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Dictionary of drugs C2

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Dictionary of pharmaceutical drugs/medications sorted alphabetically

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

A probiotic containing the anaerobic, butyric acid-forming Gram-positive bacterium Clostridium butyricum (C. butyricum), with potential immunomodulatory activity. Upon oral administration of C. butyricum-containing probiotic, C. butyricum modulates the composition of the normal gastrointestinal (GI) microflora and help maintain adequate colonization of the GI tract, thereby improving digestion and preventing GI disturbances. This bacterium creates an environment unfavorable to pathogens by adhering to human epithelial cells, thereby forming a protective mucosal barrier. This prevents attachment of pathogens and reduces the risk of infection. Dietary supplementation with this bacterium may restore or enhance intestinal immunity.

Spores of Clostridium novyi-NT, an attenuated strain of the obligate anaerobe Clostridium novyi, with potential immunostimulating and oncolytic activities. Upon intravenous administration, Clostridium novyi-NT spores germinate exclusively in hypoxic tissue, such as avascular regions of tumors. Germination results in lysis and destruction of surrounding viable tumor cells. Although C. novyi-NT spores do not proliferate in oxygenated tumor regions, they may stimulate the immune system to mount a cytolytic immune response against tumor cells, both hypoxic and well-oxygenated.

A synthetic, imidazole derivate with broad-spectrum, antifungal activity. Clotrimazole inhibits biosynthesis of sterols, particularly ergosterol, an essential component of the fungal cell membrane, thereby damaging and affecting the permeability of the cell membrane. This results in leakage and loss of essential intracellular compounds, and eventually causes cell lysis.

A preparation of autologous T-lymphocytes that have been electroporated with an mRNA encoding a chimeric antigen receptor (CAR) consisting of an anti-human hepatocyte growth factor receptor (HGFR or cMet) scFv (single chain variable fragment) and the zeta chain of the TCR/CD3 complex (CD3-zeta) coupled to the co-stimulatory molecule 4-1BB (CD137), with potential antineoplastic activities. Upon intratumoral administration, cMet CAR-mRNA electroporated autologous T lymphocytes direct T-cells to cMet-expressing tumor cells, which induces a selective toxicity in cMet-expressing tumor cells and causes tumor cell lysis. The 4-1BB co-stimulatory molecule signaling domain enhances activation and signaling after recognition of cMet. The inclusion of the 4-1BB signaling domain may increase the antitumor activity as compared to the inclusion of the CD3-zeta chain alone. The mRNA CAR is expressed for a limited amount of time, which can prevent serious, unforeseen side effects. cMet, a receptor tyrosine kinase overexpressed or mutated in many tumor cell types, plays a key role in cancer cell growth, survival, angiogenesis, invasion, and metastasis.

An orally bioavailable small molecule inhibitor of the oncoprotein c-Met (hepatocyte growth factor receptor; HGFR), with potential antineoplastic activity. Upon oral administration, AL2846 targets and binds to the c-Met protein, prevents c-Met phosphorylation and disrupts c-Met-dependent signal transduction pathways. This may induce cell death in tumor cells overexpressing c-Met or expressing constitutively activated c-Met. c-Met protein is overexpressed or mutated in many tumor cell types and plays key roles in tumor cell proliferation, survival, invasion, metastasis, and tumor angiogenesis.

A selective small-molecule inhibitor of the proto-oncogene c-Met with potential antineoplastic activity. c-Met inhibitor AMG 208 inhibits the ligand-dependent and ligand-independent activation of c-Met, inhibiting its tyrosine kinase activity, which may result in cell growth inhibition in tumors that overexpress c-Met. C-Met encodes the hepatocyte growth factor receptor tyrosine kinase, plays an important role in epithelial cell proliferation and has been shown to be overexpressed in a variety of cancers. Check for active clinical trialsusing this agent.

An orally bioavailable inhibitor of the proto-oncogene c-Met with potential antineoplastic activity. c-Met inhibitor AMG 337 selectively binds to c-Met, thereby disrupting c-Met signal transduction pathways. This may induce cell death in tumor cells overexpressing c-Met protein or expressing constitutively activated c-Met protein. c-Met protein, the product of the proto-oncogene c-Met, is a receptor tyrosine kinase also known as hepatocyte growth factor receptor (HGFR); this protein is overexpressed or mutated in many tumor cell types and plays key roles in tumor cell proliferation, survival, invasion, and metastasis, and tumor angiogenesis.

An orally bioavailable inhibitor of the proto-oncogene hepatocyte growth factor receptor (c-Met; HGFR), with potential antineoplastic activity. Upon administration, CBT-101 selectively binds to c-Met, thereby inhibiting c-Met phosphorylation and disrupting c-Met signal transduction pathways. This may induce cell death in c-Met-overexpressing tumor cells. c-Met, a receptor tyrosine kinase overexpressed or mutated in many tumor cell types, plays key roles in tumor cell proliferation, survival, invasion, metastasis, and tumor angiogenesis.

An orally bioavailable small molecule inhibitor of the oncoprotein c-Met (hepatocyte growth factor receptor; HGFR), with potential antineoplastic activity. Upon oral administration, HS-10241 targets and binds to the c-Met protein, prevents c-Met phosphorylation and disrupts c-Met-dependent signal transduction pathways. This may induce cell death in tumor cells overexpressing c-Met protein or expressing constitutively activated c-Met protein. c-Met protein is overexpressed or mutated in many tumor cell types and plays key roles in tumor cell proliferation, survival, invasion, metastasis, and tumor angiogenesis.

An orally available, small molecule inhibitor of the proto-oncogene c-Met (hepatocyte growth factor receptor [HGFR]) with potential antineoplastic activity. c-Met inhibitor JNJ-38877605 selectively binds to c-Met, thereby inhibiting c-Met phosphorylation and disrupting c-Met signal transduction pathways. This may induce cell death in tumor cells overexpressing c-Met protein or expressing constitutively activated c-Met protein. c-Met, a receptor tyrosine kinase overexpressed or mutated in many tumor cell types, plays key roles in tumor cell proliferation, survival, invasion, metastasis, and tumor angiogenesis.

An orally bioavailable inhibitor of the proto-oncogene c-Met (also known as hepatocyte growth factor receptor (HGFR)) with potential antineoplastic activity. c-Met inhibitor MSC2156119J selectively binds to c-Met, which inhibits c-Met phosphorylation and disrupts c-Met-mediated signal transduction pathways. This may induce cell death in tumor cells overexpressing c-Met protein or expressing constitutively activated c-Met protein. c-Met, a receptor tyrosine kinase overexpressed or mutated in many tumor cell types, plays key roles in tumor cell proliferation, survival, invasion, metastasis, and tumor angiogenesis.

An orally bioavailable inhibitor of the proto-oncogene c-Met (hepatocyte growth factor receptor; HGFR) with potential antineoplastic activity. Upon administration, PLB1001 selectively binds to c-Met, thereby inhibiting c-Met phosphorylation and disrupting c-Met signal transduction pathways. This may induce cell death in tumor cells overexpressing c-Met protein or expressing constitutively activated c-Met protein. c-Met, a receptor tyrosine kinase overexpressed or mutated in many tumor cell types, plays key roles in tumor cell proliferation, survival, invasion, metastasis, and tumor angiogenesis.

A chemotherapy regimen consisting of cyclophosphamide, methotrexate, and fluorouracil, which may be used in the adjuvant setting for the treatment of nonmetastatic breast cancer or alone for the treatment of metastatic breast cancer.

A peptide derived from cytomegalovirus (CMV) internal matrix protein pp65. CMV pp65 peptide antigen is used in recombinant vaccinia virus as an HLA-A-restricted epitope to produce vaccines and specific CD8+ and CD4+ cell responses against CMV infection, a serious complication of allogeneic bone marrow transplantation (BMT). In BMT, CMV infection may be prevented by passive immunization with donor-derived CMV-pp65-specific T-cell clones if provided early post-BMT.

A population of cytotoxic T lymphocytes (CTLs) specifically reactive to cytomegalovirus (CMV), Epstein-Barr virus (EBV), adenovirus (ADV) and BK virus (BKV), with potential antiviral and protective activities. T cells derived from peripheral blood mononuclear cells (PBMCs) are exposed to and activated by dendritic cells (DCs) that are loaded with specific peptides from CMV, EBV, ADV and BKV. Upon infusion of the CMV/EBV/ADV/BKV-specific CTLs, these lymphocytes target and cause lysis of CMV-, EBV-, ADV- and/or BKV-infected cells and may prevent infection and complications from CMV-, EBV-, ADV- and BKV-driven viral diseases. Opportunistic infections caused by these viruses are often seen in immunosuppressed patients. Check for active clinical trialsusing this agent.

A poloxamer-formulated, bivalent DNA vaccine containing two plasmids encoding both the human cytomegaloviral (CMV) tegument phosphoprotein 65 (pp65), a major internal matrix protein, and glycoprotein B (gB), an important CMV component responsible for attachment and entry into cells, with potential immunostimulatory properties. Upon intramuscular injection of CMVpp65/gB plasmid vaccine ASP0113, the expressed proteins may activate the immune system to mount both cellular and humoral immune responses against CMV-positive cells. This results in cell lysis of CMV-infected cells and prevents both viral replication and the development of CMV disease. This vaccine also provides active immunization and protective immunity against CMV infection in CMV-negative patients exposed to infected donor cells or tissues in transplant recipients. CMV infection can cause serious complications in patients receiving either allogeneic hematopoietic cell transplants (HCT) or solid organ transplants. The poloxamer-based delivery system enhances DNA delivery.

A peptide-based cancer vaccine containing a mutated form of the HLA-A*0201-restricted cytomegaloviral epitope CMVpp65(495-503) with potential immunostimulatory and antitumor activities. Upon subcutaneous administration, CMVpp65-A*0201 peptide vaccine may stimulate a cytotoxic T lymphocyte (CTL) response against CMV-positive cells, resulting in cell lysis. HLA-A*0201 is an MHC class I molecule that presents antigenic peptides to CD8+ T cells; epitope design restricted to epitopes that bind most efficiently to HLA-A*0201 may improve antigenic peptide immunogenicity. CMVpp65, a tegument protein of the herpes virus CMV, is the main viral antigen found in peripheral blood mononuclear cells (PBMCs) after viral infection and may activate cell-mediated immunity.

A 24-base phosphorothiolate antisense oligodeoxynucleotide (ODN) for the proto-oncogene c-myb with potential antineoplastic activity. C-myb antisense oligonucleotide G4460 binds to codon sequences 2 to 9 of c-myb mRNA, inhibiting translation of the transcript. Suppression of c-myb expression with this agent may result in the restoration of normal differentiation pathways, increased antiproliferative effects, and the induction of apoptosis in early progenitor hematopoietic cells and in tumor cells that overexpress c-myb. Tumor-cell overexpression of c-myb blocks differentiation, promotes proliferation, and inhibits apoptosis.

A preparation of non-interleukin-2 primed, tumor activated allogeneic natural killer (NK) cells with potential immunostimulating activity. The allogeneic NK cells obtained from a first or second degree relative of the patient are co-incubated with a lysate from the CTV-1 cell line, a minimally differentiated myeloid line derived from an acute myelogenous leukemia patient. Infusion of CNDO-109-activated allogeneic NK cells may be able to lyse and destroy NK-resistant tumor cells and a broad spectrum of tumor cells.

A cytokine-peptide conjugate composed of the cytokine tumor necrosis factor alpha (TNF-alpha) chemically linked to the peptide CNGRC. The peptide moiety CNGRC, a ligand for the membrane-bound metalloprotease CD13, binds to endothelial cells of the angiogenic vasculature that express CD13 (also known as aminopeptidase N); subsequently, the TNF-alpha moiety induces apoptosis in endothelial cells expressing CD13, thereby inhibiting tumor-associated angiogenesis.

An essential nutrient and natural water-soluble vitamin of the B-complex family that must combine with an intrinsic factor for absorption by the intestine, Vitamin B12 (cyanocobalamin) is necessary for hematopoiesis, neural metabolism, DNA and RNA production, and carbohydrate, fat, and protein metabolism. B12 improves iron functions in the metabolic cycle and assists folic acid in choline synthesis. B12 metabolism is interconnected with that of folic acid. Vitamin B12 deficiency causes pernicious anemia, megaloblastic anemia, and neurologic lesions.

