride also blocks the central histaminergic receptors, thereby depressing the reticular system causing sedative and hypnotic effects. In addition, promethazine hydrochloride also has centrally acting anticholinergic properties and probably mediates nausea and vomiting by acting on the medullary chemoreceptive trigger zone.

Brand name for porfiromycin

An oral solution containing a mixture of proteinases, which are produced by Streptomyces griseus, with mucolytic activity and potential diagnostic applications. Upon oral administration, pronase is able to cleave peptide chains of polypeptides into individual amino acids, thereby dissolving mucus. The removal of mucus may improve the visibility of parts of the digestive tract, such as the esophagus and the stomach, during endoscopy. Pre-treatment with pronase before endoscopic examination may help in the detection of certain cancers, such as esophageal and gastric cancer.

A water-soluble para-aminophenol derivative and ester prodrug of acetaminophen in which acetaminophen is bound to the carboxylic acid diethylglycine, with analgesic and antipyretic activities. Upon intravenous administration, propacetamol is hydrolyzed by plasma esterases into its active form acetaminophen. Although the exact mechanism of action has yet to be fully elucidated despite its widespread use, acetaminophen enters the central nervous system and acts centrally. This agent binds to cyclooxygenase (COX) and prevents the metabolism of arachidonic acid to prostaglandin. A reduction in prostaglandin formation relieves pain and reduces fever. Acetaminophen may also act centrally on cannabinoid receptors and on N-methyl-D-aspartate (NMDA) receptors.

A hypnotic alkylphenol derivative. Formulated for intravenous induction of sedation and hypnosis during anesthesia, propofol facilitates inhibitory neurotransmission mediated by gamma-aminobutyric acid (GABA). This agent is associated with minimal respiratory depression and has a short half-life with a duration of action of 2 to 10 minutes.

The hydrochloride salt of propranolol, a synthetic beta-adrenergic receptor blocker with antianginal, antiarrhythmic, and antihypertensive properties. Propranolol competitively antagonizes beta-adrenergic receptors, thereby inhibiting beta-adrenergic reactions, such as vasodilation, and negative chronotropic and inotropic effects.

A thiourea derivative with antithyroid property. Propylthiouracil (PTU) interferes with the oxidation of iodine possibly by interaction with peroxidase or a peroxidase-mediated complex reaction, thereby inhibiting synthesis of thyroid hormones tri-iodothyronine (T3) and thyroxine (T4). In addition, this agent inhibits the Type I 5'-deiodinase (D1), an enzyme involved in the peripheral conversion of thyroxine to tri-iodothyronine. This results in decreased plasma triodothyronine concentrations and decreased entrance of thyroxine into cells thereby reducing thyroid hormone activity.

Brand name for promethazine hydrochloride

Brand name for finasteride

An orally bioavailable antagonist of the prostaglandin E2 (PGE2) receptor type 4 (EP4; EP-4), with potential immunomodulating and antineoplastic activities. Upon oral administration, E7046 selectively targets, binds to and blocks the activity of immunosuppressive tumor-associated myeloid cells (TAMCs) in the microenvironment. This abolishes TAMC-dependent immunosuppression and reduces tumor cell proliferation. The presence of immunosuppressive myeloid cells in certain tumors is associated with a poor prognosis.

Brand name for concentrated, fortified, collagen protein hydrolysate liquid supplement

A cell-based vaccine derived from prostate cancer with potential immunopotentiating and antineoplastic activities. Prostate cancer vaccine ONY-P1 is derived from three irradiated allogeneic prostate cancer cell lines that represent different stages of prostate cancer and express a broad range of prostate and prostate cancer antigens. Upon administration, this vaccine may stimulate a host immune response against prostate cancer cells; in the vaccination schedule, the first two vaccinations are co-administered with bacillus Calmette-Guerin (BCG) as an adjuvant.

