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Antineoplastic agents a2

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  • Alacizumab pegol - A pegylated, cross-linked, humanized divalent-Fab' antibody fragment directed against vascular endothelial growth factor receptor-2 (VEGFR-2) with potential antiangiogenic and antitumor activities. Alacizumab pegol binds to and inhibits VEGFR-2, which may inhibit angiogenesis and tumor cell proliferation. Multivalent Fab' antibody fragments may exhibit improved retention and internalization properties compared to their parent IgGs.
  • Alanosine - An amino acid analogue and antibiotic derived from the bacterium Streptomyces alanosinicus with antimetabolite and potential antineoplastic activities. L-alanosine inhibits adenylosuccinate synthetase, which converts inosine monophospate (IMP) into adenylosuccinate, an intermediate in purine metabolism. L-alanosine-induced disruption of de novo purine biosynthesis is potentiated by methylthioadenosine phosphorylase (MTAP) deficiency. The clinical use of this agent may be limited by its toxicity profile. MTAP is a key enzyme in the adenine and methionine salvage pathways.
  • Albumin-binding cisplatin prodrug btp-114 - A proprietary, albumin-binding platinum (Pt)-based complex containing a prodrug form of the platinum compound cisplatin and a maleimide moiety, with an ability to strongly and selectively bind human serum albumin (HSA), and with potential antineoplastic activity. Upon intravenous administration, the maleimide group of BTP-114 rapidly conjugates with HSA in the bloodstream; this prolongs the blood circulation, enhances the half-life, and alters the biodistribution of BTP-114, as compared to cisplatin alone. Thus, BTP-114 demonstrates enhanced extravasation to the tumor, an increased accumulation in the tumor tissue and enhanced uptake by cancer cells. The prodrug form is reduced in the hypoxic tumor cell environment, which releases the highly cytotoxic active metabolite cisplatin. Once inside the tumor cell, cisplatin binds to nucleophilic groups, such as GC-rich sites, in DNA and induces intrastrand and interstrand DNA cross-links, resulting in apoptosis and cell growth inhibition. Compared to cisplatin alone, BTP-114 has improved selectivity towards tumor tissue, thereby enhancing efficacy while reducing systemic toxicities.
  • Aldesleukin - A recombinant analog of the endogenous cytokine interleukin-2 (IL-2) with immunoregulatory and antineoplastic activities. Aldesleukin binds to and activates the IL-2 receptor, followed by heterodimerization of the cytoplasmic domains of the IL-2R beta and gamma(c) chains; activation of the tyrosine kinase Jak3; and phosphorylation of tyrosine residues on the IL-2R beta chain, resulting in an activated receptor complex. Various cytoplasmic signaling molecules are recruited to the activated receptor complex and become substrates for regulatory enzymes that are associated with the receptor complex. This agent enhances lymphocyte mitogenesis; stimulates long-term growth of human IL-2 dependent cell lines; enhances lymphocyte cytotoxicity; induces lymphokine-activated killer (LAK) cell and natural killer (NK) cell activities; and induces expression of interferon-gamma. Aldesleukin may induce T cell-mediated tumor regression in some tumor types.
  • Aldoxorubicin - A 6-maleimidocaproyl hydrazone derivative prodrug of the anthracycline antibiotic doxorubicin (DOXO-EMCH) with antineoplastic activity. Following intravenous administration, aldoxorubicin binds selectively to the cysteine-34 position of albumin via its maleimide moiety. Doxorubicin is released from the albumin carrier after cleavage of the acid-sensitive hydrazone linker within the acidic environment of tumors and, once located intracellularly, intercalates DNA, inhibits DNA synthesis, and induces apoptosis. Albumin tends to accumulate in solid tumors as a result of high metabolic turnover, rapid angiogenesis, hypervasculature, and impaired lymphatic drainage. Because of passive accumulation within tumors, this agent may improve the therapeutic effects of doxorubicin while minimizing systemic toxicity.
  • Alectinib - An orally available inhibitor of the receptor tyrosine kinase anaplastic lymphoma kinase (ALK) with antineoplastic activity. Upon administration, alectinib binds to and inhibits ALK kinase, ALK fusion proteins as well as the gatekeeper mutation ALKL1196M known as one of the mechanisms of acquired resistance to small-molecule kinase inhibitors. The inhibition leads to disruption of ALK-mediated signaling and eventually inhibits tumor cell growth in ALK-overexpressing tumor cells. 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.
  • Alefacept - A recombinant dimeric fusion protein consisting of the extracellular CD2-binding domain of the human leukocyte function-associated antigen 3 (LFA-3; CD58) linked to the Fc portion of human immunoglobulin G1 (IgG1) with potential immunosuppressive activity. Alefacept binds to the CD2 receptor expressed on the majority of T lymphocytes, blocking the binding of endogenous LFA-3, located on antigen-presenting cells (APCs), to the CD2 receptor; the activation and proliferation of T lymphocytes in response to LFA-3 binding is thus inhibited. In addition, binding of the IgG1 moiety of this agent to the Fc gamma receptor on the surface of natural killer (NK)cells may bridge NK cells and target T lymphocytes, initiating NK cell-mediated apoptosis of T lymphocytes.
  • Alemtuzumab - A recombinant DNA-derived humanized monoclonal antibody directed against the cell surface glycoprotein, CD52. Alemtuzumab is an IgG1 kappa with human variable framework and constant regions, and complementarity-determining regions derived from a rat monoclonal antibody. This agent selectively binds to CD52, thereby triggering a host immune response that results in lysis of CD52 + cells. CD52 is a glycoprotein expressed on the surface of essentially all normal and malignant B and T cells, a majority of monocytes, macrophages and natural killer (NK) cells, a subpopulation of granulocytes, and tissues of the male reproductive system.
  • Alestramustine - The l-alanine ester form of estramustine, a combination of the nitrogen mustard normustine coupled via a carbamate to estradiol, with antineoplastic activity. Upon conversion of alestramustine to estramustine, estramustine binds to microtubule-associated proteins (MAPs) and beta tubulin, thereby interfering with microtubule dynamics and leading to microtubule disassembly and cell cyle arrest. Due to the estrogen moiety, this agent is able to selectively bind to and be taken up by estrogen receptor-positive cells.
  • Alflutinib mesylate - The mesylate salt form of alflutinib, an orally available selective inhibitor of the epidermal growth factor receptor (EGFR) mutant form T790M, with potential antineoplastic activity. Upon administration, alflutinib specifically binds to and inhibits the tyrosine kinase activity of EGFR T790M, a secondarily acquired resistance mutation. This prevents EGFR T790M-mediated signaling and leads to cell death in EGFR T790M-expressing tumor cells. EGFR, a receptor tyrosine kinase that is mutated in many tumor cell types, plays a key role in tumor cell proliferation and tumor vascularization. Compared to some other EGFR inhibitors, alflutinib may have therapeutic benefits in tumors with T790M-mediated drug resistance.
  • Algenpantucel-l - A cancer vaccine comprised of irradiated allogeneic pancreatic cancer cells transfected to express murine alpha-1,3-galactosyltransferase with potential antitumor activity. Vaccination is associated with the expression of murine alpha-1,3-galactosyl (alpha-gal) carbohydrate residues on cell membrane glycoproteins and glycolipids of the vaccine pancreatic cancer cell allograft; murine alpha-gal epitopes, not present on human cells, then induce a hyperacute rejection of the vaccine pancreatic cancer cell allograft. The hyperacute rejection involves the binding of pre-existing human anti-alpha-gal antibodies (which naturally occur against gut flora) to murine alpha-gal epitopes, resulting in the rapid activation of antibody-dependent cell-mediated cytotoxicity (ADCC) towards allograft cells. The host immune system then attacks endogenous pancreatic cancer cells, resulting in ADCC towards endogenous pancreatic cancer cells.
  • Alisertib - A second-generation, orally bioavailable, highly selective small molecule inhibitor of the serine/threonine protein kinase Aurora A kinase with potential antineoplastic activity. Alisertib binds to and inhibits Aurora A kinase, which may result in disruption of the assembly of the mitotic spindle apparatus, disruption of chromosome segregation, and inhibition of cell proliferation. Aurora A kinase localizes to the spindle poles and to spindle microtubules during mitosis, and is thought to regulate spindle assembly. Aberrant expression of Aurora kinases occurs in a wide variety of cancers, including colon and breast cancers.
  • Alitretinoin - An orally- and topically-active naturally-occurring retinoic acid with antineoplastic, chemopreventive, teratogenic, and embryotoxic activities. Alitretinoin binds to and activates nuclear retinoic acid receptors (RAR) and retinoid X receptors (RXR); these activated receptors act as transcription factors, regulating gene expression that results in the inhibition of cell proliferation, induction of cell differentiation, and apoptosis of both normal cells and tumor cells.
  • Alk inhibitor asp3026 - An orally available, small molecule inhibitor of the receptor tyrosine kinase anaplastic lymphoma kinase (ALK), with potential antineoplastic activity. Upon oral administration, ASP3026 binds to and inhibits ALK tyrosine kinase, ALK fusion proteins and ALK point mutation variants. Inhibition of ALK leads to the disruption of ALK-mediated signaling and the inhibition of cell growth in ALK-expressing tumor cells. ALK belongs to the insulin receptor superfamily and plays an important role in nervous system development. ALK is not expressed in healthy adult human tissue but ALK dysregulation and gene rearrangements are associated with a series of tumors. Additionally, ALK mutations are associated with acquired resistance to small molecule tyrosine kinase inhibitors.
  • Alk inhibitor plb 1003 - An orally available small molecule inhibitor of the receptor tyrosine kinase anaplastic lymphoma kinase (ALK), with potential antineoplastic activity. Upon oral administration, PLB1003 selectively binds to and inhibits wild-type ALK, ALK fusion proteins and ALK point mutation variants. Inhibition of ALK leads to the disruption of ALK-mediated signaling and inhibits tumor cell growth in ALK-expressing tumor cells. ALK belongs to the insulin receptor superfamily and plays an important role in nervous system development. ALK is not expressed in healthy adult human tissue but ALK dysregulation and gene rearrangements are associated with a series of tumors. ALK mutations are associated with acquired resistance to small molecule tyrosine kinase inhibitors.
  • Alk inhibitor ro5424802 - An orally available inhibitor of the receptor tyrosine kinase anaplastic lymphoma kinase (ALK) with antineoplastic activity. Upon administration, ALK inhibitor RO5424802 binds to and inhibits ALK kinase, which leads to a disruption of ALK-mediated signaling and eventually inhibits tumor cell growth in ALK-overexpressing tumor cells. 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. Additionally, ALK mutations are associated with acquired resistance to small molecule tyrosine kinase inhibitors.
  • Alk inhibitor tae684 - A small molecule inhibitor of the receptor tyrosine kinases (RTKs) anaplastic lymphoma kinase (ALK) and nucleophosmin-anaplastic lymphoma kinase (NPM-ALK), with potential antineoplastic activity. Upon administration, TAE684 binds to and inhibits ALK and NPM-ALK tyrosine kinases, which leads to a disruption of ALK- and NPM-ALK mediated signaling and eventually inhibits tumor cell growth in ALK- and NPM-ALK overexpressing tumor cells. 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. NPM-ALK is an oncogenic fusion protein associated with ALK-positive anaplastic large cell lymphoma. ALK mutations are also associated with acquired resistance to small molecule tyrosine kinase inhibitors.