Brand name for cyanocobalamin

An orally bioavailable small-molecule inhibitor of mitogen-activated protein kinase kinase 1 (MAP2K1 or MEK1), with potential antineoplastic activity. Cobimetinib specifically binds to and inhibits the catalytic activity of MEK1, resulting in inhibition of extracellular signal-related kinase 2 (ERK2) phosphorylation and activation and decreased tumor cell proliferation. Preclinical studies have demonstrated that this agent is effective in inhibiting the growth of tumor cells bearing a B-RAF mutation, which has been found to be associated with many tumor types. A threonine-tyrosine kinase and a key component of the RAS/RAF/MEK/ERK signaling pathway that is frequently activated in human tumors, MEK1 is required for the transmission of growth-promoting signals from numerous receptor tyrosine kinases.

A locked nucleic acid (LNA)-based oligonucleotide inhibitor of microRNA (miRNA) 155 (miR-155), with potential antineoplastic activity. Upon administration, cobomarsen targets, binds to and inhibits miR-155. This silences miR-155 and prevents the translation of certain tumor promoting genes, which leads to the induction of cancer cell apoptosis and the inhibition of tumor cell growth. miR-155, an oncogenic single-stranded, non-coding RNA that is critical to the regulation of gene expression, is overexpressed in certain tumor cell types. Up-regulation of miR-155 plays a key role in increased tumor cell proliferation and survival. The LNA is an RNA analog in which the ribose ring is locked in a particular confirmation that increases stability. Compared to the unmodified oligonucleotide, the LNA-modified oligonucleotide shows increased affinity for its target miR-155.

A homeopathic herbal formulation with potential anti-emetic activity. Cocculus/nux vomica/tabacum/petroleum extract contains equal homeopathic units of the following extracts: extract of Cocculus indicus (fish berry), the fruit of the southeast Asian/Indian climbing plant Anamirta cocculus; extract of the seeds of Strychnos nux vomica (poison nut), an evergreen tree native to southeast Asia; extract of Nicotiana tabacum (tobacco); and petroleum. Although the exact mechanism(s) of action for this formulation has yet to be fully elucidated, alkaloids in these plant extracts have been shown to relieve nausea, vomiting, and, in some cases, dizziness.

A dietary supplement containing cocoa extract derived from the cacao bean, with potential vasodilating, anti-inflammatory, cardiovascular protective, neuroprotective, cognition enhancing and chemopreventive activities. Cocoa extract contains flavonoids, including high levels of epicatechin, catechin, procyanidins and xanthines, such as theobromine. Upon oral administration, the bioactive ingredients in the cocoa extract inhibit angiotensin-converting enzyme (ACE) and increase the production of nitric oxide (NO) through the activation of endothelial nitric oxide synthase (eNOS). This causes vasodilation, improves blood flow, and decreases blood pressure. The cocoa extract also improves insulin sensitivity, enhances cognition, and decreases the production of pro-inflammatory molecules. In addition, this extract exerts antioxidant effects and is able to scavenge reactive oxygen species (ROS). As a result, healthy cells are protected from oxidative stress and DNA damage.

The phosphate salt of codeine, a naturally occurring phenanthrene alkaloid and opioid agonist with analgesic, antidiarrheal and antitussive activities. Codeine mimics the actions of endogenous opioids by binding to the opioid receptors at many sites within the central nervous system (CNS). Stimulation of mu-subtype opioid receptors results in a decrease in the release of nociceptive neurotransmitters such as substance P, GABA, dopamine, acetylcholine and noradrenaline; in addition, the codeine metabolite morphine induces opening of G-protein-coupled inwardly rectifying potassium (GIRK) channels and blocks the opening of N-type voltage-gated calcium channels, resulting in hyperpolarization and reduced neuronal excitability. Stimulation of gut mu-subtype opioid receptors results in a reduction in intestinal motility and delayed intestinal transit times. Antitussive activity is mediated through codeine’s action on the cough center in the medulla.

A naturally occurring benzoquinone important in electron transport in mitochondrial membranes. Coenzyme-Q functions as an endogenous antioxidant; deficiencies of this enzyme have been observed in patients with many different types of cancer and limited studies have suggested that coenzyme-Q may induce tumor regression in patients with breast cancer. This agent may have immunostimulatory effects.

Brand name for folitixorin

An orally bioavailable dietary supplement composed of an extract from the beans of green coffee (Coffea arabica), which are unprocessed and unroasted, with potential anti-inflammatory, antioxidant and chemopreventive activities. Coffea arabica extract contain high amounts of phenolic compounds and their derivatives, such as chlorogenic acid (CGA), and alkaloids, such as caffeine. As many of the active components in the Coffea arabica are antioxidant compounds, upon administration, they scavenge free radicals, protect against oxidation of low-density lipoprotein (LDL), and inhibit cell damage due to reactive oxygen species (ROS). This inhibits oxidative stress and protects against DNA damage. The components in the extract also inhibit enzymes involved in inflammation, cell replication and DNA synthesis, and induce the expression of antioxidant enzymes. They also induce anti-inflammatory-mediated pathways, decrease nuclear factor Kappa-B (NF-kB) activation and decrease the expression of pro-inflammatory cytokines. This may inhibit growth and induce apoptosis of cancer cells. In addition, Coffea arabica extract upregulates the expression of anti-inflammatory adipokines (adipocytokines), such as adiponectin, and reduces the expression of pro-inflammatory adipokines, such as tumor necrosis factor-alpha (TNF-a), leptin and interleukin 6 (IL-6), thereby further preventing inflammation and inflammation-induced cancer. Adipokines are normally secreted by adipose tissue and play a key role in the regulation of glucose and fat metabolism, insulin sensitivity and inflammation.

A dietary supplement containing coffee, with potential gastrointestinal (GI) tract stimulating activity. Following consumption of the dietary supplement, the coffee may both stimulate peristalsis and increase bowel movement. The supplement may also stimulate the central nervous system, suppress appetite and cause weight loss.

An alkaloid isolated from Colchicum autumnale with anti-gout and anti-inflammatory activities. The exact mechanism of action by which colchicine exerts its effect has not been completely established. Colchicine binds to tubulin, thereby interfering with the polymerization of tubulin, interrupting microtubule dynamics, and disrupting mitosis. This leads to an inhibition of migration of leukocytes and other inflammatory cells, thereby reducing the inflammatory response to deposited urate crystals. Colchicine may also interrupt the cycle of monosodium urate crystal deposition in joint tissues, thereby also preventing the resultant inflammatory response. Overall, colchicine decreases leukocyte chemotaxis/migration and phagocytosis to inflamed areas, and inhibits the formation and release of a chemotactic glycoprotein that is produced during phagocytosis of urate crystals.

An I 131 radioiodinated synthetic analogue of the neurotransmitter norepinephrine, manufactured with a proprietary process, with radioisotopic and potential antineoplastic activities. cold contaminant-free iobenguane I 131 (MIBG) localizes to adrenergic tissue and may be used to image or eradicate tumor cells that accumulate and metabolize norepinephrine. This agent is manufactured using a technology that avoids the production of unwanted "cold contaminants" (i.e., carrier molecules), which may cause undesirable side effects and compete with MIBG for binding on target receptor sites.

Brand name for North American ginseng extract AFX-2

A hydrochloride salt form of colesevelam, a non-absorbed polymer that binds bile acids in the intestine and lowers serum lipids.

The sodium salt of colistimethate, a broad-spectrum polymyxin antibiotic against most aerobic Gram-negative bacteria except Proteus bacteria. Colistimethate sodium contains the pentasodium salt of the penta(methanesulfonic acid) derivative of colistin A as the major component and a small proportion of the petasodium salt of the pentamethanesulfonate derivative of colistin B. Colistins are cyclic polypeptides produced from Bacillus colistinus or B. polymyxa and function as a surfactant which penetrates into and disrupts the bacterial cell membrane, thereby resulting in bactericidal effect. Check for active clinical trialsusing this agent.

A topical preparation containing collagen, aloe vera, vitamin E, and lidocaine hydrochloride with wound-healing activity. The four ingredients of collagen/aloe vera/vitamin E/lidocaine topical hydrogel may promote wound repair and new tissue growth in which : collagen, a structural protein in connective tissue, provides a connective tissue matrix for the attachment of various cells involved in wound repair; aloe vera carbohydrate polymers provide a moist wound environment; vitamin E promotes blood vessel formation; and lidocaine acts as a local anesthetic.

Collagenases are enzymes that degrade collagen fibers. These enzymes play an important role in connective tissue metabolism and are produced by specific cells involved in both repair and remodeling processes.

A nanoparticle delivery system for recombinant human tumor necrosis factor (TNF) consisting of recombinant TNF bound to pegylated colloidal gold nanoparticles with potential antineoplastic activity. Upon intravenous administration, colloidal gold-bound recombinant human TNF travels through the bloodstream, avoiding immune detection and uptake by the reticuloendothelial system because of nanoparticle pegylation. Due to their size, the colloidal gold nanoparticles exit the circulatory system only at hyperpermeable tumor neovasculature sites; TNF then binds to and activates tumor cell TNF receptors, which may result in an increase in tumor cell apoptosis and a reduction in tumor cell proliferation. Compared to the administration of unbound TNF, colloidal gold-bound TNF may improve the efficacy and safety of TNF administration by delivering TNF specifically to tumor tissue.

A colloidal, isotonic, physiologically balanced, plasma volume substitute containing succinylated gelatine and electrolytes, with potential nephroprotective properties. Upon intravenous administration, colloidal modified fluid gelatin plasma substitute expands the blood volume, restores intravascular volume and increases blood flow, thereby preventing hypovolemia, hypotension and shock and may decrease the accumulation of nephrotoxic agents in the kidneys.

A colloidal oatmeal-based skin cream with potential moisturizing and skin protecting activity. Upon application to the skin, colloidal oatmeal cream forms a protective barrier and thereby prevents water loss, provides moisture to the skin and protects the skin from damage.

A peptide cancer vaccine consisting of a combination of six synthetic polypeptides directed against cancer testis antigens (CTAs) frequently expressed in colorectal cancers, with potential antineoplastic and immunostimulatory activities. Colorectal cancer peptide vaccine PolyPEPI1018 potentially elicits a cytotoxic T-lymphocyte response against colorectal tumors expressing the CTAs associated with the vaccine, which may result in a reduction in tumor cell proliferation.

Brand name for therapeutic progesterone

Brand name for colistimethate sodium

Brand name for ferumoxtran-10

Brand name for deglycosylated ricin A chain-conjugated anti-CD19/anti-CD22 immunotoxins

The diphosphate prodrug of the stilbenoid combretastatin A1, originally isolated from the plant Combretum caffrum, with vascular-disrupting and antineoplastic activities. Upon administration, combretastatin A1 diphosphate (CA1P) is dephosphorylated to the active metabolite combretastatin A1 (CA1), which promotes rapid microtubule depolymerization; endothelial cell mitotic arrest and apoptosis, destruction of the tumor vasculature, disruption of tumor blood flow and tumor cell necrosis may ensue. In addition, orthoquinone intermediates, metabolized from combretastatin A1 by oxidative enzymes found to be elevated levels in some tumor types, may bind to tumor cell thiol-specific antioxidant proteins and DNA, and stimulate oxidative stress by enhancing superoxide/hydrogen peroxide production. CA1 binds to tubulin at the same site as colchicine but with higher affinity.

Brand name for cabozantinib-s-malate

Brand name for nicotine lozenge

A synthetic macrocyclic peptide inhibitor of the terminal complement protein C5, with potential anti-inflammatory and cell protective activities. Upon subcutaneous administration, complement C5 inhibitor RA101495 binds to a unique site in terminal complement protein C5, which blocks C5 cleavage into C5a and C5b and prevents the C5b-dependent assembly of the membrane-attack complex (MAC). RA101495 also inhibits the interaction between C5b and C6, thereby further blocking MAC assembly. This prevents MAC-mediated lysis and destruction of red blood cells (RBCs) that occurs in complement-mediated diseases, such as paroxysmal nocturnal hemoglobinuria (PNH), generalized myasthenia gravis (gMG) and lupus nephritis (LN). C5, a complement pathway protein, is expressed at high levels by the liver.