Brand name for cholecalciferol/d-alpha tocopherol/L-selenomethionine/green tea extract/saw palmetto berry extract/daidzein/genistein/lycopene prostate health supplement

A dendritic cell (DC)-based cancer vaccine composed of autologous dendritic cells (DCs) activated with a prostate tumor cell lysate containing tumor-associated antigens (TAAs) with potential immunostimulatory and antineoplastic activities. Upon administration, the prostate tumor antigen-activated autologous DC vaccine may stimulate an anti-tumoral cytotoxic T-lymphocyte (CTL) response against prostate cancer cells expressing prostate tumor cell-specific antigens, which may result in prostate tumor cell lysis.

A genetically-engineered protein formed by the fusion of prostatic acid phosphatase (PAP) and sargramostim (GM-CSF). Vaccination with antigen-presenting cells (APC) loaded with prostatic acid phosphatase-sargramostim fusion protein may elicit a cytotoxic T-cell response against tumor cells that express PAP.

Brand name for rilimogene galvacirepvec/rilimogene glafolivec

A proprietary formulation comprised of the serine protease inhibitor tranexamic acid (TXA), polyethylene glycol (PEG), electrolytes, and sugar, with potential GI protective activity. After reconstitution in water and upon oral or enteral administration before abdominal surgery, TXA in the protease inhibitor formulation LB1148 targets and inhibits several serine proteases in the gastrointestinal (GI) tract, thereby preventing and protecting the intestinal mucosa against degradation, which preserves gastrointestinal (GI) integrity, function and motility. By inhibiting digestive proteases, the intestinal mucosal barrier is preserved during acute physiologic shock, which may prevent multi-organ failure, postoperative ileus and surgical intra-abdominal adhesions. PEG enhances transport of TXA through the GI tract. The other components provide energy and balance dietary electrolytes, thereby promoting healing of the GI barrier.

A recombinant antibody prodrug composed of a monoclonal antibody directed against the tumor-associated antigen (TAA) programmed cell death 1 ligand 1 (PD-L1; B7-H1; CD274) that is linked to a proprietary masking peptide through a protease-cleavable linker on the amino terminus of the light chain domain of the antibody, with potential immune checkpoint inhibitory and antineoplastic activities. Upon administration, the linkage system is stable in the circulation and, upon extravasation into the tumor microenvironment, the peptide mask is cleaved by tumor-associated proteases. These proteases are present in high concentrations and aberrantly activated in the tumor microenvironment, while expressed as inactive forms, at much lower concentrations, in normal, healthy tissue. Protease cleavage of the linker enables binding of the unmasked, fully active monoclonal antibody moiety of CX-072 to PD-L1, which is over expressed on certain cancer cells. This blocks the binding to and activation of its receptor programmed cell death 1 (PD-1) on T lymphocytes, thereby enhancing the T-cell-mediated anti-tumor immune response and reversing PD-L1/PD-1-mediated T-cell suppression. PD-L1 binding to PD-1 on T cells suppresses the immune system and results in immune evasion. Compared to the unmodified PD-L1 antibody, peptide masking of CX-072 minimizes binding to PD-L1 in normal tissues, thereby decreasing autoimmune-based side effects while retaining anti-tumor activity.

An orally available, selective small molecule inhibitor of protein arginine methyltransferase 5 (PRMT5), with potential antiproliferative and antineoplastic activities. Although the mechanism of action has not been completely determined, PRMT5 inhibitor GSK3326595 binds to the substrate recognition site of PRMT5 following oral administration and inhibits its methyltransferase activity, which decreases the levels of both monomethylated and dimethylated arginine residues in histones H2A, H3 and H4 and modulates the expression of genes involved in several cellular processes, including cell proliferation. Therefore, this agent may increase the expression of antiproliferative genes and/or decrease the expression of genes that promote cell proliferation and may lead to decreased growth of rapidly proliferating cells, including cancer cells. PRTM5, an arginine methyltransferase that can catalyze the formation of both omega-N monomethylarginine (MMA) and symmetrical dimethylarginine (sDMA) on histones and a variety of other protein substrates, is overexpressed in several neoplasms.