  • Alk inhibitor wx-0593 - An orally available, small molecule inhibitor of the receptor tyrosine kinase (RTK) anaplastic lymphoma kinase (ALK), with potential antineoplastic activity. Upon oral administration, WX-0593 binds to and inhibits ALK tyrosine kinase, ALK fusion proteins, ALK point mutation variants ALK L1196M, ALK C1156Y, and EGFR L858R/T790M. Inhibition of ALK leads to the disruption of ALK-mediated signaling and the inhibition of cell growth in ALK-expressing tumor cells. ALK belongs to the insulin receptor superfamily and plays an important role in nervous system development. ALK is not expressed in healthy adult human tissue but ALK dysregulation and gene rearrangements are associated with a series of tumors. Additionally, ALK mutations are associated with acquired resistance to small molecule tyrosine kinase inhibitors.
  • Alk/c-met inhibitor tq-b3139 - An orally available, small molecule inhibitor of the receptor tyrosine kinases anaplastic lymphoma kinase (ALK) and hepatocyte growth factor receptor (c-Met; HGFR), with potential antineoplastic activity. Upon oral administration, TQ-B3139 binds to and inhibits the activity of ALK and c-Met, which leads to the disruption of ALK- and c-Met-mediated signaling and the inhibition of cell growth in ALK- and c-Met-expressing tumor cells. ALK and c-Met, overexpressed or mutated in many tumor cell types, play key roles in tumor cell proliferation, survival, invasion and metastasis.
  • Alk/fak/pyk2 inhibitor ct-707 - An orally available inhibitor of the receptor tyrosine kinase anaplastic lymphoma kinase (ALK), focal adhesion kinase (FAK) and proline-rich tyrosine kinase 2 (Pyk2), with potential antineoplastic activity. Upon administration, ALK/FAK/Pyk2 inhibitor CT-707 selectively binds to and inhibits ALK , FAK and Pyk2. The inhibition leads to disruption of ALK- , FAK- and Pyk2-mediated signal transduction pathways and eventually inhibits tumor cell growth in ALK-, FAK- and Pyk2-overexpressing tumor cells. Expression of these tyrosine kinases is dysregulated in various tumor types; they play a key role in tumor cell migration, proliferation, survival, and tumor angiogenesis.
  • Alk/ros1/met inhibitor tq-b3101 - An orally available, small molecule inhibitor of the receptor tyrosine kinases anaplastic lymphoma kinase (ALK), C-ros oncogene 1 (ROS1) and Met (hepatocyte growth factor receptor; HGFR; c-Met), with potential antineoplastic activity. Upon oral administration, TQ-B3101 targets, binds to and inhibits the activity of ALK, ROS1 and c-Met, which leads to the disruption of ALK-, ROS1- and c-Met-mediated signaling and the inhibition of cell growth in ALK-, ROS1- and c-Met-expressing tumor cells. ALK, ROS1 and c-Met, overexpressed or mutated in many tumor cell types, play key roles in tumor cell proliferation, survival, invasion and metastasis.
  • Alk/trk inhibitor tsr-011 - An orally available inhibitor of both the receptor tyrosine kinase anaplastic lymphoma kinase (ALK) and the tropomyosin-related kinases (TRK) TRKA, TRKB, and TRKC, with potential antineoplastic activity. Upon administration, ALK/TRK inhibitor TSR-011 binds to and inhibits both ALK and TRK kinases. The inhibition leads to disruption of ALK- and TRK-mediated signaling and impedes tumor cell growth in ALK/TRK-overexpressing tumor cells. 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. TRK, a family of receptor tyrosine kinases activated by neurotrophins, is mutated in a variety of cancer cell types and plays an important role in tumor cell growth and survival.
  • Alk-2 inhibitor tp-0184 - An orally bioavailable inhibitor of activin A receptor type 1 (activin receptor-like kinase 2; ALK2; ALK-2; ACRV1), with potential antineoplastic activity. Upon oral administration, ALK-2 Inhibitor TP-0184 targets, binds to and inhibits the activity of ALK-2. This prevents ALK-2-mediated signaling and inhibits cell growth in ALK-2-overexpressing tumor cells. In addition, in cancer and inflammatory conditions, ALK-2 is upregulated in response to increased signaling of pro-inflammatory cytokines, especially interleukin-6 (IL-6), and enhances the secretion of hepcidin, a peptide liver hormone and a key modulator of iron homeostasis. Blocking ALK-2-mediated pathways in inflammation and cancer leads to a decrease of hepcidin expression and restores plasma iron levels, thereby preventing low serum iron levels and anemia of chronic disease (ACD). ALK-2, a serine/threonine receptor kinase, is constitutively activated due to activating mutations or upregulated upstream signaling pathways in inflammatory conditions and certain types of cancer.
  • Alk-fak inhibitor cep-37440 - An orally available dual kinase inhibitor of the receptor tyrosine kinase anaplastic lymphoma kinase (ALK) and focal adhesion kinase (FAK), with potential antineoplastic activity. Upon administration, ALK-FAK inhibitor CEP-37440 selectively binds to and inhibits ALK kinase and FAK kinase. The inhibition leads to disruption of ALK- and FAK-mediated signal transduction pathways and eventually inhibits tumor cell growth in ALK- and FAK-overexpressing tumor cells. ALK belongs to the insulin receptor superfamily and plays an important role in nervous system development; its dysregulation and gene rearrangements are associated with a variety of tumors. The cytoplasmic tyrosine kinase FAK, a signal transducer for integrins, is upregulated and constitutively activated in various tumor types; it plays a key role in tumor cell migration, proliferation, survival, and tumor angiogenesis.
  • Alkotinib - An orally available inhibitor of multiple kinases, including the receptor tyrosine kinase anaplastic lymphoma kinase (ALK) and c-ros oncogene 1 (ROS1), with potential antineoplastic activity. Upon oral administration, alkotinib binds to and inhibits the wild-type, point mutations and fusion proteins of ALK and ROS1. Inhibition of these kinases leads to the disruption of downstream signaling pathways and the inhibition of proliferation in tumor cells which these kinases are overexpressed, rearranged or mutated.
  • Alkylglycerol/rosemary capsules - An orally available capsule containing alkylglycerols and Rosmarinus officinalis extracts standardized to diterpenes, including carnosic acid and carnosol, with potential antineoplastic and anti-inflammatory activities. Upon administration, carnosic acid and carnosol may induce apoptosis by decreasing apoptosis regulator B-cell lymphoma 2 (Bcl-2) expression, decrease tumor cell growth through inhibition of mammalian target of rapamycin (mTOR) phosphorylation, and inhibit metastatic activity by preventing the adhesion of tumor cells to type I collagen and fibronectin. Additionally, these diterpenes may decrease inflammation by downregulating cyclooxygenase (COX) type 2 (COX-2) protein synthesis. Alkylglycerols (alkyl-Gro) are bioactive ether lipids that may, through a not yet fully elucidated mechanism, inhibit tumor cell growth and metastases.
  • Allodepleted t cell immunotherapeutic atir101 - A cell-based immunotherapeutic product containing T-lymphocyte-enriched leukocytes that are devoid of alloreactive T-lymphocytes, that can potentially be used to restore lymphocyte levels after stem cell transplantations and are derived from partially matched (haploidentical) family donors for blood cancer patients who do not have a matching stem cell donor available. Host alloreactive T-cells, which can cause graft-versus-host disease (GVHD), are eliminated from the donor lymphocytes ex vivo using photodynamic therapy. After allogeneic hematopoietic stem cell transplantation (HSCT), allodepleted T cell immunotherapeutic ATIR101 is administered. This maintains a T-cell-mediated immune response against tumor cells and the donor T-cells can prevent opportunistic infections. ATIR101 does not cause severe, acute GVHD. In addition, administration of ATIR101 eliminates the need for immunosuppressants.
  • Allogeneic aml antigen-expressing dendritic cell vaccine - A cancer vaccine consisting of allogeneic, immortalized dendritic precursor cells derived from a patient with acute myelogenous leukemia (AML), with potential immunostimulatory and antineoplastic activities. Upon ex vivo stimulation and expansion of the precursor cells into mature, fully functional dendritic cells (DCs) and subsequent administration, the allogeneic AML antigen-expressing DC vaccine may elicit a potent cytotoxic T-cell (CTL) and antibody response against AML antigen-expressing cells, resulting in tumor cell death.
  • Allogeneic anti-bcma car-transduced t-cells allo-715 - A preparation of allogeneic, 'off-the-shelf' (OTS), universal transcription activator-like effector nuclease (TALEN)-engineered, gene-edited T-lymphocytes that have been transduced with a vector expressing a chimeric antigen receptor (CAR) containing a single chain variable fragment (scFv) derived from a monoclonal antibody specific for the human tumor-associated antigen (TAA) B-cell maturation antigen (BCMA; tumor necrosis factor receptor superfamily member 17; TNFRSF17), with potential immunostimulating and antineoplastic activities. Using TALEN technology, the T-cell receptor (TCR) alpha chain (TRAC) and CD52 genes are deleted from the CAR T-cells. Upon administration, the allogeneic anti-BCMA CAR-transduced T-cells ALLO-715 specifically recognize and induce selective toxicity in BCMA-expressing tumor cells. BCMA, a receptor for both a proliferation-inducing ligand (APRIL) and B-cell activating factor (BAFF), is a member of the tumor necrosis factor receptor superfamily (TNFRSF). BCMA is found on the surfaces of plasma cells, is overexpressed on malignant plasma cells and plays a key role in plasma cell proliferation and survival. Deletion of the CD52 gene makes the modified donor T-cells resistant to an anti-CD52 monoclonal antibody treatment, that is used during lymphodepletion. The knockout of TRAC eliminates TCR expression and is intended to abrogate the potential induction of graft-versus-host disease (GvHD) by the donor T-cells. The donor-derived, gene-edited CAR T cells have reduced production times and have increased availability when compared to autologous CAR-T cells, which use the patient's own cells and are produced on an individual basis. In addition, if the ALLO-715 cells cause unacceptable side effects, the incorporated CD20-based off-switch permits selective depletion of the ALLO-715 cells when the anti-CD20 monoclonal antibody rituximab is administered.