An orally bioavailable inhibitor of complement factor D (FD; CFD), a serine protease that cleaves complement factor B, with potential complement system inhibiting activity. Upon administration, complement FD inhibitor ACH-4471 targets, binds to and blocks the activity of FD, and thereby inhibits cleavage of complement factor B into Ba and Bb in the alternative pathway of the complement cascade. This inhibits FD-mediated signaling and activation of the alternative complement pathway (ACP), blocks complement-mediated hemolysis in paroxysmal nocturnal hemoglobinuria (PNH) and prevents ACP-induced tissue damage. FD plays a key role in the activation of the ACP.

A traditional Chinese medicine (TCM) formulation composed of compound Kushen injection (CKI) containing aqueous extracts from the roots of Kushen (Radix Sophorae Flavescentis) and Baituling (Rhizoma Smilacis Glabrae), with potential antineoplastic and immunomodulating activities. CKI contains numerous chemicals including alkaloids, such as matrine and oxymatrine, flavonoids, alkylxanthones, quinones, triterpene glycosides, fatty acids, and essential oils. Although the exact mechanism(s) of action through which CKI exerts its effects has yet to be fully elucidated, CKI is able to interfere with the activation of various signal transduction pathways, such as the Wnt/beta-catenin signaling pathway, inhibit nuclear factor-kappa B (NF-κB) activation, and block the activity of multiple receptor tyrosine kinases, such as epidermal growth factor receptor (EGFR) and vascular endothelial growth factor receptor (VEGFR). CKI induces apoptosis in and inhibits proliferation, migration, invasion and adhesion of tumor cells. CKI also modulates the production of inflammatory mediators.

A multiple electrolyte, isotonic, crystalloid solution for intravenous infusion containing sodium chloride, potassium chloride, calcium chloride dihydrate, and sodium lactate, which can restore the electrolyte balance, normalize pH, and provide water for hydration. Upon intravenous administration, the compound sodium lactate solution will replace any lost body fluids and electrolytes thereby providing hydration as well as normalizing electrolyte concentrations. In addition, conversion of sodium lactate to bicarbonate increases plasma bicarbonate levels, which facilitates the removal of hydrogen ions from the blood stream, raises blood pH and normalizes the acid-base balance.

A fully human monoclonal agonist antibody directed against the extracellular domain of human TRAIL (tumor necrosis factor-related apoptosis-inducing ligand) receptor 2 (TR-2) with potential antineoplastic activity. Conatumumab mimics the activity of native TRAIL, binding to and activating TR-2, thereby activating caspase cascades and inducing tumor cell apoptosis. TR-2 is expressed by a variety of solid tumors and cancers of hematopoietic origin.

Brand name for desmopressin acetate

A formulation containing concentrated beetroot crystals, with potential antioxidant and protective activities. Concentrated beetroot crystals contain antioxidants, including betacyanin, which scavenge free radicals, and high levels of nitrates and folic acid. Intake of concentrated beetroot crystals leads to the conversion of nitrate to nitric oxide (NO). This may have a beneficial effect on blood flow and blood pressure through the stimulation of NO-mediated vasodilation. Additionally, this agent may decrease fatigue and increase physical performance.

A liquid-based nutritional supplement containing enzyme-hydrolyzed concentrated protein derived from collagen, and fortified with L-tryptophan, with potential anti-cachexic and wound-healing activities. The concentrated, fortified, collagen protein hydrolysate liquid supplement contains all essential and non-essential amino acids. Upon oral administration, this supplement may improve both gastric functioning and gastrointestinal (GI) health, thereby reducing vomiting and diarrhea. The hydrolyzed protein helps to alleviate the digestive burden and allows for fast and efficient absorption and utilization of the protein. This may prevent both malnutrition and weight loss.

Brand name for methylphenidate hydrochloride

An antibody-drug conjugate (ADC) composed of a conditionally active biologic (CAB) antibody against AXL receptor tyrosine kinase (AXL; UFO) conjugated to an as of yet undisclosed cytotoxic agent, with potential antineoplastic activity. Upon administration of CAB-AXL-ADC BA3011, the anti-AXL antibody becomes activated through an as of yet not fully elucidated process only under the unique microphysical conditions that are present in the tumor microenvironment (TME) as a result of the glycolytic metabolism of cancer cells, and not in the microenvironment of normal, healthy tissues. Upon selective binding to AXL-expressing tumor cells and internalization, the cytotoxic agent kills the tumor cells through an as of yet undisclosed mechanism of action (MoA). AXL, a member of the TAM (TYRO3, AXL and MER) family of receptor tyrosine kinases normally expressed on many normal, healthy cells and overexpressed by many tumor cell types, plays a key role in tumor cell proliferation, survival, invasion and metastasis; its expression is associated with drug resistance and poor prognosis. The CAB antibody allows for efficient and reversible binding to AXL-expressing tumor cells under conditions that are present only in the TME, thereby maximizing efficacy while minimizing toxicity by avoiding activation and thus binding of the antibody to normal, healthy AXL-expressing cells under normal conditions.

A replication competent, oncolytic adenovirus serotype 5 (Ad5) with its knob domain of fiber protein substituted by that of the serotype 3 (Ad5/3-delta24), with potential oncolytic activity. Upon administration, oncolytic adenovirus Ad5/3-delta24 binds to specific Ad3 receptors that are highly expressed on certain tumor cells. This results in the replication of oncolytic adenovirus Ad5/3-delta24 in tumor cells and induces tumor cell lysis which may potentially result in the activation of a systemic immune response against tumor-associated antigens. The Ad5/3-delta24 has a 24 base-pair deletion in constant region 2 of the E1A gene which allows for selective replication in cells that are defective in the retinoblastoma gene (Rb) or cyclin-dependent kinase inhibitor-2A (CDKN2A or p16INK4a). As most tumor cells are defective in the Rb/p16 pathway, this virus selectively replicates in these cells. The replacement of the Ad5 fiber knob, which mediates viral-cell receptor binding, allows for a Coxsackie-adenovirus receptor (CAR)-independent infection of tumor cells; CAR expression is often deficient on cancer cells.

Purified orally bioavailable female sex hormones isolated from pregnant mare urine or synthetically derived from plant materials and primarily conjugated as sulfate esters. Estrogen binds to and activates specific nuclear receptors, which, in turn, bind to estrogen response elements (EREs) in target genes, resulting in histone acetylation, alteration of chromatin conformation, and initiation of transcription.

A combination preparation of conjugated estrogens and the selective estrogen receptor modulator (SERM) bazedoxifene that can be used for hormone replacement purposes. The conjugated estrogens increase the diminishing levels of estrogen in menopausal and postmenopausal women by binding to and activating estrogen receptors (ERs), which, in turn, bind to estrogen response elements (EREs) in target genes; this results in the transcription of estrogen-regulated genes. Maintaining adequate estrogen levels decreases symptoms such as hot flashes, night sweats, irregular menstruation, fat redistribution, mood swings, sleep disorders, vaginal dryness and osteoporosis. Bazedoxifene specifically binds to and activates ERs in certain tissues, including liver, bone, breast, and endometrium, and also promotes the transcription of estrogen-regulated genes in these tissues. However, bazedoxifene acts as an estrogen antagonist in uterine and breast tissue, thereby blocking the proliferative effects of estrogen-binding to ER-positive cells in these tissues.

A slightly altered form of linoleic acid, an omega-6 fatty acid important to human health found in beef and dairy fats.

Brand name for theophylline

Brand name for autologous tumor infiltrating lymphocytes LN-144

An aqueous colloidal nanoemulsion containing perfluorocarbon (PFC) polymers that can be used as a tracer for cell tracking purposes during fluorine-19 (19F) magnetic resonance imaging (MRI). Upon administration of the contrast agent CS-1000 to cells ex vivo, this agent freely enters the cells. Upon introduction of these cells into the patient and subsequent 19F MRI, the amount of fluorine can be detected and cellular persistence, survival and distribution of the treated cells can be assessed. The emulsion allows for fast entry of the fluorinated polymers into cells; the polymers do not degrade and remain in the cells.

The dihydrochloride salt form of copanlisib, a phosphoinositide 3-kinase (PI3K) inhibitor with potential antineoplastic activity. Copanlisib hydrochloride inhibits the activation of the PI3K signaling pathway, which may result in inhibition of tumor cell growth and survival in susceptible tumor cell populations. Activation of the PI3K signaling pathway is frequently associated with tumorigenesis and dysregulated PI3K signaling may contribute to tumor resistance to a variety of antineoplastic agents.

A chemotherapy regimen consisting of cyclophosphamide, vincristine sulfate, prednisone and dacarbazine used for the treatment of male children with classical Hodgkin lymphoma (HL).

Brand name for duvelisib

A derivative of the original MOPP regimen consisting of cyclophosphamide, vincristine, procarbazine and prednisone used as an initial treatment for Hodgkin's lymphoma. Also used for the treatment of non-Hodgkin's lymphoma.

A regimen consisting of cyclophosphamide, vincristine, prednisone and procarbazine (COPP) alternating with doxorubicin, bleomycin and vinblastine (ABV), used in combination with radiation therapy for the treatment of low-risk, childhood Hodgkin's lymphoma.

A formulation containing the compound copper chloride (CuCl2), that can potentially be used to enhance Cu levels in cancer cells in order to elevate the antitumor activity of chemotherapeutic agents that are dependent on Cu for their activity. Upon intravenous administration of CuCl2, the mineral Cu is selectively taken up by and accumulates in cancer cells. In the presence of certain chemotherapeutic agents whose mechanism of action (MoA) is dependent on Cu, this formulation may enhance their cytotoxic activity.

A radiopharmaceutical composed of the nonspecific perfusion agent ethylglyoxal bis(thiosemicarbazone) (ETS) linked to the beta-emitting, radioisotope copper Cu 62, with potential tumor imaging activity upon positron emitting tomography (PET). Upon injection, copper Cu 62-ETS distributes to various organs, especially the kidneys and the myocardium. Upon PET imaging, tumor blood flow can be visualized and the efficacy of antineoplastic and anti-angiogenic chemotherapeutics can be assessed. Cu62-ETS has a short half life of 9.74 minutes. ETS has an enhanced hyperemic response compared to other perfusion agents.

A radioconjugate consisting of a lipophilic, neutral, bioreductive copper-bis(thiosemicarbazone) complex, copper-diacetyl-bis(N4-methylthiosemicarbazone) (Cu-ATSM), labeled with the beta-emitting radioisotope copper Cu 62, with hypoxia-selective and positron emitting tomography (PET) radioimaging activities. With a high membrane permeability and low reduction potential, copper Cu 62-ATSM easily enters cells. This agent can only be reduced by mitochondria found in hypoxic cells with abnormally high electron concentrations. This chemical reaction traps Cu 62-ATSM in the cell, which allows for the selective accumulation of this agent in hypoxic cells compared to normoxic cells. The extent of copper Cu 62-ATSM retention in tissue is inversely related to the state of tissue oxygenation allowing the quantitation of tissue hypoxia with PET. This provides information about diagnosis, prognosis, treatment options and outcomes for certain cancers. The short half-life of copper Cu 62 (9.7 minutes) reduces the amount of radiation a patient is subjected to and allows for several imaging studies to be performed. Hypoxic tumors are associated with increased malignancy and resistance to radiation and chemotherapy.

A radioconjugate consisting of a lipophilic, bioreductive copper(II)bis(thiosemicarbazone) complex, copper-pyruvaldehyde-bis(N4-methylthiosemicarbazone) (Cu-PTSM), linked to the beta-emitting, radioisotope copper Cu 62, with potential perfusion and positron emitting tomography (PET) tumor imaging activities. Upon injection, the distribution of copper Cu 62-PTSM correlates with blood flow. This agent’s high membrane permeability allows for rapid diffusion into cells. Once it enters the cell, 62Cu-PTSM is then reduced by the mitochondria, which prevents diffusion of the agent out of the cell. Upon PET imaging, tumor blood flow can be visualized and tumor perfusion can be assessed. Compared with other copper radionuclides, the short half-life of copper Cu 62 (9.7 minutes) reduces the amount of radiation a patient is subjected to and allows for several imaging studies to be performed. PTSM lacks selectivity for hypoxic cells. Check for active clinical trialsusing this agent.