An orally available protein kinase C (PKC) inhibitor with potential immunosuppressive and antineoplastic activities. Upon oral administration, protein kinase C inhibitor LXS196 binds to and inhibits PKC, which prevents the activation of PKC-mediated signaling pathways. This may lead to the induction of cell cycle arrest and apoptosis in susceptible tumor cells. PKC, a serine/threonine protein kinase overexpressed in certain types of cancer cells, is involved in tumor cell differentiation, proliferation, invasion and survival.

A water soluble inhibitor of the protein phosphatase 2A (PP2A), with potential chemo- and radiotherapy enhancing activity. Upon injection, PP2A inhibitor LB-100 inhibits the removal of phosphate groups from proteins essential for cell cycle progression. When used with radio- or chemotherapy treatment, this agent prevents the activation of PP2A-mediated repair mechanisms and allows for malignant cells to progress through the cell cycle without having their damaged DNA repaired. This enhances the cytotoxic effect of the chemotherapeutic or radiotherapeutic agent and results in tumor cell apoptosis. PP2A, a serine/threonine phosphatase that plays a key role in the control of cell growth and DNA damage repair.

A formulation containing protein-stabilized liposome nanoparticles encapsulating the poorly water-soluble, second-generation taxane analog docetaxel with antineoplastic activity. Docetaxel binds to and stabilizes the beta-tubulin subunit, thereby inhibiting microtubule disassembly which results in cell-cycle arrest at the G2/M phase and cell death. This agent also inhibits pro-angiogenic factors such as vascular endothelial growth factor (VEGF) and displays immunomodulatory and pro-inflammatory properties by inducing various mediators of the inflammatory response. Compared to the use of toxic carriers to increase solubilization of docetaxel, protein-stabilized liposomal docetaxel improves drug solubility while avoiding carrier-associated toxicity.

Enzymes produced and secreted by the pancreas which aid in the proteolysis of proteins in the digestive tract. Pancreatic proteolytic enzymes include trypsin, chymotrypsin and carboxypeptidase; these enzymes are secreted as zymogens, inactive precursors of the enzymes, and are activated in the lumen of the digestive canal. Another proteolytic enzyme, enteropeptidase, is associated with the brush border of enterocytes; this enzyme catalyses the conversion of trypsinogen into trypsin which, in turn, can activate a number of other pancreatic zymogens.

Brand name for pantoprazole sodium

Brand name for PV-10

Brand name for sipuleucel-T

Brand name for albuterol sulfate

Brand name for medroxyprogesterone acetate

Brand name for promethazine hydrochloride

Brand name for modafinil

An orally bioavailable androgen receptor (AR) antagonist with potential antineoplastic activity. Upon oral administration, proxalutamide binds to AR in target tissues, inhibits androgen-induced receptor activation, and facilitates the formation of inactive complexes that cannot translocate to the nucleus. This prevents binding to and transcription of AR-responsive genes that regulate prostate cancer cell proliferation. In addition, proxalutamide induces AR downregulation, thereby further preventing AR-mediated signaling. This ultimately leads to an inhibition of growth in AR-expressing prostate cancer cells. AR is overexpressed in prostate cancer and plays a key role in prostate cancer cell proliferation.

A peptide vaccine containing the prostate specific antigen (PSA) with potential antineoplastic activity. PSA, a glycoprotein secreted by prostatic epithelial and ductal cells, is overexpressed in prostate cancer cells and is used as a tumor marker for both diagnosis and treatment evaluation. Vaccination with PSA peptide vaccine may produce anti-PSA antibodies as well as elicit a cytotoxic T-cell (CTL) response against prostate cancer cells expressing this antigen, thereby decreasing tumor cell growth.

An autologous dendritic cell vaccine with potential immunostimulatory activity. Dendritic cells harvested from a prostate cancer patient are transfected with the mRNA encoding for prostate specific antigen (PSA), a tumor marker secreted by prostatic epithelial and ductal cells. When reintroduced back to the patient, these PSA RNA pulsed autologous dendritic cells may elicit a cytotoxic T-cell (CTL) response against PSA-positive prostate cancer cells.