  • Allogeneic anti-bcma/cs1 bispecific car-t cells - A preparation of allogeneic T-lymphocytes that have been genetically modified to express a chimeric antigen receptor (CAR) targeting both the tumor-associated antigens (TAAs) B-cell maturation antigen (BCMA; TNFRSF17) and human CS1 (CD2 subset 1; SLAM family member 7; SLAMF7; CD319; CRACC), with potential immunomodulating and antineoplastic activities. Upon administration, the allogeneic anti-BCMA/CS1 bispecific CAR-T cells target and bind to tumor cells expressing BCMA and/or CS1 and induce selective cytotoxicity in those cells. BCMA, a receptor for both a proliferation-inducing ligand (APRIL) and B-cell activating factor (BAFF), is a member of the tumor necrosis factor receptor superfamily (TNFRSF). BCMA is found on the surfaces of plasma cells, is overexpressed on malignant plasma cells and plays a key role in plasma cell proliferation and survival. SLAMF7 is a member of the signaling lymphocytic activation molecule (SLAM) family of transmembrane receptors that modulate the function of immune cells through immunoreceptor tyrosine-based switch motifs (ITSMs) and intracellular adaptor proteins. SLAMF7 is highly expressed on certain malignant plasma cells and is minimally expressed on healthy immune cells. Targeting the two different TAAs highly expressed on malignant plasma cells may improve coverage and protect against antigen escape and resistance as tumor cells would need to lose both antigens.
  • Allogeneic anti-bcma-car t-cells pbcar269a - A preparation of allogeneic, off-the-shelf, T-lymphocytes that have been genetically modified using a proprietary synthetic nuclease-based system to express a chimeric antigen receptor (CAR) targeting the tumor-associated antigen (TAA) B-cell maturation antigen (BCMA; tumor necrosis factor receptor superfamily member 17; TNFRSF17), with potential immunostimulating and antineoplastic activities. Upon administration, allogeneic anti-BCMA-CAR T-cells PBCAR269A specifically recognize and kill BCMA-expressing tumor cells. BCMA, a receptor for both a proliferation-inducing ligand (APRIL) and B-cell activating factor (BAFF), is a member of the tumor necrosis factor receptor superfamily (TNFRSF). BCMA is found on the surfaces of plasma cells, is overexpressed on malignant plasma cells and plays a key role in plasma cell proliferation and survival.
  • Allogeneic anti-cd19 car t-cells allo-501a - A preparation of allogeneic, frozen, 'off-the-shelf', universal transcription activator-like effector nuclease (TALEN)-engineered, gene-edited T-lymphocytes expressing a chimeric antigen receptor (CAR) targeting the tumor-associated antigen (TAA) CD19, with potential immunostimulating and antineoplastic activities. Using TALEN technology, the T-cell receptor (TCR) alpha chain and CD52 genes are deleted from the CAR19 T-cells. Upon administration, allogeneic anti-CD19 CAR T-cells ALLO-501A specifically target and bind to CD19-expressing tumor cells, thereby selectively lysing CD19-expressing tumor cells. CD19 antigen is a B-cell specific cell surface antigen expressed in all B-cell lineage malignancies. Deletion of the CD52 gene makes the modified donor T-cells resistant to the anti-CD52 monoclonal antibody alemtuzumab, which is used during lymphodepletion. The knockout of the TCR alpha gene eliminates TCR expression and is intended to abrogate the potential induction of graft-versus-host disease (GvHD) by the donor T-cells. ALLO-501A lacks the rituximab recognition domains of ALLO-501.
  • Allogeneic anti-cd19 universal car-t cells cta101 - A preparation of allogeneic, off-the-shelf (OTS), universal, gene-edited T-lymphocytes expressing a chimeric antigen receptor (CAR) targeting the tumor-associated antigen (TAA) CD19, with potential immunomodulating and antineoplastic activities. Upon administration, allogeneic anti-CD19 universal CAR-T cells CTA101 specifically target and bind to CD19-expressing tumor cells, thereby selectively lysing CD19-expressing tumor cells. CD19 antigen is a B-cell specific cell surface antigen overexpressed in B-cell lineage malignancies. CTA101 is genetically engineered to prevent graft-versus-host disease (GvHD) by the donor T-cells. OTS CAR-T cells require reduced production times when compared to autologous CAR-T cells.
  • Allogeneic anti-cd19-car t-cells pbcar0191 - A preparation of allogeneic, off-the-shelf, T-lymphocytes that have been genetically modified using a proprietary synthetic nuclease-based system to express a chimeric antigen receptor (CAR) targeting the tumor-associated antigen (TAA) CD19 (cluster of differentiation 19) with potential immunostimulating and antineoplastic activities. Upon administration, allogeneic anti-CD19-CAR T-cells PBCAR0191 specifically recognize and kill CD19-expressing tumor cells. CD19 antigen is a B-cell specific cell surface antigen, which is expressed in all B-cell lineage malignancies and normal B-cells.
  • Allogeneic anti-cd20 car t-cells lucar-20s - A preparation of donor-derived T-lymphocytes that have been genetically modified to express a chimeric antigen receptor (CAR) targeting the tumor-associated antigen (TAA) CD20 (cluster of differentiation 20), with potential immunostimulating and antineoplastic activities. Upon administration, allogeneic anti-CD20 CAR T-cells LUCAR-20S specifically recognize and kill CD20-expressing tumor cells. The CD20 antigen, a non-glycosylated cell surface phosphoprotein, is a B-cell specific cell surface antigen expressed in B-cell lineage malignancies.
  • Allogeneic anti-cd20-car t-cells pbcar20a - A preparation of allogeneic, off-the-shelf (OTS), T-lymphocytes, derived from healthy donors, that have been genetically modified using a proprietary synthetic endonuclease-based system to express a chimeric antigen receptor (CAR) targeting the tumor-associated antigen (TAA) CD20 (cluster of differentiation 20), with potential immunostimulating and antineoplastic activities. Upon administration, allogeneic anti-CD20-CAR T-cells PBCAR20A specifically recognize and kill CD20-expressing tumor cells. The CD20 antigen, a non-glycosylated cell surface phosphoprotein, is a B-cell specific cell surface antigen expressed in B-cell lineage malignancies.
  • Allogeneic autophagosome-enriched vaccine dpv-001 - An off-the-shelf (OTS) autophagosome-enriched tumor vaccine composed of dendritic cell (DC)-targeting microvesicles containing short lived proteins (SLiPs) and defective ribosomal products (DRiPs) derived from tumor cells, with potential immunostimulating and antineoplastic activities. The DriPs- and SLiPs-filled autophagosome microvesicles are made by treating two human non-small cell lung cancer (NSCLC) cell lines, UbiLT3 (non-specific histopathology) and UbiLT6 (adenocarcinoma-like) with both a proteasome inhibitor, to prevent protein degradation, and an autophagy inducer. DPV-001 contains a wide variety of NSCLC-derived TAAs, many as immunogenic altered-peptide ligands (APL), and numerous damage-associated molecular pattern molecules (DAMPs) with Toll-like receptor (TLR) 2, 3, 4, 7 and 9 agonist activities. Upon administration of allogeneic autophagosome-enriched vaccine DPV-001, the proteins in the vaccine target DCs and may stimulate the immune system to mount cytotoxic T-lymphocyte (CTL) and helper T-lymphocyte responses against the TAAs. The TAAs are overexpressed in a variety of cancer cell types other than NSCLC. The tumor-associated SLiPS and DRiPs are highly unstable and normally degraded by tumor cell proteasomes. They are typically not processed and cross-presented by antigen-presenting cells (APCs).
  • Allogeneic b7.1/hla-a1 transfected tumor cell vaccine - An allogeneic whole cell vaccine, derived from irradiated allogenic tumor cells manipulated to express human B7.1 (CD80 antigen) and human leukocyte antigen (HLA) A1, with potential antitumor activity. Vaccination with allogeneic B7.1/HLA-A1 transfected tumor cell vaccine may elicit a cytotoxic T lymphocyte (CTL) response against similar host tumor cells, resulting in decreased tumor cell proliferation.
  • Allogeneic cd123car-cd28-cd3zeta-egfrt-expressing t-lymphocytes - A preparation of genetically modified allogeneic T-cells transduced with a replication-incompetent, self-inactivating lentiviral vector expressing a hinge-optimized, chimeric antigen receptor (CAR), comprised of a CD28 co-stimulatory signaling domain fused to CD3 zeta, the single-chain variable fragment of CD123 antigen (interleukin-3 receptor alpha chain or IL3RA), and a truncated form of the human epidermal growth factor receptor (EGFRt), with potential immunostimulating and antineoplastic activities. Upon intravenous administration, allogeneic CD123CAR-CD28-CD3zeta-EGFRt-expressing T-lymphocytes are directed to and induce selective toxicity in CD123-expressing tumor cells. CD123 is normally expressed on committed blood progenitor cells in the bone marrow; its overexpression is associated with increased leukemic cell proliferation and aggressiveness. Devoid of both ligand binding domains and tyrosine kinase activity, EGFRt both facilitates detection of the administered T-cells in vivo and can promote elimination of those cells following a cetuximab-induced antibody-dependent cellular cytotoxicity (ADCC) response. The costimulatory signaling domain enhances both proliferation of T-cells and antitumor activity. Hinge optimization prevents recognition of the CAR by Fc receptors (FcRs).
  • Allogeneic cd123-specific universal car123-expressing t-lymphocytes - Allogeneic, off-the-shelf, universal transcription activator-like effector nuclease (TALEN)-engineered T-lymphocytes that have been genetically modified to express a chimeric antigen receptor (CAR) targeting the tumor-associated antigen (TAA) human interleukin-3 receptor alpha chain (IL3RA; cluster of differentiation 123; CD123), with potential immunomodulating and antineoplastic activities. Upon transfusion of allogeneic CD123-specific universal CAR123-expressing T-lymphocytes (UCART123), these cells target and bind to cancer cells expressing CD123. This induces selective toxicity in and causes lysis of CD123-expressing tumor cells. CD123 is normally expressed on committed blood progenitor cells in the bone marrow; its overexpression is associated with both increased leukemic cell proliferation and aggressiveness. Using TALEN technology, the UCART123 cells no longer express the endogenous T-cell receptor (TCR) thereby abrogating the potential induction of graft-versus-host disease (GvHD) by the donor T-cells.
  • Allogeneic cd19car-transfected cytokine-induced killer cells - A preparation of allogeneic cytokine-induced killer (CIK) cells derived from peripheral blood mononuclear cells (PBMCs) transfected with the Sleeping Beauty (SB) transposon, CD19CAR (CARCIK-CD19), with potential immunomodulatory and antineoplastic activities. CIK cells are CD3- and CD56-positive, non-major histocompatibility complex (MHC)-restricted, natural killer (NK)-like T-lymphocytes. Upon infusion following an allogeneic stem cell transplantation, the CARCIK-CD19 cells bind to CD19-expressing tumor cells, thereby inducing selective toxicity in CD19-expressing tumor cells. CIK cells may have enhanced cytotoxic activity compared to lymphokine-activated killer (LAK) cells. CD19 is a B-cell specific cell surface antigen expressed in all B-cell lineage malignancies.