A radioimmunoconjugate consisting of a humanized monoclonal antibody directed against the human carcinoembryonic antigen, carcinoembryonic antigen-related cell adhesion molecule 5 (CEA or CEACAM5), which is conjugated with the radioisotope copper Cu 64 via the chelator tetra-azacyclododecanetetra-acetic acid (DOTA), with potential use as an imaging agent during positron emission tomography (PET). Upon administration, the antibody moiety of copper Cu 64 anti-CEA monoclonal antibody M5A specifically binds to cells expressing CEA. Upon binding, the radioisotope moiety can be detected using PET, thereby allowing the imaging and quantification of CEA-expressing tumor cells. CEA, a tumor associated antigen and a member of the CEA family of proteins, plays a key role in cell migration, cell invasion, and cell adhesion and is overexpressed by a variety of cancer types.

A radioimmunoconjugate containing daratumumab, a human immunoglobulin G1 kappa (IgG1k) monoclonal antibody directed against the cell surface glycoprotein CD38, conjugated with the bifunctional, macrocyclic chelating agent tetra-azacyclododecanetetra-acetic acid (DOTA), and labeled with the radioisotope copper Cu 64, with potential diagnostic properties upon positron emission tomography (PET) imaging. The monoclonal antibody moiety of copper Cu 64-DOTA-daratumumab specifically targets and binds to cell surface antigen CD38. Upon binding, the radioisotope moiety may be detected using PET, thereby allowing the imaging and quantification of CD38-expressing tumor cells. CD38, a cell surface glycoprotein, is expressed on various hematopoietic cells and is overexpressed on multiple myeloma (MM) cells.

A radioconjugate labeled with the positron-emitting radioisotope, copper Cu 64, and also composed of plerixafor, a bicyclam and hematopoietic stem cell-mobilizing agent that targets the chemokine receptor CXCR4, with tumor imaging potential using positron emission tomography (PET)/computed tomography (CT). Upon administration, the plerixafor moiety blocks the binding of stromal cell-derived factor-1alpha (SDF-1alpha or CXCL12) to the cellular receptor CXCR4. In turn, the CXCR4-expressing tumor cells can be visualized using PET/CT and the resulting images could be used to predict a tumor's response to certain treatments. The expression of CXCR4 on cancer cells has been correlated with increased tumor cell survival, tumor progression, and increased metastatic potential.

A peptide analog of pituitary adenylate cyclase-activating peptide (PACAP) radiolabeled with the positron-emitting radioisotope copper Cu 64, with potential diagnostic ability upon positron emission tomography (PET) imaging. The peptide moiety of copper Cu 64 TP3805 is able to bind to vasoactive intestinal peptide/pituitary adenylate cyclase activating peptide receptors 1 (VPAC1). Upon PET imaging, the cancer cells expressing VPAC1 can be visualized and this may allow for early detection. The oncogenic product VPAC1 is overexpressed in a variety of cancer cell types, moreover, it is overexpressed in 100% of breast tumors at the onset of the cancer. Compared to other positron-emitting radioisotopes, Cu 64 has a longer half life. Check for active clinical trialsusing this agent.

A diagnostic radioimmunoconjugate comprised of the recombinant humanized monoclonal antibody trastuzumab conjugated with the positron-emitting radioisotope copper Cu 64. Copper Cu 64 trastuzumab binds to the extracellular domain of human epidermal growth factor receptor 2 (HER2), allowing the detection of HER2 distribution using positron emission tomography (PET).

A radioconjugate consisting of a lipophilic copper(II)bis(thiosemicarbazone) labeled with the positron- and beta-emitting isotope (64)Cu with hypoxia-selective and antineoplastic activities. With a high membrane permeability and redox potential, copper Cu 64-ATSM is preferentially taken up by hypoxic cells compared to normoxic cells; the extent of retention in tissue is inversely related to the state of tissue oxygenation allowing the quantitation of tissue hypoxia by positron emission tomography (PET). In addition, the radioactive copper moiety of this agent may deliver a selective cytotoxic dose of beta radiation to hypoxic tumor cells.

A radioconjugate containing LLP2A, a high-affinity peptidomimetic ligand for the tumor-associated antigen (TAA) very-late-antigen-4 (VLA-4; VLA 4; alpha4beta1 integrin; CD49d/CD29), conjugated, via the chelator 1,4,8,11-tetraazacyclotetradecane-1-(methane phosphonic acid)-8-(methane carboxylic acid) (CB-TE1A1P), to the radioisotope copper Cu 64, and conjugated to polyethylene glycol (PEG) chains that can potentially be used as a diagnostic imaging agent of VLA-4-expressing tumor cells using positron-emitting tomography (PET). Upon administration, copper Cu 64-CB-TE1A1P-PEG4-LLP2A targets, binds to and is taken up by VLA-4-expressing tumor cells. Upon PET, the VLA-4-expressing tumor cells can be visualized, and the tumor can be assessed. VLA-4, a transmembrane adhesion receptor overexpressed and activated on various tumor cell types and surrounding stroma, plays an important role in tumor growth, angiogenesis, metastasis, drug resistance and immune responses. Pegylation optimizes the pharmacokinetic profile of 64Cu-LLP2A.

A radioimmunoconjugate containing a bivalent monospecific tandem immunoglobulin fragment (B-Fab) derived from the humanized monoclonal antibody DS6 targeting the tumor-associated mucin-1 (MUC1)-sialoglycotope CA6 conjugated with the bifunctional, macrocyclic chelating agent 1,4,7,10-tetra-azacyclododecane-1,4,7,10-tetra-acetic acid (DOTA) and labeled with the radioisotope copper Cu 64 with potential use as an imaging agent for CA6-expressing tumors using positron emission tomography (PET). The B-Fab moiety of copper Cu 64-DOTA B-Fab binds, with high affinity, to the cell surface antigen CA6. Upon binding, the radioisotope moiety may be detected using PET, thereby allowing the imaging and quantification of CA6-expressing tumor cells. This tracer could be used to select patients who could benefit from and to monitor efficacy of CA6-targeted anti-cancer therapies. Compared to DS6, the antibody fragment allows for increased tumor penetration, faster blood clearance, and more rapid renal elimination. The CA6 epitope is found on a variety of solid tumors.

A radiotracer composed of AE105, a urokinase-type plasminogen activator receptor (uPAR) peptide antagonist, conjugated with DOTA and labeled with the radionuclide copper Cu 64, with potential imaging activity upon positron emission tomography (PET). Upon administration, the AE105 moiety of copper Cu 64-DOTA-AE105 targets and binds to uPAR-expressing tumor cells. Upon PET imaging, the copper Cu 64 moiety can be visualized, uPAR-expressing tumor cells can be quantified and the degree of tumor aggressiveness can be assessed. uPAR expression is correlated with increased tumor invasiveness and aggressiveness as well as a poor prognosis.

A radioimmunoconjugate of the fully human monoclonal antibody against the third member of the epidermal growth factor receptor (EGFR), HER3 or ERBB3, conjugated with the bifunctional, macrocyclic chelating agent tetra-azacyclododecanetetra-acetic acid (DOTA) and labeled with radioisotope copper Cu 64, with potential diagnostic properties upon positron emission tomography (PET) imaging and antineoplastic activity. The antibody moiety of copper Cu 64-DOTA-anti-HER3 monoclonal antibody U3-1287 binds to and blocks the activation of HER3, thereby resulting in the inhibition of EGFR-dependent PI3K/AKT signaling and the subsequent inhibition of cellular proliferation and differentiation. The Cu 64 moiety may be detected using positron emission tomography (PET), thereby allowing the imaging and quantification of HER3-expressing tumor cells. HER3, which lacks the kinase domain conveying ligand-binding signaling by forming heterodimers with other EGFR members that have kinase activity, is frequently overexpressed in solid tumors.

A radiotracer composed of ECL1i (extracellular loop 1 inverso; d(LGTFLKC)), an allosteric peptidic modulator of CC chemokine receptor type 2 (CCR2), conjugated with 1,4,7,10-tetra-azacyclododecane-1,4,7,10-tetra-acetic acid (DOTA) and labeled with the radionuclide copper Cu 64, with potential imaging activity upon positron emission tomography (PET). Upon administration, the ECL1i moiety targets and allosterically binds to CCR2 expressing tumor cells. Upon PET imaging, the copper Cu 64 moiety can be visualized, thereby allowing the quantification of CCR2-expressing cells. CCR2, a G-protein coupled receptor expressed on the surface of monocytes and macrophages, stimulates the migration and infiltration of these cell types, and plays a significant role in angiogenesis, inflammation, tumor cell migration, and proliferation. Quantification of CCR2 may help predict chemotherapy resistance and identify early metastatic disease in certain cancers.

A radioimmunoconjugate containing rituximab, a recombinant chimeric murine/human antibody directed against the human CD20 antigen, conjugated with the bifunctional, macrocyclic chelating agent tetra-azacyclododecanetetra-acetic acid (DOTA) and labeled with the radioisotope copper Cu 64 with potential diagnostic properties upon positron emission tomography (PET) imaging. The monoclonal antibody moiety of copper Cu 64-DOTA-Rituximab specifically binds to cell surface antigen CD20. Upon binding, the radioisotope moiety may be detected using PET, thereby allowing the imaging and quantification of CD20-expressing tumor cells. CD20 is a non-glycosylated phosphoprotein that is exclusively expressed on B cells during most stages of B cell development and is often overexpressed in B-cell malignancies.

A radioimmunoconjugate containing the recombinant humanized monoclonal antibody trastuzumab conjugated with the bifunctional, macrocyclic chelating agent tetra-azacyclododecanetetra-acetic acid (DOTA) and labeled with the radioisotope copper Cu 64 with radioisotopic activity and potential use as an imaging agent. The trastuzumab moiety of copper Cu 64-DOTA-trastuzumab binds with high affinity to the extracellular domain of human epidermal growth factor receptor 2 (HER2). Upon binding, the radioisotope moiety may be detected using positron emission tomography (PET), thereby allowing the imaging and quantification of HER2-expressing tumor cells. HER2, a tyrosine kinase and client protein of heat shock protein 90 (Hsp90), may be overexpressed on the cell surfaces of various tumor cell types.

A radioconjugate containing the biphosphonate alendronate conjugated with the bifunctional, macrocyclic chelating agent 1,4,7,10-tetra-azacyclododecane-1,4,7,10-tetra-acetic acid (DOTA) and labeled with the radioisotope copper Cu 64, with potential use as an imaging agent for microcalcifications in mammary tumors using positron emission tomography (PET). Upon administration of the copper Cu-64 alendronate, the alendronate moiety targets and binds to hydroxyapatite crystals found in malignant tumors. Upon binding and PET imaging, the radioisotope moiety is detected, thereby allowing differentiation between malignant tumors, benign tumors and normal tissue, as the highest uptake of 64Cu-DOTA-alendronate occurs in malignant tumors while the lowest uptake occurs in benign tumors and normal mammary tissue.

The orally bioavailable copper salt of D-gluconic acid. In addition to its roles as an enzyme cofactor for cytochrome C oxidase and superoxide dismutase, copper forms complexes with the thiocarbamate disulfiram (DSF) forming DSF-copper complexes, which enhances the DSF-mediated inhibition of the 26S proteasome; proteasome inhibition may result in inhibition of cellular protein degradation, cessation of cell cycle progression, inhibition of cellular proliferation, and the induction of apoptosis in susceptible tumor cell populations.

An element with atomic symbol Cu, atomic number 29, and atomic weight 63. Check for active clinical trialsusing this agent.

A population of allogeneic expanded cord blood (CB)-derived cytotoxic T lymphocytes (CTLs) that are specifically reactive to cytomegalovirus (CMV), Epstein-Barr virus (EBV), adenovirus (AdV), and human polyomavirus type I (BKV), with potential antiviral activity. Infusion of the CB-derived CMV/AdV /EBV/BKV-specific CTLs into CB hematopoietic stem cell transplant (HSCT) recipients may provide virus-specific cellular immunity, thereby preventing the infection or reactivation of certain viral-associated diseases.

A preparation of human umbilical cord blood (UCB)-derived and ex vivo-expanded allogeneic natural killer (NK) cells, with immunomodulating and cytotoxic activities. Upon infusion of the cord blood-derived expanded allogeneic NK cells, these cells recognize and bind to tumor cells, and secrete perforins, granzymes, and cytokines, which cause cancer cell lysis.

Brand name for amiodarone hydrochloride

A purine nucleoside antimetabolite and antibiotic isolated from the fungus Cordyceps militaris with potential antineoplastic activity. Cordycepin is an adenosine analogue, which is readily phosphorylated to its mono-, di-, and triphosphate intracellularly. Triphosphate cordycepin can be incorporated into RNA, and inhibits transcription elongation and RNA synthesis due to the absence of a hydroxyl moiety at the 3' position. Because it can be converted to an inactive metabolite by adenosine deaminase, this agent must be administered with an adenosine deaminase inhibitor in order to be effective. Cordycepin has displayed cytotoxicity against some leukemic cell lines in vitro.