A prostate cancer vaccine containing prostate specific antigen (PSA) combined with the cytokines, interleukin-2 (IL-2) and granulocyte macrophage-colony-stimulating factor (GM-CSF), with potential antineoplastic activity. Upon intradermal vaccination, PSA/IL-2/GM-CSF vaccine may activate the immune system to induce a cytotoxic T-cell (CTL) response against prostate cancer cells expressing this antigen, thereby decreasing tumor cell growth. PSA, a glycoprotein secreted by prostatic epithelial and ductal cells, is overexpressed by prostate cancer cells. IL-2 stimulates natural killer (NK) cells and cytotoxic T-cells against the PSA-expressing tumor cells. GM-CSF promotes antigen presentation to dendritic cells and further stimulates a tumor-specific cytotoxic T-lymphocyte (CTL) response.

A plasmid DNA vaccine encoding the tumor-associated antigens (TAAs) prostate-specific antigen (PSA) and prostate-specific membrane antigen (PSMA), with potential immunoactivating and antineoplastic activities. Upon intramuscular delivery and electroporation of the PSA/PSMA DNA plasmid INO-5150, both PSA and PSMA are translated in cells which then activate the immune system. This induces cytotoxic T-lymphocyte (CTL) responses against tumor cells expressing PSA and PSMA. This may result in both immune-mediated tumor cell death and the inhibition of tumor cell proliferation. PSA and PSMA are overexpressed on a variety of cancer cell types. The DNA encoding the TAAs in INO-5150 is based on both human and other primate antigen gene sequences. As the plasmid genes differ from the human gene sequences encoding these antigens, INO-5150 may overcome immune tolerance to human TAAs.

A cancer vaccine comprised of a synthetic peptide with an amino acid sequence corresponding to positions 154-163 of the amino acid sequence for prostate-specific antigen (PSA) with a leucine substitution at position 155. Upon administration, PSA:154-163(155L) peptide vaccine may elicit a cytotoxic T-cell response against tumor cells that express PSA.

A cell-based cancer vaccine composed of autologous dendritic cells (DCs) pulsed with the prostate-specific tumor associated antigens (TAAs) prostate specific antigen (PSA) and prostate acid phosphatase (PAP), and conjugated to the immunostimulant keyhole limpet hemocyanin (KLH), with potential immunostimulatory and antineoplastic activities. Upon administration, prostate cancer antigen/KLH-pulsed autologous dendritic cell vaccine may stimulate the immune system to mount anti-tumoral cytotoxic T lymphocyte (CTL) and antibody responses against prostate cancer cells expressing PSA and PAP, which may result in prostate cancer cell lysis. KLH is an immunogenic carrier and serves as an immunostimulant to improve antigenic immune recognition and T-cell responses and can be used to evaluate vaccine efficacy.

A preparation containing the inactivated Pseudomonas aeruginosa bacterium with potential immunomodulating activity. Upon inoculation, Pseudomonas aeruginosa preparation may stimulate the immune system, increasing macrophage and natural killer cell activity; it may be used thereby in cancer adjuvant treatments, and it may reduce the incidence of infection.

A tryptamine alkaloid, isolated from various genera of fungi including the genus Psilocybe, with hallucinogenic, anxiolytic, and psychoactive activities. In vivo, psilocybine is rapidly dephosphorylated into the active compound psilocin, which activates serotonin 2A (5-HT2A) receptors in the central nervous system (CNS), mimicking the effects of serotonin.