  • Allogeneic cd19-specific car-modified cd8 plus central memory-derived virus-specific t cells - A preparation of allogeneic Epstein-Barr virus (EBV)- and human cytomegalovirus (CMV)-specific CD8+ central memory-derived T effector-lymphocytes that have been genetically modified to express a chimeric antigen receptor (CAR) anti-CD19/CD3 zeta chain fusion protein coupled to the intracellular signal domain of CD28 antigen, with potential immunostimulating, anti-viral and antineoplastic activities. Upon infusion, allogeneic CD19-specific CAR-modified CD8+ central memory-derived virus-specific T cells directs the T-lymphocytes to CD19-expressing tumor cells, stimulating a selective toxicity to tumor cells which may eventually result in tumor cell lysis. CD19 antigen is a B-cell specific cell surface antigen expressed in all B-cell lineage malignancies. The viral specific T-cells exert antiviral immunity.
  • Allogeneic cd19-specific universal car19-expressing t-lymphocytes - A preparation of allogeneic, frozen, 'off-the-shelf', universal transcription activator-like effector nuclease (TALEN)-engineered, gene-edited T-lymphocytes expressing a chimeric antigen receptor (CAR) targeting the tumor-associated antigen (TAA) CD19, and containing a RQR8 transgene, with potential immunostimulating and antineoplastic activities. Using TALEN technology, the T-cell receptor (TCR) alpha chain and CD52 genes are deleted from the CAR19 T-cells. Upon infusion, allogeneic universal CD19-specific CAR-modified T cells (UCART19) specifically target and bind to CD19-expressing tumor cells, thereby selectively lysing CD19-expressing tumor cells. CD19 antigen is a B-cell specific cell surface antigen expressed in all B-cell lineage malignancies. Deletion of the CD52 gene makes the modified donor T-cells resistant to the anti-CD52 monoclonal antibody alemtuzumab, which is used during lymphodepletion. The knockout of the TCR alpha gene eliminates TCR expression and is intended to abrogate the potential induction of graft-versus-host disease (GvHD) by the donor T-cells. The gene-edited allogeneic, frozen UCART19 have reduced production times and provide off-the-shelf CAR-T cells when compared to autologous CAR-T cells, which use the patient's own cells and are produced on an individual basis. The protein expressed by the RQR8 transgene contains epitopes from CD34 and CD20, which allows tracking of the UCART19 cells with a clinically-approved anti-CD34 antibody. Additionally if the UCART19 cells cause unacceptable side effects, the CD20 portion of the protein permits selective depletion of the UCART19 cells when the anti-CD20 monoclonal antibody rituximab is administered.
  • Allogeneic cd22-specific universal car-expressing t-lymphocytes ucart22 - A preparation of allogeneic, off-the-shelf (OTS), universal transcription activator-like effector nuclease (TALEN)-engineered T-lymphocytes that have been genetically modified to express a chimeric antigen receptor (CAR) targeting the tumor-associated antigen (TAA) human CD22 with potential immunomodulating and antineoplastic activities. Upon transfusion, allogeneic CD22-specific universal CAR-expressing T-lymphocytes UCART22 express anti-CD22-CAR on their cell surfaces and bind to the CD22 antigen on tumor cell surfaces, resulting in lysis of CD22-expressing tumor cells. CD22, a cell surface glycoprotein, is expressed on mature B-cells and on most malignant B-cells.
  • Allogeneic cd3- cd19- cd57+ nkg2c+ nk cells fate-nk100 - A preparation of pharmacologically-enriched, allogeneic natural killer (NK) cells derived from a related but not completely matched human leukocyte antigen (HLA)-haploidentical donor that is seropositive for cytomegalovirus (CMV+), with potential cytolytic and antineoplastic activities. Upon leukapheresis, the donor peripheral blood mononuclear cells (PBMCs) are treated to remove T-lymphocytes (CD3+) and B-lymphocytes (CD19+). The remaining leukocytes are cultured for 7 days with the cytokine interleukin-15 (IL-15) and a small molecule inhibitor of glycogen synthase kinase 3-beta (GSK3beta) to generate the adaptive, CD3- CD19- CD57+ NKG2C+ NK cells FATE-NK100 ex vivo. Upon infusion of the allogeneic CD3- CD19- CD57+ NKG2C+ NK cells FATE-NK100, these cells selectively recognize and bind to tumor cells, and secrete perforins, granzymes, and cytokines, which results in cancer cell lysis. Exposure to CMV induces the expression of the memory-like activating receptor NKG2C and the maturation marker CD57 in the isolated NK cells, making them more potent than those not pre-exposed to CMV. CD57 both enhances the effector function of NK cells and stimulates CD16-dependent signaling. Treatment with IL-15 enhances NK cell proliferation and survival. The GSK3beta inhibitor induces preferential expansion of CD57+ NK cells that exhibit enhanced interferon (IFN)-gamma production.
  • Allogeneic cd3- cd19- selected natural killer cells - Human leukocyte antigen (HLA)-haploidentical donor-derived natural killer (NK) cells that are activated with the cytokine interleukin-15 (IL-15), with immunomodulating and antineoplastic activities. Upon leukapheresis, the HLA-haploidentical donor peripheral blood mononuclear cells (PBMCs) are treated to remove T-lymphocytes (CD3+) and B-lymphocytes (CD19+) cells. In turn, NK cells are expanded and activated with IL-15. Upon infusion of the allogeneic CD3- CD19- selected NK cells, these cells recognize and bind to tumor cells, and secrete perforins, granzymes, and cytokines, which results in cancer cell lysis.
  • Allogeneic cd34-positive e-rosetted t-cell depleted peripheral blood stem cells - A preparation of CD34+ selected peripheral blood stem cells (PBSCs) that are depleted of T-cells via erythrocyte rosetting (E-rosetting) and intended for allogeneic stem cell transplant. Administration of this particular preparation of CD34+E- T-cell depleted PBSCs may potentially reduce the occurrence of graft-versus-host disease (GvHD) without increasing the risk of graft failure or poor graft function
  • Allogeneic cd4+ memory th1-like t cells/microparticle-bound anti-cd3/anti-cd28 - A preparation consisting of allogeneic, differentiated Th1-like T cells bound to T cell-stimulating monoclonal antibodies with potential antitumor activity. More specifically, allogeneic CD4+ memory Th1-like T cells/microparticle-bound anti-CD3/anti-CD28 are composed of a proprietary preparation of mismatched, allogeneic differentiated CD4+ memory Th1-like T cells bound to paramagnetic, epoxy-covered 4.5 micron microparticles with covalently bound anti-CD3/anti-CD28 monoclonal antibodies at a 2:1 bead:cell ratio. The CD4+ memory Th1-like T cells are derived from precursors found in the circulation of a normal donor. Stimulated by the microparticle-bound monoclonal antibodies, the infused T cells produce pro-inflammatory, anti-tumor cytokines such as like IFN-gamma, TNF-beta, and IL-2, disabling tumor immune avoidance mechanisms and stimulating the host immune system to both reject the infused T cells and kill tumor cells.
  • Allogeneic cd56-positive cd3-negative natural killer cells - A population of allogeneic lymphocytes expressing the CD56 surface antigen and exhibiting a lack of CD3, with immunomodulating activity. Upon infusion of allogeneic CD56-positive CD3-negative natural killer (NK) cells, these cells are able to secrete cytokines and recognize and kill tumor cells as well as virally-infected cells. CD56 is a transmembrane glycoprotein also known as NCAM (Neural Cell Adhesion Molecule).
  • Allogeneic cd56-positive cd3-negative natural killer cells cynk-001 - A population of cryopreserved, off-the-shelf (OTS) allogeneic natural killer (NK) cells derived from human placental hematopoietic stem cells (HSCs) and expressing the CD56 surface antigen and exhibiting a lack of CD3, with potential immunomodulating, antineoplastic and antiviral activities. Upon infusion of allogeneic CD56-positive CD3-negative NK cells CYNK-001, these cells are able to recognize tumor cells as well as virally-infected cells, secrete perforins, granzymes and cytokines, and induce apoptosis in tumor and virally-infected cells.
  • Allogeneic cd8+ leukemia-associated antigens specific t cells nexi-001 - A preparation of allogeneic CD8+ T cells targeting multiple undisclosed leukemia-associated antigens, with potential immunomodulating and antineoplastic activities. Following peripheral blood mononuclear cell (PBMC) collection from the original stem cell donor and ex vivo priming and expansion, the allogeneic CD8+ leukemia-associated antigens specific T cells NEXI-001 are re-introduced into the leukemia patient, where they target and kill tumor cells expressing these leukemia-associated antigens.
  • Allogeneic cellular vaccine 1650-g - A pluripotent, allogeneic, tumor cell vaccine composed of irradiated tumor cells from the non-small cell lung cancer (NSCLC) cell line 1650 and the immunoadjuvant recombinant granulocyte-macrophage colony stimulating factor (GM-CSF) (1650-G), with potential immunostimulating and antineoplastic activities. Upon administration, allogeneic cellular vaccine 1650-G may stimulate the immune system to exert a cytotoxic T-lymphocyte (CTL) immune response against tumor-associated antigens (TAAs) expressed on NSCLC cells. GM-CSF potentiates the antitumor immune response. The 1650 cell line is used as a source for TAAs.
  • Allogeneic cmv antigen-specific cd4+/cd8+ t-lymphocytes - A population of allogeneic T-lymphocytes specifically reactive to cytomegalovirus (CMV) with potential antiviral activity. Allogeneic CMV antigen-specific T-cells are prepared via ex vivo stimulation of donor-derived peripheral blood mononuclear cells (PBMCs) with major cytomegalovirus structural protein, pp65 (ppUL83). T-cells that secrete interferon (IFN)-gamma in response to pp65 antigen exposure are selected and expanded for administration. Administration of the CMV antigen-specific CD4+ and CD8+T-lymphocytes into hematopoietic stem cell transplant (HSCT) or immunocompromised patients infected with CMV may potentially reconstitute virus-specific responses, thereby controlling CMV infections.
  • Allogeneic crispr-cas9 engineered anti-bcma t cells ctx120 - A preparation of human allogeneic T-lymphocytes gene-edited with the clustered regularly interspaced short palindromic repeats (CRISPR)-Cas9 nuclease complex to disrupt expression of endogenous TCR and major histocompatibility complex (MHC) class I molecules and modified to express a chimeric antigen receptor (CAR) specific for the tumor-associated antigen (TAA) human B-cell maturation antigen (BCMA; tumor necrosis factor receptor superfamily member 17; TNFRSF17), with potential immunostimulating and antineoplastic activities. Upon introduction into the patient, the allogeneic CRISPR-Cas9 engineered anti-BCMA CAR T-cells CTX120 recognize and bind to BCMA-overexpressing tumor cells. This may result in a specific cytotoxic T-lymphocyte (CTL)-mediated killing of BCMA-positive tumor cells. BCMA, a receptor for proliferation-inducing ligand (APRIL) and B-cell activating factor (BAFF), is a member of the tumor necrosis factor (TNF) receptor superfamily (TNFRSF) and plays a key role in plasma cell survival. BCMA is found on the surfaces of plasma cells and overexpressed on malignant plasma cells. The disruption of endogenous TCR prevents graft-versus-host disease (GvHD). The disruption of MHC class I molecules increases the persistence of the CAR T-cells.