Brand name for carvedilol

Brand name for carvedilol phosphate extended-release capsule

Brand name for nadolol

An extract derived from the mushroom Coriolus versicolor, containing polysaccharide K (PSK) and polysaccharide-peptide (PSP), with potential immunomodulating and antineoplastic activities. Coriolus versicolor extract has been shown to stimulate the production of lymphocytes and cytokines, such as interferons and interleukins, and may exhibit antioxidant activities. However, the precise mechanism of action(s) of this agent is unknown.

Brand name for ivabradine hydrochloride

Brand name for prednisolone

Brand name for therapeutic hydrocortisone

Brand name for therapeutic hydrocortisone

Brand name for therapeutic hydrocortisone

A synthetic therapeutic agent which is chemically identical to or similar to the endogenous human corticotropin-releasing factor (hCRF). Synthesized in the hypothalamus, hCRF stimulates the anterior pituitary gland to secrete adrenocorticotropic hormone (ACTH). In cerebral edema, hCRF acts by impeding the flow of fluid from blood vessels into brain tissue, thereby decreasing edema and stabilizing intracranial pressure. This agent possesses anti-edema properties independent of adrenal gland function. Check for active clinical trialsusing this agent.

A hormone synthesized in the hypothalamus and regulates the secretion of adrenocorticotropic hormone (ACTH).

Brand name for therapeutic hydrocortisone

Brand name for therapeutic hydrocortisone

An insoluble fraction isolated from the bacterium Corynebacterium granulosum with potential cancer immunotherapeutic activity. As a non-specific immunostimulant, Corynebacterium granulosum P40 activates the reticulo-endothelial system; induces the production of certain cytokines; enhances macrophage activity; and potentiates a delayed-type hypersensitivity response when co-administered with an antigen.

Brand name for dactinomycin

Brand name for iodine I 131 monoclonal antibody TNT-1/B

Brand name for cobimetinib

Brand name for trimethoprim-sulfamethoxazole

Brand name for warfarin sodium

O hydroxycinnamic acid. Pleasant smelling compound found in many plants and released on wilting. Has anticoagulant activity by competing with Vitamin K.

Brand name for recombinant Ornithodoros moubata saliva-derived small protein complement C5 inhibitor

A naturally occurring enterovirus with potential antitumor activity. Upon intratumoral administration, coxsackievirus A21 targets and binds to intracellular adhesion molecule 1 (ICAM-1) and decay acceleration factor (DAF), both cell surface molecules that are both overexpressed on certain malignant cells. After entering the cells, coxsackievirus A21 replicates in these cancer cells, thereby causing cancer cell lysis. This results in a reduction of tumor cell growth.

Brand name for losartan potassium

An orally bioavailable quinazoline with potential antineoplastic activity. CP-724,714 selectively binds to the intracellular domain of HER2, reversibly inhibiting its tyrosine kinase activity and resulting in suppression of tumor cell growth. HER2, a member of the epidermal growth factor receptor (EGFR) family, is overexpressed in many adenocarcinomas, particularly breast cancers.

A synthetic oligodeoxynucleotide, containing unmethylated CpG motifs derived from bacterial DNA, with immunostimulatory activities. A CpG oligodeoxynucleotide (CpG ODN) binds to and activates a Toll-like receptor 9 (TLR9) and is taken up into cells by endocytosis; once internalized, it may activate numerous signaling transduction pathways resulting in the release of multiple cytokines. Through activation of TLR9, a CpG ODN can directly stimulate B-lymphocytes, dendritic and NK cells, resulting in an increase in innate immunity and antibody-dependant cell cytotoxicity (ADCC). Additionally, a CpG ODN can indirectly modulate T-cell responses, through the release of cytokines (IL-12 and IFN gamma), to induce a preferential shift to the Th1 (helper) phenotype resulting in enhanced CD8+ cellular cytotoxicity.

A synthetic, 21-mer, unmethylated CpG motif-based oligodeoxynucleotide (ODN), with immunostimulatory activity. CpG oligodeoxynucleotide GNKG168 binds to and activates Toll-like receptor 9 (TLR9) and is taken up into cells by endocytosis; once internalized, it may activate numerous signaling transduction pathways resulting in the release of multiple cytokines, such as immunoglobulins (Igs), interferons (IFNs), interleukins (ILs) and tumor necrosis factor (TNF). Through activation of TLR9, this ODN can directly stimulate B-lymphocytes, dendritic and natural killer (NK) cells, resulting in an increase in innate immunity and antibody-dependent cellular cytotoxicity (ADCC). In addition, through the release of IL-12 and IFN, this agent may induce a preferential shift to the T-helper 1(Th1) phenotype resulting in enhanced CD8+ T cell-mediated antitumor cytotoxicity.

A proprietary synthetic, aerosolized C-class CpG oligodeoxynucleotide-based (ODN) agonist of toll-like receptor 9 (TLR9), with potential immunostimulating activity. Upon inhalation, CpG ODN TLR9 agonist DV281 specifically targets, binds to and activates TLR9 expressed by plasmacytoid dendritic cells (pDCs) and B-cells. This initiates immune signaling pathways and induces a cytotoxic T-lymphocyte (CTL)-mediated immune response against antigens expressed by lung cancer cells. TLR9, a member of the TLR family, plays a fundamental role in pathogen recognition and activation of the innate immune system.

A recombinant, chimeric human fusion protein consisting of the iC3b/C3d-binding region of human complement receptor type 2 (CR2/CD21) linked to the alternative complement pathway (ACP) inhibitory domain of human factor H (fH) (CR2-fH), with potential complement system inhibiting activity. Via its C3 binding domain, TT30 selectively binds to complement-activated cell surfaces and via its fH binding domain regulates ACP activity. This suppresses excessive complement activity and may result in an inhibition of ACP-mediated hemolysis of paroxysmal nocturnal hemoglobinuria (PNH) red blood cells (RBCs) as well as preventing ACP-induced tissue damage. Factor H is a key regulator in the activation of ACP.

The monohydrate form of creatine similar or identical to endogenous creatine produced in the liver, kidneys, and pancreas. Creatine, in phosphate form, helps supply energy to muscle cells for contraction. After intense effort, when ATP deposits are depleted, creatine phosphate donates phosphate groups toward the fast synthesis of ATP. Dietary supplementation with creatine may improve muscle wasting associated with cancer and other chronic diseases.

An orally bioavailable small molecule, targeting the platelet-derived growth factor receptor (PDGFR), with potential antineoplastic activity. Crenolanib binds to and inhibits PDGFR, which may result in the inhibition of PDGFR-related signal transduction pathways, and, so, the inhibition of tumor angiogenesis and tumor cell proliferation. PDGFR, up-regulated in many tumor cell types, is a receptor tyrosine kinase essential to cell migration and the development of the microvasculature.

The besylate salt form of crenolanib, an orally bioavailable benzimidazole targeting the platelet-derived growth factor receptor (PDGFR) subtypes alpha and beta and FMS-related tyrosine kinase 3 (Flt3), with potential antineoplastic activity. Upon oral administration, crenolanib binds to and inhibits both wild-type and mutated forms of PDGFR and Flt3, which may result in the inhibition of PDGFR- and Flt3-related signal transduction pathways. This results in inhibition of tumor angiogenesis and tumor cell proliferation in PDGFR and/or Flt3 overexpressing tumor cells. PDGFR and Flt3, class III receptor tyrosine kinases, are upregulated or mutated in many tumor cell types.

Brand name for pancrelipase

Brand name for isavuconazonium sulfate

Brand name for rosuvastatin calcium

The sodium salt form of cridanimod, a small molecule that can increase progesterone receptor (PR) expression, with potential antineoplastic adjuvant activity. Upon intramuscular administration, cridanimod is able to induce the expression of PR in endometrial cancer. This could increase the sensitivity of endometrial cancer cells to progestin monotherapy. In combination with a progestin, cancer cells could be eradicated through increased PR-mediated signaling, leading to an inhibition of luteinizing hormone (LH) release from the pituitary gland, via a negative feedback mechanism, and, eventually, an inhibition of estrogen release from the ovaries. This leads to an inhibition of cellular growth in estrogen-dependent tumor cells. In addition, this agent is able to increase the production and release of interferon (IFN) alpha and beta. PR is often downregulated in endometrial cancer and makes it resistant to progestin-mediated hormone therapy.

A plasmid encoding for clustered regularly interspaced short palindromic repeats (CRISPR) targeting the promoters for the human papillomavirus (HPV) type 16 (HPV16) and 18 (HPV18) epitopes E6 and E7, and coupled to the endonuclease cas9, with potential antineoplastic activities. Upon administration and transfection of the CRISPR/Cas9-edited HPV16/18 E6/E7 plasmid, the guide RNA (gRNA) of the CRISPR moiety specifically targets and binds to complementary sites on the HPV 16/18 promoter regions for E6 and E7. Cas9 cleaves these specific DNA sites, thereby disrupting HPV16/18 E6/E7 transcription. Decreased expression of E6 and E7 induces apoptosis and decreases tumor cell proliferation in HPV-driven tumor cells. This induces the expression of certain tumor suppressor genes, such as p53 and retinoblastoma 1 (RB1), which induces tumor cell apoptosis and inhibits tumor cell proliferation.

A preparation of human T lymphocytes transduced with a chimeric antigen receptor (CAR) specific for the tumor-associated antigen (TAA) mesothelin and gene-edited with the clustered regularly interspaced short palindromic repeats (CRISPR)-Cas9 nuclease complex to eliminate endogenous TCR and programmed death 1 (PD-1; PDCD1; CD279; programmed cell death-1) expression, with potential immunostimulating and antineoplastic activities. The CRISPR guide RNA (gRNA) specifically targets and binds to complementary sites on TCRalpha, TCRbeta and PD-1. In turn, Cas9 cleaves these specific DNA sites, thereby disrupting transcription. Upon isolation, transduction, electroporation with TCRalpha, TCRbeta and PD-1 gRNAs, which are complexed to Cas9 RNA to disrupt expression of endogenous TCRalpha, TCRbeta and PD-1, expansion ex vivo, and introduction into the patient, the CRISPR-Cas9-mediated PD-1 and TCR gene-deleted anti-mesothelin CAR T cells recognize and bind to mesothelin-overexpressing tumor cells. This may result in a specific cytotoxic T-lymphocyte (CTL)-mediated killing of mesothelin-positive tumor cells. PD-1, an immune checkpoint receptor expressed on T cells, plays a key role in tumor immune evasion by binding to its ligand programmed death ligand 1 (PD-L1; cluster of differentiation 274; CD274; programmed cell death-1 ligand 1) expressed on tumor cells. By removing PD-1 from T cells, PD-1-mediated signaling is halted which may decrease T-cell exhaustion and may enhance T-cell activity against the mesothelin-expressing tumor cells. Removal of endogenous TCR reduces TCR competition for expression, increases the persistence and function of the expressed transgenic TCR, enhances resistance to T-cell exhaustion and increases T-cell activity. Mesothelin is upregulated on a variety of tumor cell types.

Brand name for indinavir sulfate

A humanized monoclonal immunoglobulin G1 anti-P-selectin antibody with vaso-protective and anti-vaso-occlusive properties. Upon administration, crizanlizumab binds to P-selectin and blocks its interaction with P-selectin glycoprotein ligand-1 (PSGL-1; SELPLG) on neutrophils and monocytes. P-selectin, a glycoprotein that functions as a cell adhesion molecule (CAM), translocates to the surface of activated endothelial cells and platelets, upon stimulation, where it binds to its ligand and mediates the rolling of platelets and neutrophils on activated endothelial cells. Therefore, blockade of p-selectin may inhibit platelet aggregation, maintain blood flow and minimize sickle cell-related pain crises (SCPC).

An orally available aminopyridine-based inhibitor of the receptor tyrosine kinase anaplastic lymphoma kinase (ALK) and the c-Met/hepatocyte growth factor receptor (HGFR) with antineoplastic activity. Crizotinib, in an ATP-competitive manner, binds to and inhibits ALK kinase and ALK fusion proteins. In addition, crizotinib inhibits c-Met kinase, and disrupts the c-Met signaling pathway. Altogether, this agent inhibits tumor cell growth. ALK belongs to the insulin receptor superfamily and plays an important role in nervous system development. ALK dysregulation and gene rearrangements are associated with a series of tumors.