A recombinant antibody derivative composed of tri-specific T-cell activating construct (TriTAC) directed against the human tumor-associated antigen (TAA) prostate-specific membrane antigen (PSMA; FOLH1) and the CD3 antigen found on T lymphocytes and an albumin-binding domain, with potential immunostimulating and antineoplastic activities. Upon administration, PSMA/CD3 tri-specific T-cell antibody construct HPN424 targets and binds PSMA on tumor cells and CD3 on cytotoxic T lymphocytes (CTLs), thereby bringing PSMA-expressing tumor cells and CTLs together, which results in the CTL-mediated cell death of PSMA-expressing tumor cells. The albumin-binding domain targets and binds to serum albumin, thereby extending the serum half-life of HPN424. PSMA is overexpressed on the surface of metastatic and hormone-refractory prostate tumor cells.

A peptide-based cancer vaccine containing epitopes of T cell receptor gamma-chain alternate reading frame protein (TARP) and prostate-specific membrane antigen (PSMA) in combination with a Poly IC-LC immunoadjuvant, with potential antineoplastic activity. Upon administration, PSMA/TARP peptide vaccine may stimulate a host cytotoxic T-cell (CTL) response against TARP- and PSMA-expressing tumor cells, resulting in tumor cell cytotoxicity. The nuclear protein TARP and PSMA are commonly expressed in prostate cancer cells.

A proprietary preparation of polymeric nanoparticles containing the second-generation taxane docetaxel, targeted to prostate-specific membrane antigen (PSMA), with antineoplastic activity. PSMA-targeted docetaxel nanoparticles BIND-014 carry docetaxel within a matrix of polylactic acid covered with a coating of polyethylene glycol; embedded on the surface of the polyethylene glycol coating are ligands targeted to PSMA. BIND-014 allows gradual release of docetaxel upon degradation of the polylactic acid, and the PEG encapsulation escapes the host immune response while PSMA ligands on the surface restrict the cytotoxic effect to PSMA-expressing cells. Docetaxel binds to and stabilizes the beta-tubulin subunit, thereby inhibiting microtubule disassembly which results in cell-cycle arrest at the G2/M phase and cell death. PSMA is a cell-surface antigen that is abundantly present on the surface of cancer cells and on the neovasculature that feeds a wide variety of tumor types.

A radioconjugate composed of the phosphoramidate agent CTT1057, a human prostate specific membrane antigen (PSMA) inhibitor, and labeled with the radioisotope fluorine F 18, with potential use as a tracer for PSMA-expressing tumors during positron emission tomography (PET). Upon intravenous administration of PSMA-targeted PET imaging agent fluorine F 18 CTT-1057, the CTT-1057 moiety targets and irreversibly binds to the extracellular domain of PSMA-expressing tumor cells. Upon rapid internalization, and following PET imaging, PSMA-expressing tumor cells can be detected. PSMA, a tumor-associated antigen (TAA) and type II transmembrane protein, is expressed on the membrane of prostatic epithelial cells and overexpressed on prostate tumor cells.

An injectable, water soluble, small molecule drug conjugate (SMDC) containing a ligand specific for prostate-specific membrane antigen (PSMA), conjugated via a stable, enzyme-cleavable linker to the cytotoxic agent tubulysin B hydrazide (TubBH), with potential antineoplastic activity. Upon administration of PSMA-targeted tubulysin B-containing conjugate EC1169, the PSMA ligand specifically targets and binds to PSMA, a protein which is abundantly expressed on the surface of metastatic and hormone-refractory prostate cancer cells as well as on the neovasculature of many solid tumors. This allows for the specific delivery of TubBH to PSMA-expressing cancer cells. Upon internalization and cleavage, tubulysin B binds to tubulin and inhibits microtubule polymerization, which blocks cell division and results in G2/M phase arrest, tumor cell apoptosis and a decrease in PSMA-expressing tumor cells.

A radioconjugate composed of 2-[3-(1, 3-dicarboxy propyl)-ureido] pentanedioic acid (DUPA), a prostate-specific membrane antigen (PSMA)-targeting ligand, linked to the radioisotope technetium Tc 99m (Tc99m), that can potentially be used as a radioimaging agent for PSMA-overexpressing tumor cells. Upon administration, the PSMA-targeting moiety of EC0652 targets and binds to PSMA-expressing tumors. Upon uptake and single-photon emission computed tomography (SPECT) imaging, PSMA-expressing tumors can be visualized and identified. In turn, PSMA-overexpression can be used to evaluate both the efficacy of and response to certain PSMA-targeting cytotoxic agents. PSMA, a tumor-associated antigen (TAA), is overexpressed by most prostate cancers.