  • Allogeneic crispr-cas9 engineered anti-cd19 car t cells ctx110 - A preparation of human allogeneic T-lymphocytes transduced with a chimeric antigen receptor (CAR) specific for the tumor-associated antigen (TAA) CD19 and gene-edited with the clustered regularly interspaced short palindromic repeats (CRISPR)-Cas9 nuclease complex to eliminate endogenous TCR, with potential immunostimulating and antineoplastic activities. Upon introduction into the patient, the allogeneic CRISPR-Cas9 engineered anti-CD19 CAR T-cells CTX110 recognize and bind to CD19-overexpressing tumor cells. This may result in a specific cytotoxic T-lymphocyte (CTL)-mediated killing of CD19-positive tumor cells. Removal of endogenous TCR reduces the risk of graft-versus-host disease (GvHD). CD19 antigen is a B-cell specific cell surface antigen expressed in all B-cell lineage malignancies.
  • Allogeneic crispr-cas9 engineered anti-cd70 car-t cells ctx130 - A preparation of human allogeneic T-lymphocytes gene-edited with the clustered regularly interspaced short palindromic repeats (CRISPR)-Cas9 nuclease complex to disrupt expression of endogenous TCR and major histocompatibility complex (MHC) class I molecules and modified to express a chimeric antigen receptor (CAR) specific for the tumor-associated antigen (TAA) human cluster of differentiation 70 (CD70), with potential immunostimulating and antineoplastic activities. Upon introduction into the patient, the allogeneic CRISPR-Cas9 engineered anti-CD70 CAR T-cells CTX130 recognize and bind to CD70-overexpressing tumor cells. This may result in a specific cytotoxic T-lymphocyte (CTL)-mediated killing of CD70-positive tumor cells. CD70, the ligand for the costimulatory receptor CD27 and a member of the tumor necrosis factor (TNF) family, is found on the surfaces of various types of cancer cells. Disruption of endogenous TCR prevents graft-versus-host disease (GvHD); the disruption of MHC class I molecules increases the persistence of the CAR T-cells.
  • Allogeneic cs1-specific universal car-expressing t-lymphocytes ucartcs1a - A preparation of allogeneic, off-the-shelf (OTS), universal transcription activator-like effector nuclease (TALEN)-engineered T-lymphocytes that have been genetically modified to express a chimeric antigen receptor (CAR) targeting the tumor-associated antigen (TAA) human CS1 (CD2 subset 1; SLAM family member 7; SLAMF7; CD319; CRACC), with potential immunomodulating and antineoplastic activities. Upon transfusion of allogeneic CS1-specific universal CAR-expressing T-lymphocytes UCARTCS1A, these cells target and bind to cancer cells expressing CS1. This induces selective toxicity in and causes lysis of CS1-expressing tumor cells. SLAMF7 is a member of the signaling lymphocytic activation molecule (SLAM) family of transmembrane receptors that modulate the function of immune cells through immunoreceptor tyrosine-based switch motifs (ITSMs) and intracellular adaptor proteins. SLAMF7 is highly expressed on certain malignant plasma cells and is minimally expressed on healthy immune cells.
  • Allogeneic dendritic cell-myeloma idiotype vaccine - A cell-based vaccine composed of allogeneic dendritic cells pulsed ex-vivo with an autologous myeloma idiotype with potential antineoplastic activity. Upon administration, allogeneic dendritic cell-myeloma idiotype vaccine may stimulate the host immune system to mount a specific cytotoxic T-lymphocyte (CTL) response against myeloma cells, resulting in cell lysis.
  • Allogeneic epstein-barr virus-specific cytotoxic t-lymphocytes - A preparation of allogeneic Epstein-Barr virus (EBV) specific cytotoxic T-lymphocytes (CTL) with potential antineoplastic activity. Upon administration, the allogeneic EBV-specific CTLs are either harvested from a donor with an EBV-positive tumor or are donor CTLs activated against EBV-specific antigens ex vivo. Administration into a patient exerts a CTL response against EBV-positive tumor cells or EBV-infected cells. This results in cell lysis and inhibition of cancer cell proliferation. EBV, a ubiquitous human herpes virus, is associated with various malignancies, including nasopharyngeal carcinoma, Hodgkin disease, non-Hodgkin lymphoma, and other lymphomas.
  • Allogeneic glioblastoma stem-like cell line lysate-pulsed autologous dendritic cell vaccine - A cell-based cancer vaccine composed of autologous dendritic cells (DCs) pulsed with lysates from an allogeneic glioblastoma (GBM) stem-like cell line, with potential immunostimulatory and antineoplastic activities. Upon administration allogeneic glioblastoma stem-like cell line lysate-pulsed autologous dendritic cell vaccine exposes the immune system to GBM stem cell antigens, which may result in cytotoxic T lymphocyte (CTL) and antibody responses against GBM cells. This leads to GBM cell lysis. GBM stem-like cells contain a specific range of antigens that are essential for the neoplastic growth and survival of GBM cells.
  • Allogeneic gm-csf-based myeloma cell vaccine - An allogeneic tumor cell vaccine containing myeloma cancer cells transfected with the granulocyte macrophage-colony-stimulating factor (GM-CSF) gene with potential antineoplastic activity. Upon vaccination, allogeneic GM-CSF-based myeloma cellular vaccine secretes GM-CSF, which may potentiate a tumor-specific cytotoxic T-lymphocyte (CTL) response against myeloma cancer cell-associated antigens.
  • Allogeneic gm-csf-secreting breast cancer vaccine - An allogenic vaccine consisting of irradiated breast cancer cells transfected with the granulocyte macrophage-colony-stimulating factor (GM-CSF) gene. Upon vaccination, the genetically modified cells secrete GM-CSF, thereby potentiating a tumor-specific T cell response against breast cancer cell-asociated antigens.
  • Allogeneic gm-csf-secreting breast cancer vaccine sv-br-1-gm - A vaccine consisting of irradiated allogeneic breast cancer cells, derived from the breast cancer cell line SV-BR-1 that are transfected with the immunostimulant granulocyte-macrophage colony-stimulating factor (GM-CSF; CSF2) gene, with potential immunostimulating and antineoplastic activities. Upon intradermal administration of the allogeneic GM-CSF-secreting breast cancer vaccine SV-BR-1-GM, the genetically-modified cells secrete GM-CSF. This potentiates a tumor-specific cytotoxic T-lymphocyte (CTL) immune response against breast cancer cells.
  • Allogeneic gm-csf-secreting lethally irradiated pancreatic tumor cell vaccine - An allogeneic tumor vaccine composed of lethally irradiated allogeneic pancreatic tumor cells that are genetically modified to secrete the immunostimulatory cytokine granulocyte-macrophage colony-stimulating factor (GM-CSF), with potential immunostimulating and antineoplastic activities. Upon intradermal injection, allogeneic GM-CSF-secreting lethally irradiated pancreatic tumor cell vaccine secretes GM-CSF at the injection site. In turn, GM-CSF may stimulate the body's immune system against tumor cells by attracting and enhancing the activation of antigen-presenting cells (APCs), such as dendritic cells (DCs). This promotes antigen presentation to T-lymphocytes and induces a cytotoxic T-lymphocyte (CTL) response against the pancreatic tumor cells expressing the pancreatic tumor-associated antigens (TAAs).
  • Allogeneic gm-csf-secreting lethally irradiated prostate cancer vaccine - An allogeneic whole cell vaccine expressing human granulocyte macrophage-colony stimulating factor (GM-CSF) with potential antineoplastic activity. Tumor cells from prostate cancer patients are harvested and then genetically modified to secrete GM-CSF, an immune stimulatory growth factor that plays a key role in stimulating the body's immune responses against tumor cells. Because the vaccine is derived from allogenic cells, it has demonstrated a favorable side effect profile than other approaches of delivering long-lasting GM-CSF.
  • Allogeneic gm-csf-secreting lethally irradiated whole melanoma cell vaccine - An allogeneic cancer vaccine composed of lethally irradiated whole melanoma cancer cells that are genetically modified to secrete the immunostimulatory cytokine granulocyte-macrophage colony-stimulating factor (GM-CSF), with potential immunostimulating and antineoplastic activities. Upon intradermal injections, allogeneic GM-CSF-secreting lethally irradiated whole melanoma cell vaccine secretes GM-CSF. In turn, GM-CSF may stimulate the body's immune system against tumor cells by enhancing the activation of dendritic cells (DCs) and promoting antigen presentation to both B- and T-lymphocytes. In addition, GM-CSF promotes antibody-dependent cellular cytotoxicity (ADCC), and increases interleukin-2-mediated lymphokine-activated killer cell function.
  • Allogeneic gm-csf-secreting myeloma vaccine - An allogeneic plasma cell myeloma vaccine consisting two multiple myeloma cell lines, H929 and U266, admixed with GM-CSF-secreting K562 cells, with potential antineoplastic and immunopotentiating activities. Upon administration, the secreted GM-CSF modulates the proliferation and differentiation of a variety of hematopoietic progenitor cells, with some specificity towards stimulation of leukocyte production, and may reverse treatment-induced neutropenia. This agent also promotes antigen presentation, upregulates antibody-dependent cellular cytotoxicity (ADCC), increases interleukin-2-mediated lymphokine-activated killer cell (LAK) function and may augment host antitumoral immunity. For safety, the myeloma cells are irradiated prior to vaccination.
  • Allogeneic gm-csf-secreting tumor vaccine panc 10.05 pcdna-1/gm-neo - An allogeneic cancer vaccine composed of lethally irradiated, whole pancreatic cancer cells transfected with a plasmid carrying the gene for cytokine granulocyte-macrophage colony-stimulating factor (GM-CSF), with potential immunostimulating and antineoplastic activities. Allogeneic GM-CSF-secreting tumor vaccine PANC 10.05 pcDNA-1/GM-Neo secretes GM-CSF thereby activating dendritic cells, promoting antigen presentation to B- and T-cells, and promoting a cytotoxic T-lymphocyte (CTL) response. This may eventually kill tumor cells. The pancreatic tumor cells are derived from the PANC 10.05 tumor cell line.
  • Allogeneic gm-csf-secreting tumor vaccine panc 6.03 pcdna-1/gm-neo - An allogeneic cancer vaccine composed of lethally irradiated, whole pancreatic cancer cells transfected with a plasmid carrying the gene for cytokine granulocyte-macrophage colony-stimulating factor (GM-CSF), with potential immunostimulating and antineoplastic activities. Allogeneic GM-CSF-secreting tumor vaccine PANC 6.03 pcDNA-1/GM-Neo secretes GM-CSF thereby activating dendritic cells, promoting antigen presentation to B- and T-cells, and promoting a cytotoxic T-lymphocyte (CTL) response. This may eventually kill tumor cells. The pancreatic tumor cells are derived from the PANC 6.03 tumor cell line.
  • Allogeneic hadv antigen-specific t-lymphocytes - A population of allogeneic T-lymphocytes specifically reactive to human adenovirus (HAdV) with potential antiviral activity. Allogeneic HAdV antigen-specific T-cells are prepared via ex vivo stimulation of donor-derived peripheral blood mononuclear cells (PBMCs) with HAdV hexon protein. T-cells that secrete interferon (IFN)-gamma in response to HAdV antigen exposure are selected and expanded for administration. Infusion of the HAdV antigen-specific T-lymphocytes into hematopoietic stem cell transplant (HSCT) patients infected with HAdV may potentially reconstitute virus-specific responses, thereby controlling HAdV infections.