A modulator of the E3 ubiquitin ligase complex containing cereblon (CRL4-CRBN E3 ubiquitin ligase), with immunomodulating and pro-apoptotic activities. Upon administration CC-220 specifically binds to the cereblon (CRBN) part of the ligase complex, thereby affecting the ubiquitin E3 ligase activity, and targeting certain substrate proteins for ubiquitination. This induces the proteasome-mediated degradation of certain transcription factors, including Ikaros (IKZF1) and Aiolos (IKZF3) which are transcriptional repressors in T cells. This leads to a reduction of their protein levels, and the modulation of the immune system, including activation of T lymphocytes. In addition, this leads to a downregulation of other proteins, including interferon regulatory factor 4 (IRF4), which plays a key role in the proliferation of certain cancer cell types. CRBN, the substrate recognition component of the E3 ubiquitin ligase complex, plays a key role in the ubiquitination of certain proteins.

An oligomeric proanthocyanidin extracted from the latex produced by the tree Croton lechleri (Euphorbiaceae), with antidiarrheal, and potential antiviral and antimicrobial activities. Upon oral administration, crofelemer acts locally within the gastrointestinal (GI) tract by inhibiting both the cystic fibrosis transmembrane conductance regulator (CFTR) chloride ion (Cl-) channel and the calcium-activated Cl- channel (CaCC) expressed on the luminal surface of enterocytes. This inhibits the secretion of chloride ions into the intestinal lumen and prevents high volume water loss. By normalizing Cl- and water balance in the intestines, crofelemer relieves secretory diarrhea.

A small molecule tubulin polymerization inhibitor with potential antineoplastic activity. Crolibulin binds to the colchicine-binding site on beta-tubulin and inhibits the polymerization of tubulin into microtubules, which may result in cell cycle arrest, the induction of apoptosis, and the inhibition of tumor cell proliferation. As a vascular disruption agent (VDA), this agent also disrupts tumor neovascularization, which may result in a reduction in tumor blood flow and tumor hypoxia and ischemic necrosis.

A solution containing a high concentration of cromolyn sodium, with potential mast cell stabilizing, anti-tussive and anti-inflammatory activities. Upon inhalation of PA101 via a nebulizer, cromolyn blocks calcium ion influx into mast cells, thereby preventing the degranulation of mast cells in the lungs. This blocks the release of pro-inflammatory mediators from mast cells, such as histamine and slow-reacting substance of anaphylaxis (SRS-A), and prevents both bronchoconstriction and an inflammatory response. In indolent systemic mastocytosis (ISM), PA101 may be able to reduce the symptoms associated with this disease. Check for active clinical trialsusing this agent.

A specific complex of toxic proteins from the venom of Crotalus durissus terrificus (South American rattlesnake). It can be separated into a phospholipase A and crotapotin fragment; the latter consists of three different amino acid chains, potentiates the enzyme, and is specifically neurotoxic.

An orally available crystalline formulation of genistein, a soy-derived isoflavone and phytoestrogen with potential antineoplastic, chemosensitizing, and antioxidant activities. Similar to genistein, crystalline genistein formulation AXP107-11 increases expression of phosphatase and tensin homolog (PTEN), which deactivates protein kinase Akt and mitogen-activated protein kinases (MAPK1 and 3; ERK2 and 1), thereby disrupting PI3K/Akt signal transduction and inducing apoptosis. This agent also induces antioxidant enzymes through AMP-activated protein kinase (AMPK) activation, inhibits NF-kB activation and decreases inflammation response, thereby sensitizing tumors to chemotherapy. Compared to genistein itself, this crystalline formulation shows improved solubility and bioavailability.

An orally bioavailable inhibitor of colony stimulating factor 1 receptor (CSF-1R; CSF1R), with potential antineoplastic activity. CSF1R inhibitor BLZ945 selectively binds to CSF1R expressed on tumor-associated macrophages (TAMs), blocks the activity of CSF1R, and inhibits CSF1R-mediated signal transduction pathways. This inhibits the activity and proliferation of TAMs, and reprograms the immunosuppressive nature of existing TAMs. Altogether, this reduces TAM-mediated immune suppression in the tumor microenvironment, re-activates the immune system, and improves anti-tumor cell responses mediated by T-cells. CSF1R, also known as macrophage colony-stimulating factor receptor (M-CSFR) and CD115 (cluster of differentiation 115), is a cell-surface receptor for its ligand, colony stimulating factor 1 (CSF1); this receptor is overexpressed by TAMs in the tumor microenvironment, and plays a major role in both immune suppression and the induction of tumor cell proliferation.

An orally bioavailable inhibitor of the tyrosine kinase receptor colony stimulating factor 1 receptor (CSF1R; CSF-1R; C-FMS; CD115; M-CSFR), with potential antineoplastic, macrophage checkpoint-inhibitory and immunomodulating activities. Upon administration, CSF1R inhibitor DCC-3014 targets and binds to CSF1R expressed on monocytes, macrophages, and osteoclasts and inhibits the binding of the CSF1R ligands colony-stimulating factor-1 (CSF-1) and interleukin-34 (IL-34), to CSF1R. This prevents CSF1R activation and CSF1R-mediated signaling in these cells. This blocks the production of inflammatory mediators by macrophages and monocytes and reduces inflammation. By blocking the recruitment to the tumor microenvironment and activity of CSF1R-dependent tumor-associated macrophages (TAMs), DCC-3014 inhibits the immunomodulating activity by macrophages and enhances T-cell infiltration and antitumor T-cell immune responses, which inhibits the proliferation of tumor cells. TAMs play key roles in the tumor microenvironment and allow for immune suppression; TAMs promote inflammation, tumor cell proliferation, angiogenesis, invasiveness and survival.

A probody composed of ipilimumab, a recombinant human immunoglobulin (Ig) G1 monoclonal antibody directed against the human T-cell receptor cytotoxic T-lymphocyte-associated antigen 4 (CTLA4; CTLA-4), linked to a proprietary masking peptide that covers the active antigen-binding site of the antibody through a protease-cleavable linker, with potential immune checkpoint inhibitory and antineoplastic activities. Upon administration of CTLA-4-directed probody BMS-986249, the masking peptide is cleaved by tumor-associated proteases upon extravasation into the tumor microenvironment (TME). Protease-mediated removal of the linker enables binding of the unmasked monoclonal antibody moiety to CTLA-4, which is expressed on certain T cells. This inhibits the CTLA4-mediated downregulation of T-cell activation, and leads to both activation of tumor infiltrating T-effector cells and a cytotoxic T lymphocyte (CTL)-mediated immune response against cancer cells. CTLA4, an inhibitory receptor and member of the immunoglobulin superfamily expressed on activated effector T cells (Teffs) and regulatory T cells (Tregs), plays a key role in the inhibition of T-cell activity and downregulation of the immune system. The peptide masking of BMS-986249 minimizes binding to CTLA-4 in normal tissues and may reduce systemic toxicity, when compared to ipilimumab. Tumor-associated proteases are present in high concentrations and aberrantly activated in the TME. Check for active clinical trialsusing this agent.

A vaccine composed of synthetic peptides derived from beta-human chorionic gonadotropin (hCG) conjugated to diphtheria toxoid. Vaccination with this peptide may elicit the host immune response against hCG-producing cancer cells.

Brand name for daptomycin

Brand name for Lactobacillus rhamnosus GG

Brand name for penicillamine

Brand name for penicillamine

The oil extracted from the root tuber of Curcuma xanthorrhiza. Curcuma xanthorrhiza oil is used primarily in skincare preparations.

A phytopolylphenol pigment isolated from the plant Curcuma longa, commonly known as turmeric, with a variety of pharmacologic properties. Curcumin blocks the formation of reactive-oxygen species, possesses anti-inflammatory properties as a result of inhibition of cyclooxygenases (COX) and other enzymes involved in inflammation; and disrupts cell signal transduction by various mechanisms including inhibition of protein kinase C. These effects may play a role in the agent's observed antineoplastic properties, which include inhibition of tumor cell proliferation and suppression of chemically induced carcinogenesis and tumor growth in animal models of cancer.

An orally available preparation containing curcumin, quercetin, hyaluronic acid, and chondroitin sulfate with potential radioprotective activity. Upon administration, the glycosaminoglycans may improve barrier function and reduce inflammation and irritation in the genitourinary tract caused by radiotherapy.

A water-soluble, nano-sized formulation composed of nanoparticles encapsulating the poorly water-soluble curcumin, a signal transducer and activator of transcription 3 (Stat3), nuclear factor Kappa B (NF-kB) and poly-tyrosine kinase inhibitor (TKI), and the antineoplastic anthracycline antibiotic doxorubicin, with potential antineoplastic activity. Upon administration of the curcumin/doxorubicin-encapsulating nanoparticle IMX-110, the curcumin moiety targets and inhibits the activation of STAT3 and NF-kB and prevents STAT3- and NF-kB-mediated signaling pathways, both of which are activated in a variety of human cancers and plays a key role in neoplastic transformation, uncontrolled tumor cell proliferation, tumor resistance to apoptosis, metastasis and immune evasion. The doxorubicin moiety intercalates into DNA and interferes with topoisomerase II activity. This inhibits DNA replication and RNA synthesis, leading to tumor cell growth inhibition and apoptosis. This agent also interacts with cell membrane lipids causing lipid peroxidation. Delivery of doxorubicin in nanoparticles may improve drug penetration into tumors and curcumin, by inhibiting NFkB and STAT3 activity, may circumvent the tumor cells multidrug resistance mechanisms and may therefore be effective in chemoresistant tumor cells. Chemotherapeutic agents, such as doxorubicin, upregulate the expression of NF-kB in tumor cells which generates chemotherapy-resistant tumor cells.

An oral capsule containing curcumin, green tea extract, Polygonum cuspidatum extract, and soybean extract, with antioxidant and potential chemopreventive activities. The antioxidants in curcumin/green tea extract/Polygonum cuspidatum extract/soybean extract capsule bind to and neutraliize free-radicals, which may prevent their genotoxic and carcinogenic effects.

A proprietary topical gel formulation containing an extract of curcumin, the polyphenol derived from the plant Curcuma longa, with potential anti-inflammatory, antioxidant, and wound healing activities. Upon topical administration to the affected areas, curcumin inhibits a variety of pro-inflammatory enzymes and reduces the production of certain pro-inflammatory mediators. Curcumin also blocks the formation of reactive oxygen species (ROS), neutralizes free radicals and prevents oxidative stress and DNA damage. In addition, curcumin inhibits phosphorylase kinase (PhK) in the skin, which prevents multiple PhK-mediated signal transduction pathways that are induced upon skin injury. This further prevents inflammation, promotes healing and reduces scar tissue formation. The proprietary curcumin-based gel also provides moisture to the skin and contains tetrahydropiperine (THP), which is derived from black pepper fruit and increases skin uptake of curcumin.

The eicosasodium salt of a mixed-backbone antisense oligodeoxynucleotide with chemosensitizing properties. Custirsen inhibits testosterone-repressed prostate message-2 (TRPM-2). Administration of custirsen abrogates the anti-apoptotic effect of TRPM-2, thereby sensitizing cells to chemotherapy and resulting in tumor cell death. TRPM-2 is an anti-apoptotic clusterin that is overexpressed by prostate cancer cells and is associated with chemoresistance.

A formulation composed of DOTAP:cholesterol liposome nanoparticles complexed with the plasmid C-VISA BiKDD, with potential antineoplastic activity. C-VISA BikDD: liposome consists of a pancreatic-cancer-specific expression vector “VISA” (VP16-GAL4-WPRE integrated systemic amplifier) and a pancreatic-cancer-specific promoter CCKAR (cholecystokinin type A receptor) (CCKAR-VISA or C-VISA) which drives expression of the gene BikDD, a mutant form of the potent proapoptotic gene Bik (Bcl-2 interacting killer). Upon administration and transduction into pancreatic tumor cells, expression of BikDD by C-VISA BikDD:liposome may induce pancreatic tumor cell apoptosis and suppress pancreatic tumor cell proliferation. BikDD binds with greater affinity to anti-apoptotic proteins bcl-2, bcl-xl, bcl-w and Mcl-1 and is more potent than wild-type Bik. DOTAP:cholesterol liposome is composed of cationic lipid dioleoyl-trimethylammonium propane (DOTAP) and cholesterol at molar ratio of 1:1.