Brand name for curcumin-based gel

A naturally-derived stilbenoid structurally related to resveratrol, with potential antioxidant, anti-inflammatory, pro-apoptotic, antineoplastic and cytoprotective activities. Upon administration, pterostilbene exerts its antioxidant activity by scavenging reactive oxygen species (ROS), thereby preventing oxidative stress and ROS-induced cell damage. It may also activate the nuclear factor erythroid 2-related factor 2 (Nrf2)-mediated pathway and increase the expression of various antioxidant enzymes, such as superoxide dismutase (SOD). In addition, pterostilbene is able to inhibit inflammation by reducing the expression of various inflammatory mediators, such as interleukin (IL) 1beta, tumor necrosis factor alpha (TNF-a), inducible nitric oxide synthase (iNOS), cyclooxygenases (COX), and nuclear factor kappa B (NF-kB). It also inhibits or prevents the activation of many signaling pathways involved in carcinogenesis, increases expression of various tumor suppressor genes while decreasing expression of certain tumor promoting genes and directly induces apoptosis in tumor cells.

A cancer vaccine containing plasmid DNA encoding human prostatic acid phosphatase (PAP) (pTVG-HP) with potential immunostimulatory and antineoplastic activities. Upon administration, pTVG-HP plasmid DNA vaccine may stimulate the host immune system to generate a cytotoxic T lymphocyte (CTL) response against PAP-expressing prostate cancer cells. PAP or prostatic specific acid phosphatase (PSAP) is a tumor associated antigen (TAA) that may be overexpressed in prostate cancer.

Brand name for dornase alfa inhalation solution

A plasmid DNA vaccine containing mammalian expression vector pUMVC3, encoding epitopes of human insulin-like growth factor-binding protein 2 (hIGFBP-2) with potential immunostimulating and antineoplastic activities. Upon vaccination, pUMVC3-hIGFBP-2 multi-epitope plasmid DNA vaccine may activate the immune system to mount a cytotoxic T-lymphocyte (CTL) response against hIGFBP-2-expressing cells. The tumor associated antigen (TAA) hIGFBP-2, a member of the insulin like growth factor receptor family, is overexpressed in a number of cancer cell types and its expression has been associated with increased invasiveness.

A polyepitope plasmid DNA vaccine containing the mammalian expression vector pUMVC3 encoding epitopes derived from three tumor-associated antigens (TAAs): human insulin-like growth factor-binding protein 2 (IGFBP2), human epidermal growth factor receptor 2 (HER2; ERBB2) and insulin-like growth factor 1 receptor (IGF1R), with potential immunostimulating and antineoplastic activities. Upon intradermal vaccination, pUMVC3-IGFBP2-HER2-IGF1R plasmid DNA vaccine transfects local keratinocytes, which process the plasmid, express the epitopes and present them to antigen-presenting cells (APCs). This activates the immune system to mount a combined response from specific T helper type 1 (Th1) cells, memory T cells and cytotoxic T lymphocytes (CTL) against IGFBP2-, HER2-, and IGF1R-expressing tumor cells. IGFBP2, HER2, and IGF1R are tumor-associated proteins overexpressed in certain tumor cell types, and play key roles in cellular proliferation and survival.

Brand name for mercaptopurine

Brand name for mercaptopurine

Brand name for mercaptopurine oral suspension

Brand name for rostaporfin

Juice made form dark, purple grapes that contain polyphenols with antioxidant and potential cardiovascular protecting activities. Purple grape juice contains high amounts of flavonoids that may increase antioxidant activity and reduce oxidative stress, reduce low-density lipoprotein (LDL), and improve nitric oxide formation, endothelial function and vasodilation.