  • Allogeneic hla-a2/4-1bb ligand-expressing melanoma vaccine - An allogeneic melanoma cell vaccine derived from a cell line with high expression of melanoma associated antigens and genetically modified to express both HLA-A2 and 4-1BB ligand, with potential immunostimulating and antineoplastic activities. Upon administration, the 4-1BB ligand of the allogeneic HLA-A2/4-1BB ligand-expressing melanoma vaccine binds to 4-1BB on activated T-lymphocytes, which induces a strong immune response against HLA-A2 positive melanoma cells.
  • Allogeneic hpv-specific cytotoxic t lymphocytes - A population of allogeneic cytotoxic T-lymphocytes (CTLs) that are specifically reactive to human papillomavirus (HPV), with potential antiviral and antineoplastic activities. Upon infusion of the allogeneic HPV-specific CTLs, these CTLs induce selective toxicity in HPV-positive cancer cells and other HPV-infected cells. HPV is associated with various cancer cell types.
  • Allogeneic ic9/cd19-car-cd28-zeta-2a-il15-transduced cord blood-derived natural killer cells - A preparation of allogeneic, umbilical cord blood (CB)-derived natural killer cells (NKs) transduced with a retroviral vector expressing interleukin-15 (IL-15) and encoding a chimeric antigen receptor (CAR) specific for the tumor-associated antigen (TAA) CD19 that is coupled to the co-stimulatory domains of CD28 and to the zeta chain of the TCR/CD3 complex (CD3-zeta), and is linked to the suicide gene inducible caspase 9 (iCasp9; iC9), with potential immunomodulating and antineoplastic activities. Upon transfusion, the allogeneic iC9/CD19-CAR-CD28-zeta-2A-IL15-transduced CB-NKs recognize, bind to and induce selective cytotoxicity in CD19-expressing tumor cells. The iCasp9 safety switch consists of a full-length caspase 9, including its caspase recruitment domain, linked to a human FK506 drug-binding domain with an F36V mutation (FKBP12-F36V). If the administered NK cells lead to unacceptable side effects, the chemical homodimerizer AP1903 can be administered; AP1903 binds to the FKBP12-F36V drug-binding domain, activates caspase 9, and results in apoptosis of the administered NK cells. CD19 antigen is a B-cell specific cell surface antigen expressed in all B-cell lineage malignancies. IL-15 enhances the cytotoxic effect of the NK cells.
  • Allogeneic il13-zetakine/hytk-expressing-glucocorticoid resistant cytotoxic t lymphocytes grm13z40-2 - A preparation of glucocorticoid receptor (GR) negative, allogeneic cytotoxic T-lymphocytes (CTLs) expressing a membrane-tethered interleukin 13 (IL13) cytokine chimeric T-cell antigen receptor (zetakine), with potential antineoplastic activity. Upon transfection of donor T-lymphocytes with a plasmid encoding a fusion protein of the IL13-zetakine and the selection-suicide expression enzyme HyTK, these modified CTLs are expanded and introduced into a patient with glioblastoma multiforme (GBM). This agent specifically targets IL13 receptor alpha2, a glioma-restricted cell-surface epitope; the CTLs exert their cytolytic effect thereby killing IL13Ra2-expressing glioma cells. In addition, IL13-zetakine redirected CTLs induce production of certain cytokines. Furthermore, due to the fact that these CTLs are GR negative, they can be used concomitantly with glucocorticoid therapy. The IL13-zetakine consists of an extracellular IL-13 E13Y mutein-human IgG4 hinge-Fc chimera fused to human cytoplasmic CD3-zeta via the transmembrane domain of human CD4.
  • Allogeneic irradiated melanoma cell vaccine csf470 - An allogeneic cancer vaccine composed of a mixture of lethally irradiated whole melanoma cancer cells obtained from four different melanoma cell lines, with potential immunostimulating and antineoplastic activities. Upon intradermal injections, allogeneic irradiated melanoma cell vaccine may stimulate the body's immune system to exert a cytotoxic T-lymphocyte response and antibody-dependent cellular cytotoxicity (ADCC) against the melanoma cancer cells.
  • Allogeneic large multivalent immunogen breast cancer vaccine - A cancer vaccine, containing human-specific large multivalent immunogens (LMIs) isolated from the membrane fraction of cells from a breast cancer cell line, with potential immunostimulatory and antineoplastic activities. Upon administration, allogeneic large multivalent immunogen breast cancer vaccine may stimulate a cytotoxic T lymphocyte (CTL) immune response against tumor cells that express the breast cancer cell-specific LMIs.
  • Allogeneic large multivalent immunogen melanoma vaccine lp2307 - A cancer vaccine, containing human-specific large multivalent immunogen (LMI) isolated from plasma membrane fractions of the melanoma cell lines MSM-M1 and MSM-M2, with potential immunostimulating and antineoplastic activities. Upon administration, allogeneic large multivalent immunogen melanoma vaccine LP2307 may stimulate a CD8+ cytotoxic T lymphocyte (CTL) response against melanoma tumor cells that express melanoma-specific LMI.
  • Allogeneic lmp1/lmp2-specific cytotoxic t-lymphocytes - A preparation of cytotoxic T-lymphocytes (CTL), specifically reactive to the Epstein-Barr virus (EBV) latent membrane proteins (LMP) 1 and 2, with potential antineoplastic activity. Peripheral blood mononuclear cells (PBMC) are collected from a donor and are exposed ex vivo to dendritic cells (DCs) transfected with a replication-deficient adenovirus encoding EBV LMP1/2 to generate LMP1/2-specific CTL which are subsequently expanded. Administration of allogeneic LMP1-/LMP2- specific CTL to patients with LMP1/2-positive tumors may result in a specific CTL response against tumor cells expressing LMP1 and LMP2, resulting in cell lysis and inhibition of tumor cell proliferation. As tumor associated antigens (TAAs), LMP1 and LMP2 are expressed in various malignancies including nasopharyngeal cancer and EBV-positive Hodgkin lymphoma.
  • Allogeneic melanoma vaccine agi-101h - A cancer vaccine derived from two gentically modified human melanoma cell lines with potential antineoplastic activity. Allogeneic melanoma vaccine AGI-101H consists of a 1:1 mixture of cells from two genetically modified human melanoma cell lines, designated as Mich1H6 and Mich2H6, that have been gamma-irradiated to render the cells non-proliferative. Upon administration, this vaccine may stimulate a cytotoxic immune response against melanoma tumor cells.
  • Allogeneic mesothelioma tumor lysate-pulsed autologous dendritic cell vaccine - A cell-based cancer vaccine composed of autologous dendritic cells (DCs) pulsed with a mixture of lysates from five allogeneic mesothelioma tumor cell lines, with potential immunostimulatory and antineoplastic activities. Upon leukapheresis, DCs are loaded with allogeneic mesothelioma tumor cell lysates. Upon re-administration of the allogeneic mesothelioma tumor lysate-pulsed autologous DC vaccine, the immune system is exposed to an undefined amount of mesothelioma-associated antigens, which stimulates the induction of a specific cytotoxic T-lymphocyte (CTL) response against mesothelioma tumor cells and leads to tumor cell lysis.
  • Allogeneic natural killer cell line mg4101 - A population of allogeneic, cytotoxic natural killer (NK) cells with potential antitumor activity. Allogeneic natural killer cell line MG4101 is derived from cells of a normal, healthy donor upon leukapheresis and activation.
  • Allogeneic natural killer cell line nk-92 - A proprietary, human cytotoxic cell line composed of allogeneic, activated, interleukin-2 (IL-2) dependent-natural killer cells derived from a 50-year old male patient with rapidly progressive non-Hodgkin's lymphoma, with potential antineoplastic activity. As NK-92 cells are devoid of killer inhibitory receptors (KIRs; also called killer cell immunoglobulin-like receptors), which are negative regulators of NK cell activity, cancer cells are unable to suppress the cancer cell killing ability of the NK-92 cells. Upon infusion of the allogeneic NK cell line NK-92, the NKs recognize and bind to tumor cells. This leads to the secretion and release of perforins, granzymes, cytokines and chemokines, which results in cancer cell lysis and apoptosis. In addition, NK-92 cells express high affinity Fc receptors, which bind to therapeutic antibodies; therefore, this agent can enhance antibody dependent cellular cytotoxicity (ADCC) of co-administered therapeutic antibodies.
  • Allogeneic nicotinamide-expanded natural killer cells - Allogeneic, nicotinamide (NAM)-expanded natural killer (NK) cells, with potential cytolytic and antineoplastic activities. Upon administration, the allogeneic NAM-expanded NK cells may lyse cancer cells. These cells also secrete pro-inflammatory cytokines, which further stimulate an anti-tumor immune response. Ex-vivo treatment with the vitamin B3 derivative NAM increases the in-vivo homing, retention and proliferation potential of the NK cells.
  • Allogeneic nkg2dl-targeting car-grafted gamma delta t cells - A preparation of a subset of allogeneic T-lymphocytes that express only gamma chain and delta chain T-cell receptors (TCRs) and that are engineered to express a chimeric antigen receptor (CAR) encoding for human natural-killer group 2, member D receptor protein (NKG2D or KLRK1; natural killer cell activating receptor group 2D), with potential immunomodulating and antineoplastic activities. Upon administration of the NKG2DL-targeting CAR-grafted gamma delta T cells, these cells specifically target and bind to tumor cells expressing NKG2D ligands (NKG2DL). This induces secretion of pro-inflammatory cytokines and results in the lysis of NKG2DL-expressing tumor cells. In addition, these cells target, bind to and kill NKG2DL-expressing tumor-associated endothelial cells in the neovasculature and immunosuppressive cells, such as regulatory T-cells (Tregs) and myeloid-derived suppressor cells (MDSCs) in the tumor microenvironment (TME) that express NKG2D ligands. Gamma/delta T-lymphocytes play a key role in the activation of the immune system and do not require major histocompatibility complex (MHC)-mediated antigen presentation to exert their cytotoxic effect. Ligands for NKG2D, such as MHC class I chain-related protein A (MICA), MICB, and members of the UL16-binding proteins (ULBP)/retinoic acid early transcript 1 (RAET1) family, are overexpressed on infected cells and most cancer cell types, but are not expressed on most normal, healthy cells.