A regimen consisting of cyclophosphamide, vincristine and prednisone used to treat indolent forms of non-Hodgkin lymphoma. It is also used for the treatment of chronic lymphocytic leukemia.

An orally bioavailable, selective and reversible antagonist of CXC chemokine receptor 2 (CXCR2), with potential anti-inflammatory and antineoplastic activities. Upon administration, CXC chemokine receptor 2 antagonist AZD5069 directly binds to CXCR2 and inhibits its activation. This inhibits CXCR2-mediated signaling and may inhibit tumor cell proliferation in CXCR2-overexpressing tumor cells. In addition, AZD5069 reduces both neutrophil recruitment and migration from the systemic circulation into sites of inflammation, including the lung mucosa; it may also prevent neutrophil migration from the bone marrow. This results in the reduction of inflammation, mucus production, and neutrophil proteinase-mediated tissue destruction in the lung. CXCR2, a G protein-coupled receptor protein also known as IL-8 receptor B (IL-8RB), is upregulated in a variety of tumor cell types and plays a key role in tumor cell proliferation and progression; it is known to be elevated in several inflammatory diseases, such as chronic obstructive pulmonary disease (COPD), asthma and fibrotic pulmonary disorders.

An orally bioavailable, selective and reversible antagonist of C-X-C motif chemokine receptors 1 (CXCR1) and 2 (CXCR2), with potential anti-inflammatory and antineoplastic activities. Upon administration CXCR1/2 inhibitor SX-682 selectively and allosterically binds to CXCR 1 and 2 and inhibits their activation by tumor-secreted chemokines. This inhibits CXCR1/2-mediated signaling, reduces both recruitment and migration of immunosuppressive myeloid-derived suppressor cells (MDSCs) and neutrophils in the tumor microenvironment (TME), inhibits inflammatory processes and abrogates the immunosuppressive-induced nature of the TME. This allows effector cells, such as natural killer (NK) cells and cytotoxic T lymphocytes (CTLs), to kill and eliminate cancer cells. This inhibits tumor cell migration, metastasis, angiogenesis and tumor cell proliferation. CXCR1 and 2, G protein-coupled receptor proteins located on myeloid cells and certain tumor cells, play key roles in the immunosuppressive nature of the TME, tumor metastasis, therapy-resistance and myeloid cell suppression. They play a key role in inflammation and their expression is elevated in several inflammatory-driven diseases.

An orally available small molecule antagonist of the G protein-coupled receptor, C-X-C motif chemokine receptor 2 (CXCR2), with potential immunomodulating and antineoplastic activities. Upon administration, QBM076 binds to and inhibits the activation of CXCR2, resulting in reduced neutrophil recruitment, myeloid-derived suppressor cell (MDSC) accumulation, and may potentially slow tumorigenesis and metastatic processes. CXCR2 is upregulated in a variety of cancer types, predominately in neutrophils/MDSCs rather than tumor cells, and is thought to contribute to tumor cell proliferation, invasion, and metastasis.

An orally bioavailable inhibitor of CXC Chemokine Receptor 4 (CXCR4) with potential antineoplastic activity. CXCR4 antagonist BL-8040 selectively binds to the chemokine receptor CXCR4, preventing the binding of stromal derived factor-1 (SDF-1 or CXCL12) to the CXCR4 receptor and subsequent receptor activation, which may result in decreased tumor cell proliferation and migration. In addition, inhibition of CXCR4 may induce mobilization of hematopoietic cells from the bone marrow into blood. The G protein-coupled receptor CXCR4 plays an important role in chemotaxis and angiogenesis and is upregulated in several tumor cell types; SDF-1/CXCR4 interaction induces retention of hematopoietic cells in the bone marrow. Check for active clinical trialsusing this agent.

An orally bioavailable inhibitor of C-X-C chemokine receptor type 4 (CXCR4), with potential antineoplastic activity. Upon administration, USL311 binds to CXCR4, thereby preventing the binding of stromal-cell derived factor-1 (SDF-1 or CXCL12) to CXCR4 and inhibiting CXCR4 activation, which may result in decreased proliferation and migration of CXCR4-expressing tumor cells. CXCR4, a chemokine receptor belonging to the G protein-coupled receptor (GPCR) family, plays an important role in chemotaxis and angiogenesis, and is upregulated in several tumor cell types.

An orally bioavailable inhibitor of CXCR4 with potential antineoplastic and antiviral activities. CXCR4 inhibitor MSX-122 binds to the chemokine receptor CXCR4, preventing the binding of stromal derived factor-1 (SDF-1) to the CXCR4 receptor and receptor activation, which may result in decreased tumor cell proliferation and migration. CXCR4, a chemokine receptor belonging to the GPCR (G protein-coupled receptor) gene family, plays an important role in chemotaxis and angiogenesis and is upregulated in several tumor cell types; it is also a co-receptor for HIV entry into T cells.

An orally bioavailable inhibitor of C-X-C chemokine receptor type 4 (CXCR4), with potential antineoplastic and immune checkpoint inhibitory activities. Upon administration, the CXCR4 inhibitor X4P-001 selectively binds to CXCR4 and prevents the binding of CXCR4 to its ligand, stromal cell-derived factor 1 (SDF-1 or CXCL12). This inhibits receptor activation and results in decreased proliferation and migration of CXCR4-overexpressing tumor cells. In addition, inhibition of CXCR4 prevents the recruitment of regulatory T-cells and myeloid-derived suppressor cells (MDSCs) to the tumor microenvironment, thereby abrogating CXCR4-mediated immunosuppression and enabling the activation of a cytotoxic T-lymphocyte-mediated immune response against cancer cells. The G protein-coupled receptor CXCR4, which is upregulated in several tumor cell types, induces the recruitment of immunosuppressive cells in the tumor microenvironment, suppresses immune surveillance, and promotes tumor angiogenesis and tumor cell proliferation. It is also a co-receptor for HIV entry into T cells.

An inhibitor of CXC chemokine receptor 4 (CXCR4), with potential antineoplastic activity. Upon subcutaneous administration, CXCR4 inhibitor LY2510924 binds to the chemokine receptor CXCR4, thereby preventing CXCR4 binding to its ligand, stromal derived factor-1 (SDF-1), and subsequent receptor activation. This may result in decreased tumor cell proliferation and migration. CXCR4, a chemokine receptor belonging to the G protein-coupled receptor (GPCR) gene family, plays an important role in chemotaxis and angiogenesis and is upregulated in several tumor cell types.

An essential nutrient and natural water-soluble vitamin of the B-complex family that must combine with an intrinsic factor for absorption by the intestine. Cyanocobalamin is necessary for hematopoiesis, neural metabolism, DNA and RNA production, and carbohydrate, fat, and protein metabolism. B12 improves iron functions in the metabolic cycle and assists folic acid in choline synthesis. B12 metabolism is interconnected with that of folic acid. Vitamin B12 deficiency causes pernicious anemia, megaloblastic anemia, and neurologic lesions.

A quadruple mixture composed of the corticosteroid dexamethasone, the aminoglycoside antibiotic gentamicin, the vitamin cyanocobalamin (vitamin B12), and the local anesthetic agent procaine, with antimucositis activity. Upon oral administration of the cyanocobalamin/dexamethasone/gentamicin/procaine formulation, the active ingredients prevent or inhibit inflammation and infection of the oral mucosa and reduce the associated pain. This may prevent or treat radiation-induced oral mucositis (OM).

A cell-based cancer vaccine comprised of autologous dendritic cells (DCs) pulsed with cyclin B1 peptide, with potential immunostimulatory and antineoplastic activities. Upon administration, cyclin B1 peptide-pulsed autologous dendritic cell vaccine may stimulate anti-tumoral cytotoxic T lymphocyte (CTL) and anti-cyclin B1 antibody responses against cyclin B1-expressing cancer cells, resulting in tumor cell lysis. Cyclin B1, a key regulator of the cell cycle and cell division, is overexpressed in a variety of cancer cells.

An orally bioavailable inhibitor of cyclin dependent kinases 8 and 19 (CDK8/19), with potential antineoplastic and chemoprotective activities. Upon oral administration, CDK8/19 inhibitor BCD 115 binds to and inhibits the activity of CDK8/19, which prevents activation of CDK8/19-mediated oncogenic signaling pathways, blocks selective transcription of certain tumor promoting genes, and inhibits proliferation of CDK8/19-overexpressing tumor cells. CDKs are serine/threonine kinases involved in the regulation of the cell cycle and may be overexpressed in certain cancer cell types. CDK8 plays a key role in transcription regulation and is an important oncogenic driver in a variety of cancer cell types.

An orally bioavailable, cyclin-dependent kinase (CDK) inhibitor, with potential antineoplastic activity. Upon administration, PF-06873600 selectively targets, binds to and inhibits the activity of CDKs. Inhibition of these kinases leads to cell cycle arrest, induction of apoptosis and inhibition of tumor cell proliferation. CDKs, ATP-dependent serine/threonine kinases that are important regulators of cell cycle progression and cellular proliferation, are frequently overexpressed in tumor cells.

A centrally acting muscle relaxant, chemically similar to amitriptyline hydrochloride with antidepressant activity. The exact mechanism of action of cyclobenzaprine hydrochloride has not been fully determined. However, it primarily acts at the brain stem to reduce tonic somatic motor activity, influencing both gamma and alpha motor neurons. This leads to a reduction in muscle spasms.

A formulation of camptothecin, an alkaloid isolated from the Chinese tree Camptotheca acuminata, conjugated with to a hydrophilic, cyclodextrin-based linear polymer with potential antineoplastic activity. Upon intravenous administration, camptothecin is slowly released from the formulation at the tumor site and taken up by tumor cells. 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. Compared to camptothecin alone, the cyclodextrin-based polymer formulation has a prolonged half life and greatly improves the biodistribution of camptothecin resulting in an accumulation of camptothecin at the tumor site, which enhances tumor exposure while greatly reducing toxic side effects. In addition, cyclodextrin-based polymer-camptothecin may be able to overcome certain kinds of multidrug resistance.

Brand name for cyclobenzaprine hydrochloride

A non-metabolizable synthetic amino acid, formed through the cyclization of the amino acid leucine, with immunosuppressive, antineoplastic, and cytostatic activities. Cycloleucine competitively inhibits the enzyme methionine adenosyltransferase, resulting in the inhibition of S-adenosylmethionine (SAM) synthesis from methionine and ATP, and subsequent nucleic acid methylation and polyamine production; RNA, and perhaps to a lesser extent, DNA biosyntheses and cell cycle progression are finally disrupted. This agent is also a competitive inhibitor at the glycine modulatory site of the N-methyl-D-aspartate (NMDA) receptor.

A pro-drug carbocyclic analogue of cytidine with antineoplastic and antiviral activities. Cyclopentenyl cytosine (CPEC) is converted to the active metabolite cyclopentenyl cytosine 5'-triphosphate (CPEC-TP); CPEC-TP competitively inhibits cytidine triphosphate (CTP) synthase, thereby depleting intracellular cytidine pools and inhibiting DNA and RNA synthesis. This agent may also induce differentiation of some tumor cell types. The antiviral activity of this agent is broad-spectrum.

A synthetic alkylating agent chemically related to the nitrogen mustards with antineoplastic and immunosuppressive activities. In the liver, cyclophosphamide is converted to the active metabolites aldophosphamide and phosphoramide mustard, which bind to DNA, thereby inhibiting DNA replication and initiating cell death.

A natural cyclic polypeptide immunosuppressant isolated from the fungus Beauveria nivea. The exact mechanism of action of cyclosporine is not known but may involve binding to the cellular protein cytophilin, resulting in inhibition of the enzyme calcineurin. This agent appears to specifically and reversibly inhibit immunocompetent lymphocytes in the G0-or G1-phase of the cell cycle. T-lymphocytes are preferentially inhibited with T-helper cells as the primary target. Cyclosporine also inhibits lymphokine production and release.

An topical ophthalmic formulation containing cyclosporine, an undecapeptide produced by the fungus Beauveria nivea, with immunosuppressant and anti-inflammatory activities. The exact therapeutic mechanism of action of cyclosporine is not known but may involve binding to the cellular protein cytophilin, resulting in inhibition of the enzyme calcineurin. This agent appears to specifically and reversibly inhibit immunocompetent lymphocytes in the G0-or G1-phase of the cell cycle. T-lymphocytes are preferentially inhibited with T-helper cells as the primary target. Cyclosporine also inhibits lymphokine production and release.