An injectable ten percent solution of rose bengal disodium, an iodinated fluorescein derivative, with potential antineoplastic and radiosensitizing activities. When injected into tumor tissue, PV-10 specifically targets and concentrates in tumor cells, producing cytotoxic singlet oxygen when exposed to ionizing radiation. In addition, PV-10 may stimulate an anti-tumor immune response.

An attenuated, replication-competent, oncolytic strain of Newcastle disease virus. PV701 selectively lyses tumor cells. The selectivity of this agent is related to defects in the interferon-mediated antiviral response found in tumor cells. Check for active clinical trials using this agent.

An embolic material composed of microspheres of polyvinyl alcohol (PVA) polymers. These water-soluble, compressible microspheres may be used to encapsulate various therapeutic agents; drug-loaded microspheres can then be used as a drug delivery vehicle during embolization of tumor vasculature.

An embolic material composed of microspheres of polyvinyl alcohol (PVA) polymers loaded with doxorubicin hydrochloride with antineoplastic activity. Doxorubicin hydrochloride-loaded microspheres may be used as a drug delivery vehicle during embolization of tumor vasculature. Doxorubicin intercalates DNA, interferes with catalytic activity of topoisomerase II, and causes DNA adducts and other DNA damage, resulting in tumor cell growth inhibition and apoptosis. When used in tumor vasculature embolization, this preparation may provide more tumor-specific treatment with doxorubicin compared to the systemic administration of doxorubicin, thereby reducing the systemic toxicity of doxorubicin.

A cancer vaccine containing xenogenic DNA from rhesus macaque (Macaca mulatta) that encodes prostate specific antigen (PSA) with potential immunostimulating and antineoplastic activities. Upon repeated intradermal administration via electroporation, pVAXrcPSAv53l vaccine may induce a cytotoxic T-lymphocyte (CTL) response against PSA-expressing prostate cancer cells. Rhesus PSA is 89% homologous to human PSA.

A topical formulation consisting of a polyvinylidene fluoride (PVDF) polymer resin containing the macrolide sirolimus (rapamycin), produced by the organism Streptomyces hygroscopicus, with immunosuppressive activity. Upon application of topical PVDF/sirolimus, sirolimus migrates from the PVDF polymer resin into the skin. Once inside cells, sirolimus binds to the immunophilin FK binding protein-12 (FKBP-12) and forms a sirolimus:FKBP-12 complex. This complex binds to and inhibits the activity of the serine/threonine kinase mammalian target of rapamycin (mTOR), which may result in the suppression of cytokine-driven T-cell activation and proliferation.

Brand name for French maritime pine bark extract

A synthetic pyrazinoic acid amide derivative with bactericidal property. Pyrazinamide is particularly active against slowly multiplying intracellular bacilli (unaffected by other drugs) by an unknown mechanism of action. Its bactericidal action is dependent upon the presence of bacterial pyrazinamidase, which removes the amide group to produce active pyrazinoic acid. Pyrazinamide is an important component of multidrug therapy for tuberculosis.

A congener of pyridine 2-diazohydroxide. Pyrazine diazohydroxide forms DNA adducts via the reactive pyrazine diazonium ion, thereby inhibiting DNA synthesis.

A nucleoside analog. Pyrazofurin potently inhibits orotidine 5'-monophosphate (OMP) decarboxylase, thereby interfering with de novo synthesis of uridine nucleotides and resulting in cytotoxicity. This agent also causes a rapid depletion of the pyrimidine deoxynucleotide pool, thereby inhibiting DNA synthesis and cell replication.

A 9-methoxy acridine compound containing a reducible 5-nitro substituent. Pyrazoloacridine appears to intercalate into DNA and inhibit RNA synthesis, DNA synthesis, and the activities of topoisomerases I and II, thereby causing cytotoxicity.