  • Allogeneic pd-l1 tumor-targeted high-affinity natural killer cells - A preparation of natural killer (NK) cells that are derived from NK-92 cells, a human cytotoxic cell line composed of allogeneic NK cells derived from a 50-year old male patient with rapidly progressive non-Hodgkin's lymphoma (NHL), that are genetically engineered to express the high-affinity CD16/FcgammaRIIIa (158V) allele, endoplasmic reticulum (ER)-retained interleukin (IL)-2 and a chimeric antigen receptor (CAR) specific for programmed death-ligand 1 (PD-L1), with potential immunomodulating, cytolytic and antineoplastic activities. Upon infusion of the PD-L1 tumor-targeted high-affinity (ha) NK cells, the NK cells recognize and bind to tumor cells, preferentially to PD-L1-expressing tumor cells and human peripheral myeloid-derived suppressor cells (MDSCs). This leads to the secretion and release of perforins, granzymes, cytokines and chemokines, and results in cancer cell lysis and apoptosis. In addition, the incorporation of the high-affinity CD16 allele allows the NK cells to lyse tumor cells via antibody-dependent cell-mediated cytotoxicity (ADCC) mediated by tumor-antigen-specific immunoglobulin G1 (IgG1) antibodies through binding of CD16 with the Fc region of human IgG1 antibodies. IL-2 replenishes the granular stock of NK cells, leading to enhanced perforin- and granzyme-mediated lysis of tumor cells.
  • Allogeneic plasmacytoid dendritic cells expressing lung tumor antigens pdc*lung01 - An off-the-shelf (OTS) preparation composed of irradiated allogeneic plasmacytoid dendritic cells (pDCs) loaded with seven immunogenic, human leukocyte antigen (HLA)-A*02:01 serotype-restricted peptides derived from the lung tumor antigens cancer/testis antigen 1 (NY-ESO-1), melanoma antigen A3 (MAGE-A3), MAGE-A4, multi-MAGE, a peptide shared by multiple MAGE-A proteins, survivin, mucin1 (MUC1) and melanoma antigen recognized by T-cells 1 (Mart-1; Melan-A), with potential immunostimulating and antineoplastic activities. Upon administration of the allogeneic pDCs expressing lung tumor antigens PDC*lung01, the pDCs may activate the immune system to mount a specific cytotoxic T-lymphocyte (CTL) response against HLA-A*0201 positive lung cancer cells expressing the TAAs NY-ESO-1, MAGE-A3, MAGEA4, multi-MAGE, survivin, MUC1 and melan-A. The pDCs are derived from a distinct subset of dendritic cells (DCs) with a plasma cell-like morphology and express a characteristic set of surface markers and may increase the anti-tumor immune responses.
  • Allogeneic renal cell carcinoma vaccine mgn1601 - A whole cell vaccine comprised of irradiated allogeneic renal cell carcinoma (RCC) with potential immunostimulating and antineoplastic activities. Allogeneic renal cell carcinoma vaccine MGN1601 contains two active ingredients: 1) genetically modified allogeneic RCC cells that are transiently transfected with four different MIDGE (Minimalistic Immunogenically Defined Gene Expression) vectors encoding IL-7, GM-CSF, CD80 and CD154 and 2) the synthetic DNA-based immunomodulator dSLIM-30L1, a TLR9 agonist.. Vaccination results in expression of IL-7, GM-CSF, CD80 and CD154, which all contribute to the activation or enhancement of immune responses. Furthermore, administration of this RCC vaccine may elicit a cytotoxic T lymphocyte (CTL) response against similar host tumor cells, resulting in decreased tumor growth. TLR9 is a member of the TLR family, which plays a fundamental role in pathogen recognition and activation of innate immunity.
  • Allogeneic tcr alpha/beta-positive t-lymphocyte-depleted peripheral blood stem cells - A preparation of allogeneic T-cell receptor (TCR) alpha/beta-positive T cell-depleted peripheral blood stem cells (PBSCs), that can potentially be used for hematopoietic stem cell transplantation (HSCT). Allogeneic PBMCs are processed, using the proprietary CliniMACS device, to remove TCRalpha/beta T-cells, while retaining other cells, such as donor-derived natural killer (NK) cells and gamma/delta T-cells. As TCR alpha/beta-positive T-cells appear to be related to the development of graft versus host disease (GvHD), depletion of these cells may lower the risk of the recipient developing GvHD. Upon infusion of the TCR alpha/beta-positive T-cell-depleted PBSCs for allogeneic stem cell transplantation (allo SCT), the alpha/beta-positive T-cell depletion as well as the presence of allogeneic NK cells, and other cells, may facilitate engraftment, exert graft-versus-leukemia effects, enhance post-transplant immune recovery, and reduce the risk of infections and GvHD.
  • Allogeneic third-party suicide gene-transduced anti-hla-dpb1*0401 cd4+ t-cells ctl 19 - A preparation of allogeneic, third-party, CD4+ T-lymphocytes that specifically recognizes the human leukocyte antigen (HLA)-DPB1*0401 and transduced with a suicide gene, with potential antineoplastic activity. Upon administration, allogeneic third-party suicide gene-transduced anti-HLA-DPB1*0401 CD4+ T-cells CTL 19 specifically target and kill HLA-DPB1*0401-positive leukemic cells. The suicide gene causes the destruction of the T-cell clone upon the administration and presence of ganciclovir, which enhances the safety of the agent. HLA-DP is expressed by many leukemic cells.
  • Allogeneic t-lymphocytes expressing ny-eso-1-c259-specific tcr - Genetically engineered human allogeneic T-lymphocytes that are transduced with a retroviral vector encoding a T-cell receptor (TCR) specific for the cancer/testis antigen NY-ESO-1, with potential antineoplastic activity. Upon isolation, transduction, expansion ex vivo and introduction into the patient, the allogeneic T-lymphocytes expressing NY-ESO-1-C259-specific TCR specifically target and bind to NY-ESO-1-overexpressing tumor cells. This may result in the specific cytotoxic T-lymphocyte (CTL) killing of NY-ESO-1-positive cancer cells. NY-ESO-1, a tumor-associated antigen (TAA), is expressed in normal testis and on the surface of various tumor cell types.
  • Allogeneic tri-functional anti-cd19 car-nk cells - A preparation of allogeneic natural killer (NK) cells transduced with a retroviral vector expressing the immunostimulatory cytokine interleukin-15 (IL-15) and encoding a chimeric antigen receptor (CAR) specific for the tumor-associated antigen (TAA) cluster of differentiation 19 (CD19) that is coupled to the co-stimulatory domains cluster of differentiation 28 (CD28, T-cell-specific surface glycoprotein CD28), cluster of differentiation 137 (CD137; 4-1BB), and the zeta chain of the T-cell receptor (TCR)/CD3 complex (TCRzeta; CD247; CD3zeta); and a blocker for the inhibitory T-cell receptor programmed cell death protein 1 (PD-1; PDCD1; CD279), with potential immunomodulating and antineoplastic activities. Upon transfusion, the allogeneic tri-functional anti-CD19 CAR-NK cells recognize, bind to and induce selective cytotoxicity in CD19-expressing tumor cells. IL-15 enhances the cytotoxic effect of the NK cells and the activated anti-tumor T-cells. The PD-1 inhibitory domain targets and binds to programmed cell death-1 ligand 1 (PD-L1) expressed on tumor cells, thereby preventing the binding of the PD-1 on T-lymphocytes to its ligand, PD-L1 on tumor cells. This prevents PD-1/PD-L1-mediated inhibition of T-lymphocytes and leads to the activation and expansion of T-cells resulting in a cytotoxic T-lymphocyte (CTL) response against tumor cells, thereby enhancing the elimination of tumor cells. CD19 antigen is a B-cell specific cell surface antigen expressed in all B-cell lineage malignancies. The co-stimulatory signaling domains enhance both proliferation of T-cells and anti-tumor activity.
  • Allogeneic tumor cell vaccine - A vaccine composed of tumor cells isolated from the tumor of one patient, killed and processed, and administered to another patient to stimulate cytotoxic immune responses to a similar tumor cell type. The cells found in this type of whole-cell vaccine express many cell-surface tumor-associated antigens. This vaccine is frequently administered with an adjuvant immunostimulant.
  • Allosteric erbb inhibitor bdtx-189 - An orally bioavailable, irreversible, selective, small-molecule inhibitor of certain oncogenic driver, allosteric mutations of the ErbB receptor tyrosine kinases epidermal growth factor receptor (EGFR/ErbB1) and human epidermal growth factor receptor 2 (HER2/neu or ErbB2), including extracellular domain allosteric mutations of HER2, and EGFR and HER2 exon 20 insertion mutations, with potential antineoplastic activity. Upon oral administration, the allosteric ErbB inhibitor BDTX-189 selectively binds to and inhibits these allosteric ErbB mutants while sparing wild-type EGFR, which may result in the selective inhibition of cellular proliferation and angiogenesis in tumor cells and tumors expressing these allosteric ErbB mutations. EGFR and HER2, ErbB receptor tyrosine kinases mutated or overexpressed in many tumor cell types, play a key role in tumor cell proliferation and tumor vascularization.
  • Almurtide - A synthetic muramyl dipeptide (MDP) analogue with potential immunostimulating and antineoplastic activity. As a derivative of the mycobacterial cell wall component MDP, almurtide activates both monocytes and macrophages. This results in the secretion of cytokines and induces the recruitment and activation of other immune cells, which may result in indirect tumoricidal or cytostatic effects.
  • Alobresib - An orally bioavailable inhibitor of the Bromodomain and Extra-Terminal (BET) family of proteins, with potential antineoplastic activity. Upon oral administration, alobresib binds to the acetylated lysine recognition motifs in the bromodomains of BET proteins, thereby preventing the interaction between the BET proteins and acetylated histones. This disrupts chromatin remodeling and gene expression. Prevention of the expression of certain growth-promoting genes may lead to an inhibition of proliferation in BET-overexpressing tumor cells. BET proteins, comprised of BRD2, BRD3, BRD4 and BRDT, are transcriptional regulators that play an important role during development and cellular growth.
  • Alofanib - An inhibitor of the fibroblast growth factor receptor (FGFR) type 2 (FGFR2), with potential antineoplastic and anti-angiogenic activities. Upon administration, alofanib targets, allosterically binds to the extracellular domain of FGFR2 and inhibits the activity of FGFR2, which may result in the inhibition of basic FGF (bFGF)/FGFR2-related signal transduction pathways. This inhibits FGF-induced endothelial cell proliferation and migration, and inhibits the proliferation of FGFR2-overexpressing tumor cells. FGFR2, a receptor tyrosine kinase upregulated in many tumor cell types, plays a key role in cellular proliferation, migration and survival.
  • Alpelisib - An orally bioavailable phosphatidylinositol 3-kinase (PI3K) inhibitor with potential antineoplastic activity. Alpelisib specifically inhibits PI3K in the PI3K/AKT kinase (or protein kinase B) signaling pathway, thereby inhibiting the activation of the PI3K signaling pathway. This may result in inhibition of tumor cell growth and survival in susceptible tumor cell populations. Activation of the PI3K signaling pathway is frequently associated with tumorigenesis. Dysregulated PI3K signaling may contribute to tumor resistance to a variety of antineoplastic agents.