Brand name for tranexamic acid

A gene transfer preparation of a plasmid DNA encoding mouse somatostatin receptor subtype 2 (sst2) and a fusion protein of human deoxycytidine kinase (DCK) and uridine monophosphate kinase (UMK), complexed to a synthetic polycationic carrier, polyethylenimine, with antineoplastic adjuvant application. Upon administration, CYL-02 plasmid DNA expresses DCK::UMK fusion protein that converts gemcitabine into its toxic phosphorylated metabolite. Expression of sst2 protein by this agent could induce both antioncogenic and local antitumor bystander effects. A loss of sst2 gene expression often is found in pancreatic and colorectal cancers, and is the receptor for somatostatin which negatively regulates a number of processes such as epithelial cell proliferation. Combination effects of these gene products allows for less chemotherapy to cause tumor cell lysis in not only the original tumor, but in distant tumors as well.

Brand name for paclitaxel polymeric micelle formulation NANT-008

An orally bioavailable, non-steroidal, selective inhibitor of the enzyme cytochrome 450 side-chain cleavage (scc) (CYP11A1), with potential antineoplastic activity. Upon oral administration, CYP11A1 inhibitor ODM-208 targets, binds to and inhibits the activity of CYP11A1. This prevents the synthesis of all steroid hormones and their precursors. This may inhibit proliferation of hormone-positive tumor cells. CYP11A1, a mitochondrial enzyme, catalyzes the conversion of cholesterol to pregnenolone (Preg), which is the first rate-liming step in steroid hormone biosynthesis.

An orally available inhibitor of the steroid 17-alpha-hydroxylase/C17,20 lyase (CYP17A1 or CYP17), with potential antiandrogen and antineoplastic activities. Upon oral administration, CYP17 inhibitor CFG920 inhibits the enzymatic activity of CYP17A1 in both the testes and adrenal glands, thereby inhibiting androgen production. This may decrease androgen-dependent growth signaling and may inhibit cell proliferation of androgen-dependent tumor cells. The cytochrome P450 enzyme CYP17A1, localized to the endoplasmic reticulum, exhibits both 17alpha-hydroxylase and 17,20-lyase activities, and plays a key role in the steroidogenic pathway that produces steroidal hormones.

An orally available non-steroidal, lyase-selective inhibitor of the steroid 17-alpha-hydroxylase/C17,20 lyase (CYP17A1 or CYP17), with potential anti-androgenic and antineoplastic activities. Upon oral administration, CYP17 lyase inhibitor ASN001 selectively binds to and inhibits the lyase activity of CYP17A1 in both the testes and adrenal glands, resulting in a significant reduction in androgen production to castrate-range levels. This may both decrease androgen-dependent growth signaling and inhibit the proliferation of androgen-dependent tumor cells. The cytochrome P450 enzyme CYP17A1, which is localized to the endoplasmic reticulum, exhibits both 17alpha-hydroxylase and 17,20-lyase activities; it plays a key role in the steroidogenic pathway. The selective inhibition of CYP17A1 lyase activity by ASN001 prevents the increased synthesis of mineralocorticoids that is normally seen with non-selective CYP17 inhibitors, which also inhibit the 17-alpha-hydroxylase activity of CYP17A1.

An orally available inhibitor of both the steroid 17-alpha-hydroxylase/C17,20 lyase (CYP17A1 or CYP17) and androgen receptor (AR), with potential anti-androgen and antineoplastic activities. Upon oral administration, CYP17/AR inhibitor ODM 204 selectively inhibits the enzymatic activity of CYP17A1 in both the testes and adrenal glands, thereby inhibiting androgen production. This may both decrease androgen-dependent growth signaling and inhibit the proliferation of androgen-dependent tumor cells. In addition, ODM 204 binds to ARs in target tissues and inhibits androgen-induced receptor activation and AR nuclear translocation, which prevents the binding to and transcription of AR-responsive genes. This leads to an inhibition of growth in AR-expressing prostate cancer cells. The cytochrome P450 enzyme CYP17A1, which is localized to the endoplasmic reticulum, exhibits both 17alpha-hydroxylase and 17,20-lyase activities.

The hydrochloride salt of a synthetic methyl-piperidine derivative with antihistaminic and anti-serotoninergic properties. Cyproheptadine competes with free histamine (HA) for binding at HA-receptor sites, thereby competitively antagonizing histamine stimulation of HA-receptors in the gastrointestinal tract, large blood vessels, and bronchial smooth muscle. This agent also competes with free serotonin for binding at serotonin receptor sites. Cyproheptadine exhibits anticholinergic and sedative properties and has been shown to stimulate appetite and weight gain.

The acetate salt of a synthetic steroidal antiandrogen with weak progestational and antineoplastic activities. Cyproterone binds the androgen receptor (AR), thereby preventing androgen-induced receptor activation in target tissues and inhibiting the growth of testosterone-sensitive tumor cells. This agent also exerts progestational agonist properties at the level of the pituitary that reduce luteinizing hormone (LH), resulting in reductions in testicular androgen secretion and serum testosterone levels. Treatment with cyproterone alone results in incomplete suppression of serum testosterone levels.

Brand name for ramucirumab

Brand name for diethylstilbestrol

A biologically active, cysteine-rich, undenatured, bovine whey-based protein isolate with potential anti-cachexia and glutathione-enhancing properties. Upon administration of cysteine-rich whey protein isolate, cystine and glutamylcystine are taken up by cells and release free cysteine. The available cysteine allows cells to synthesize glutathione (GSH), a tripeptide made from amino acids glycine, glutamate and cysteine, thereby maintaining and increasing intracellular GSH concentrations. GSH plays a major role as an antioxidant, thereby protecting cells from oxidative damage due to harmful substances such as free radicals and reactive oxygen compounds. As IMN 1207 is rich in protein, this agent may prevent weight loss and increase body weight and strength.

Brand name for hexaminolevulinate hydrochloride

An orally available small molecule and nucleoside antimetabolite with potential antineoplastic activity. Upon administration, the cytidine analogue RX-3117 is taken up by cells through a carrier-mediated transporter, phosphorylated by uridine cytidine kinase (UCK) and then further phosphorylated to its diphosphate (RX-DP) and triphosphate forms (RX-TP). The triphosphate form is incorporated into RNA and inhibits RNA synthesis. The diphosphate RX-DP is reduced by ribonucleotide reductase (RR) to dRX-DP; its triphosphate form (dRX-TP) is incorporated into DNA. In addition, RX-3117 also inhibits DNA methyltransferase 1 (DNMT1). This eventually leads to cell cycle arrest and the induction of apoptosis. UCK is the rate-limiting enzyme in the pyrimidine-nucleotide salvage pathway.

An antimetabolite analogue of cytidine with a modified sugar moiety (arabinose instead of ribose). Cytarabine is converted to the triphosphate form within the cell and then competes with cytidine for incorporation into DNA. Because the arabinose sugar sterically hinders the rotation of the molecule within DNA, DNA replication ceases, specifically during the S phase of the cell cycle. This agent also inhibits DNA polymerase, resulting in a decrease in DNA replication and repair.

A liposomal intrathecal formulation of the antimetabolite cytarabine. As an S-phase-specific antimetabolite, cytarabine is phosphorylated by deoxycytidine kinase to a triphosphate form which competes with thymidine for incorporation into DNA; the incorporation of cytarabine triphosphate into DNA appears to inhibit DNA polymerase and so DNA synthesis, resulting in cell death.

A prodrug of the monophosphate (MP) form of the antimetabolite cytarabine (araCMP), an analogue of cytidine with a modified sugar moiety (arabinose instead of ribose), with potential antineoplastic activity. Upon administration of the cytarabine MP prodrug MB07133, the targeting moiety of this agent specifically delivers the cytarabine moiety to the liver. In turn, araCMP is selectively converted to araC triphosphate (araCTP) by a liver kinase, where it binds to and competes with cytidine for incorporation into DNA, thereby inhibiting DNA polymerase, and DNA synthesis. This leads to the inhibition of tumor cell proliferation and destruction of liver cancer cells. The liver is not able to convert araC into araCMP; araCMP is not converted into araCTP in tissues other than the liver. This enhances efficacy and minimizes systemic toxicity.

A small molecule pro-drug consisting of cytarabine, an antimetabolite analog of cytidine with a modified arabinose sugar moiety, covalently bonded to asparagine, with potential antineoplastic activity. Upon intravenous administration, cytarabine-asparagine prodrug BST-236 targets cancer cells, which often lack asparagine synthetase and are dependent on an external source of amino acids due to their high metabolic rate. Once the prodrug is inside target cells, the cytarabine component is cleaved and competes with cytidine for incorporation into DNA. The arabinose sugar moiety of cytarabine sterically hinders the rotation of the molecule within DNA, resulting in cell cycle arrest, specifically during the S phase of replication. Cytarabine also inhibits DNA polymerase, resulting in a decrease in DNA replication and repair. Because BST-236 specifically targets cancer cells, it may spare normal tissues from cytarabine-related toxicities.

A radio-sensitizing pyrimidine nucleoside with potential antineoplastic activity. Cytochlor is metabolized first to a phosphate derivative, CldCMP, by the enzyme deoxycytidine kinase and then to the active uracyl derivative, CldUMP, by the enzyme dCMP deaminase; deoxycytidine kinase and dCMP deaminase have been found in abnormally high concentrations in most cancers. CldUMP, the active metabolite, incorporates into DNA and, upon exposure to radiation, induces the formation of uracil radicals and double-strand DNA breaks.

A preparation of autologous lymphocytes with potential immunopotentiating and antineoplastic activities. Cytokine-induced killer (CIK) cells are CD3-and CD56-positive, non-major histocompatibility complex (MHC)-restricted, natural killer (NK)-like T lymphocytes, generated ex-vivo by incubation of peripheral blood lymphocytes (PBLs) with anti-CD3 monoclonal antibody, interleukin (IL)-2, IL-1, and interferon gamma (IFN-gamma) and then expanded. When reintroduced back to patients after autologous stem cell transplantation, CIK cells may recognize and kill tumor cells associated with minimal residual disease (MRD). CIK cells may have enhanced cytotoxic activity compared to lymphokine-activated killer (LAK) cells. Check for active clinical trialsusing this agent.

A preparation of activated veto cells, with potential immunostimulating and antineoplastic activities. White blood cells (WBCs), taken from either the patient or a healthy third-party donor, are processed and ex-vivo treated with an as of yet not disclosed mix of cytokines to activate specific cytotoxic veto cells. Upon administration, the veto cells specifically target and bind to tumor or foreign cells, thereby inducing apoptosis. Veto cells are able to selectively activate the immune system to only attack and kill tumor or foreign cells upon transplantation to prevent graft-versus-host disease (GvHD).

Cytotoxic T-lymphocytes (CTLs), specifically reactive to the cytomegalovirus (CMV) immediate early-1 (IE-1) protein, with immunomodulating activity. Adoptive immunotherapy with cytomegalovirus IE-1-specific cytotoxic T lymphocytes may help reconstitute CD8+ cytomegalovirus-specific CTL responses in CMV-infected immunocompromised hosts. IE-1 is one of the first CMV antigens expressed by CMV-infected cells, predominantly inducing a CD8+ CTL response.

Cytotoxic T lymphocytes (CTLs) specifically reactive to the cytomegalovirus (CMV) phosphoprotein pp65 with potential antiviral activity. To prepare CMV pp65-specific cytotoxic T lymphocytes in vitro, dendritic cells (DCs) are pulsed with CMV pp65 epitopes and then used to stimulate and propagate CMV pp65-specific cytotoxic T lymphocytes from peripheral blood mononuclear cells (PBMNCs); the CMV pp65-specific cytotoxic T lymphocyte population is then expanded so as to be sufficient for use in adoptive T lymphocyte therapy. When administered into a patient post-allogeneic hematopoietic stem cell transplantation, this agent may elicit a specific CTL response against CMV-infected host cells, which may result in the resolution of CMV infection. The CMV pp65 protein (65 kDa lower matrix phosphoprotein), the primary component of the enveloped subviral particle, is an immunodominant target for helper and cytotoxic T lymphocyte responses to CMV.

Brand name for [[liothyronine sodium)

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