The hydrochloride salt of pyridoxine, a water-soluble B vitamin. Pyridoxine is converted in the liver into the metabolically active coenzyme form pyridoxal 5'-phosphate (P5P), an essential cofactor in many enzymatic reactions in amino acid metabolism, including transamination, deamination, and decarboxylation. P5P is required for glycogenolysis and the synthesis of sphingolipids and is essential to red blood cell, nervous system, and immune system functions.

A synthetic derivative of ethyl-pyrimidine with potent antimalarial properties. Pyrimethamine is a competitive inhibitor of dihydrofolate reductase (DHFR). DHFR is a key enzyme in the redox cycle for production of tetrahydrofolate, a cofactor that is required for the synthesis of DNA and proteins. This agent is often used in combination with other antimalarials for the treatment of uncomplicated falciparum malaria.

An orally bioavailable, dual kinase inhibitor of the epidermal growth factor receptor (EGFR or HER-1) and the human epidermal growth factor receptor 2 (ErbB2 or HER-2), with potential antineoplastic activity. Upon oral administration, pyrotinib binds to and inhibits both EGFR and HER2, which may result in the inhibition of tumor growth and angiogenesis, and tumor regression in EGFR/HER2-expressing tumor cells. EGFR and HER2 are receptor tyrosine kinases that are upregulated in various tumor cell types and play major roles in tumor cell proliferation and tumor vascularization.

A synthetic derivative of hydroxamic acid with antineoplastic properties, Pyroxamide inhibits histone deacetylases involved in transcription; induces hyperacetylation of core histones, modulating chromatin structure and affecting transcription of some genes that inhibit tumor growth; and induces growth arrest and apoptosis. Pyroxamide is used in clinical studies for cancer chemotherapy.

An antibody-drug conjugate (ADC) consisting of an anti-CD19 humanized monoclonal antibody (hBU12ec) with engineered cysteines (EC-mAb) conjugated, via a maleimidocaproyl-valine-alanine dipeptide protease-cleavable linker, to the cytotoxic, DNA minor-groove crosslinking agent pyrrolobenzodiazepine (PBD) dimer (SGD-1882), with potential antineoplastic activity. Upon administration of anti-CD19 ADC SGN-CD19B, the antibody moiety targets the cell surface antigen CD19, which is found on B-cell-derived cancers. Upon antibody/antigen binding, internalization and lysosome uptake, the cytotoxic PBD moiety is released. In turn, the imine groups of the PBD moiety bind to the N2 positions of guanines on opposite strands of DNA. This induces DNA strand breaks, inhibits DNA replication, leads to G2/M cell cycle arrest, induces cell death, and inhibits the proliferation of CD19-overexpressing tumor cells. CD19, a transmembrane receptor belonging to the immunoglobulin superfamily and a B-cell specific antigen, is expressed on B-cell-derived cancers. The cysteine engineering of the EC-mAb allows for a site-specific and stable conjugation of PBD to the antibody.

A synthetic cyclic heptapeptide with potential antineoplastic activity. Pyruvate kinase (PK) inhibitor TLN-232 targets pyruvate kinase M2 (M2PK), which may disrupt tumor cell anaerobic glycolysis. M2PK is a dimeric isoform of PK and the predominant PK isoform found in tumor cells.

W8MD weight loss logo

Ad. Tired of being overweight?. W8MD's insurance Weight loss program can HELP*

Other languages:
English

Quick links: Medicine Portal | Encyclopedia‏‎‏‎ | Gray's Anatomy‏‎ | Topics‏‎ |‏‎ Diseases‏‎ | Drugs | Wellness | Obesity‏‎ | Metabolic syndrome | Weight loss*
Disclaimer: The entire contents of WIKIMD.ORG are for informational purposes only and do not render medical advice or professional services. If you have a medical emergency, you should CALL 911 immediately! Given the nature of the wiki, the information provided may not be accurate, misleading and or incorrect. Use the information on this wiki at your own risk! See full Disclaimer.
Link to this page: <a href="http://www.wikimd.org/wiki/Dictionary_of_drugs:_P">Dictionary of drugs: P</a>

  • Individual results may vary for weight loss from our sponsors.