  • Alpha fetoprotein adenoviral vector vaccine - A vaccine consisting of a recombinant adenoviral vector encoding alpha fetoprotein. After vaccination, expressed alpha fetoprotein may stimulate a cytotoxic T lymphocyte (CTL) response against tumor cells that express alpha fetoprotein, resulting in tumor cell lysis. (NCI05)
  • Alpha fetoprotein plasmid dna vaccine - A vaccine consisting of plasmid DNA encoding alpha fetoprotein. After vaccination, expressed alpha fetoprotein may stimulate a cytotoxic T lymphocyte (CTL) response against tumor cells that express alpha fetoprotein, resulting in tumor cell lysis. (NCI05)
  • Alpha galactosylceramide - A potent alpha galactosylceramide modified from marine-sponge that stimulates the immune system to exhibit antitumor activity.
  • Alpha v beta 1 inhibitor atn-161 - A small peptide antagonist of integrin alpha5beta1 with potential antineoplastic activity. ATN-161 selectively binds to and blocks the receptor for integrin alpha5beta1, thereby preventing integrin alpha5beta1 binding. This receptor blockade may result in inhibition of endothelial cell-cell interactions, endothelial cell-matrix interactions, angiogenesis, and tumor progression. Integrin alpha5beta1 is expressed on endothelial cells and plays a crucial role in endothelial cell adhesion and migration.
  • Alpha v beta 8 antagonist pf-06940434 - An antagonist of integrin alpha v beta 8, with potential antineoplastic activity. Upon administration, PF-06940434 selectively binds to and blocks the receptor for integrin alpha v beta 8, thereby preventing integrin alpha v beta 8 binding. This may result in the inhibition of cell adhesion in the tumor microenvironment (TME) and blocks the activation of the cytokine transforming growth factor-beta 1 (TGF-b1), preventing TGF-b1-mediated signal transduction. This abrogates TGF-b1-mediated immunosuppression, enhances anti-tumor immunity in the TME and promotes a cytotoxic T-lymphocyte (CTL)-mediated immune response against tumor cells leading to tumor cell death. This may lead to a reduction in TGF-b1-dependent proliferation of cancer cells. Alpha v beta 8 integrin plays a key role in tumor initiation, growth, and progression through TGF-b1 activation. It is expressed in a variety of tumor cell types and is associated with poor prognosis.
  • Alpha-1,3-galactosyltransferase-expressing allogeneic renal cell carcinoma vaccine - An allogeneic renal cell cancer (RCC) vaccine composed of cell line-derived RCCs that are genetically engineered to express the murine alpha-1,3-galactosyltransferase (GalT), with potential immunostimulatory and antineoplastic activities. Not naturally occurring in humans, GalT catalyzes the expression of foreign alpha-1,3-galactosyl (alpha-gal) carbohydrate epitopes on the cell membranes of the allogeneic RCCs present in the vaccine. This induces a hyperacute rejection reaction involving pre-existing human anti-alpha-gal antibodies, which bind to the foreign alpha-gal epitopes expressed by the allogeneic RCCs. This results in complement-mediated cytotoxicity (CMC) and antibody-dependent cell-mediated cytotoxicity (ADCC) towards endogenous RCCs with unmodified carbohydrate epitopes.
  • Alpha-1-proteinase inhibitor human - Human serum-derived alpha-1 proteinase inhibitor (alpha-1-antitrypsin or AAT) with immunomodulating and anti-inflammatory activity. Upon administration, AAT reduces the production of proinflammatory cytokines, such as tumor necrosis factor-alpha, interleukin (IL)-1 beta, IL-32, IL-6, and proteinase 3, and induces the production of anti-inflammatory cytokines, such as IL-10 and the IL-1 receptor antagonist IL-1RN. This agent also downregulates heparan sulfate and reduces the expansion of cytotoxic effector T cells, interferes with the maturation of dendritic cells and increases T regulatory cells. Altogether, AAT may attenuate acute graft-versus-host disease (GvHD) and may facilitate graft acceptance and survival. In addition, AAT enhances levels of cAMP and activation of cAMP-dependent protein kinase A. AAT, a 52kD protein and serine protease inhibitor, belongs to the serpin superfamily.
  • Alpha-fetoprotein peptide-pulsed autologous dendritic cell vaccine - A cell-based cancer vaccine comprised of autologous dendritic cells pulsed with four alpha-fetoprotein (AFP) peptides, with potential immunostimulatory and antineoplastic activities. Upon administration, AFP peptide-pulsed autologous dendritic cell vaccine may stimulate anti-tumoral cytotoxic T lymphocyte (CTL) and antibody responses against AFP-expressing cancer cells, resulting in tumor cell lysis. AFP is overexpressed in a variety of cancer cells.
  • Alpha-gal agi-134 - A synthetic alpha Gal (aGal) molecule, with potential immunomodulating and antineoplastic activities. Upon intratumoral injection of aGal AGI-134, aGal coats the cancer cell membranes and triggers an anti-aGal antibody-mediated immune response leading to an initial complement-dependent and antibody-dependent cellular cytotoxicity (ADCC). This cytotoxicity causes release from tumor cells and subsequent uptake of released tumor-associated antigens (TAAs) by antigen-presenting cells (APCs). This may activate a systemic immune response against the TAAs and may eradicate cancer cells. aGal is a cell-surface carbohydrate antigen not expressed by humans while being expressed by all other mammals and bacteria. Anti-aGal antibodies are continuously and abundantly produced by humans due to exposure to aGal present on intestinal bacteria in the digestive system.
  • Alpha-gal glycosphingolipids - A preparation of glycosphingolipids (GSL), containing the disaccharide epitope galactose-alpha-1,3-galactose (alpha-Gal), with potential antineoplastic activity. Upon intratumoral injection, alpha-Gal glycosphingolipids may stimulate the immune system to mount complement-mediated cytotoxicity (CMC) and antibody-dependent cell-mediated cytotoxicity (ADCC) responses against alpha-Gal GSL, which may result in tumor cell death; these responses involve natural anti-alpha-Gal immunoglobulins (Igs). As antibodies that occur naturally due to sensitization to alpha-Gal present on symbiotic bacterial flora, anti-alpha-Gal Igs are present in unusually high amounts in human sera. GSL represent a glycolipid subtype containing the amino alcohol sphingosine; tumor-associated GSL antigens contain various oligosaccharide residues.
  • Alpha-galactosylceramide-pulsed autologous dendritic cells - A cancer vaccine comprised of autologous dendritic cells (DCs) pulsed with the marine sponge glycolipid alpha-galactosylceramide (alpha-GalCer) with potential immunostimulatory and antimetastatic activities. Upon administration, alpha-galactosylceramide-pulsed autologous dendritic cells may result in the activation and proliferation of a subset of endogenous natural killer T (NKT) cells, B cells, and CD4+ and CD8+ T cells, and the production of interferon-gamma and interleukin-12; these cascade events may result in a T helper-1 cell-biased proinflammatory antitumor immune response. The NKT cell ligand alpha-GalCer was originally isolated from the marine sponge Agelas mauritianusis.
  • Alpha-lactalbumin-derived synthetic peptide-lipid complex alpha1h - A synthetic proteolipid complex comprised of the alpha-1 domain of alpha-lactalbumin (lactose synthase B protein) and oleic acid, with potential antineoplastic activity. Upon intravesical instillation, alpha1H selectively accumulates in the nuclei of tumor cells and binds to histones H3, H4, and H2B. By binding to histones, alpha1H disrupts chromatin assembly and interferes with intact chromatin, thereby preventing tumor cell transcription and replication. Additionally, alpha1H inhibits the phosphorylation of multiple kinases involved in cancer-associated pathways including the Ras/Raf/ERK, PI3K/AKT, p38 MAPK and JNK signaling pathways. This may inhibit tumor cell proliferation and induce apoptosis in tumor cells that are driven by the dysregulation of certain kinases and oncogenic GTPases.
  • Alpha-lipoic acid-palladium/vitamin/mineral supplement - A proprietary water- and lipid-soluble polymer-based nutritional supplement composed of a complex mixture of alpha-lipoic acid bound to palladium (Palladium Lipoic Acid Complex (PdLA)) and other minerals, vitamins and amino acids, including vitamins B1, B2 and B12, formylmethionine, acetyl cysteine, and trace amounts of molybdinum, rhodium, and ruthenium, with potential anti-oxidant and cytoprotective activities. Upon oral administration, the alpha-lipoic acid-palladium/vitamin/mineral supplement acts as a free radical scavenger, crosses the cell membrane and is able to transfer electrons from fatty acids to DNA via the electron transport chain in mitochondria, which protects against DNA damage. This could protect non-cancerous cells from the oxidative damage caused by radiation and chemotherapy. In addition, in the hypoxic conditions found within tumors, the excess electrons can generate free radicals within mitochondria and could induce both cytochrome c release and apoptosis.
  • Alpha-tocopheryloxyacetic acid - An orally bioavailable vitamin E derivative with potential antineoplastic and immunostimulating activities. Upon administration, alpha-tocopheryloxyacetic acid (alpha-TEA) induces tumor autophagy; the autophagosomes formed, which carry tumor associated antigens (TAAs), allow for increased cross-presentation of TAAs by professional antigen-presenting cells (APCs). This activates a T cell-mediated T helper type 1 (TH1) response, generates a cytotoxic T-lymphocyte (CTL) response against cancer cells, and reduces the frequency of regulatory T-cell (Treg) differentiation. In addition, alpha-TEA modulates the release of various cytokines and chemokines and induces tumor cell apoptosis. Altogether, this results in decreased tumor cell proliferation.
  • Alpha-type-1 polarized dendritic cells - A mature polarized dendritic cell with potent immunostimulating activity. Treating dendritic cells (DCs) with interferon-alpha (IFN-a) and polyinosinic:polycytidylic acid (p-I:C) in addition to a cytokine cocktail (tumor necrosis factor alpha/Interleukin-1beta/IFN-gamma) produces mature but not exhausted alpha type-1 polarized DCs (alphaDC1) that are capable of: 1) high responsiveness to other lymphoid chemokines, and 2) producing high level of interleukin-12p70 (IL-12p70). Therefore, alphaDC1 has a much more significant capability of inducing helper T cell (CD4+ T-cell) responses in comparison with the "gold standard" DCs. When pulsed with specific tumor associated antigens (TAAs), alphaDC1 is able to induce a potent cytotoxic T lymphocyte (CTL) response against TAAs; as a result it can be used as a cancer vaccine.
  • Alsevalimab - A fully human, glycoengineered monoclonal antibody targeting B7-H4 (V-set domain-containing T-cell activation inhibitor 1; VTCN1; B7x; B7S1) with potential antineoplastic and immune checkpoint inhibitory activities. Upon intravenous administration, alsevalimab binds to B7-H4 on the surface of tumor cells, thereby preventing B7-H4 binding to T-cells and abrogating the B7-H4-mediated negative regulation of T-cell activation. This increases a cytotoxic T-lymphocyte (CTL)-mediated immune response against B7-H4-expressing tumor cells. In addition, the afucosylated Fc region of the anti-B7-H4 monoclonal antibody FPA150 enhances its binding affinity for human FcgammaRIIIa receptors (CD16) on natural killer (NK) cells, resulting in enhanced antibody-dependent cellular cytotoxicity (ADCC) against B7-H4-expressing tumor cells. B7-H4, a member of the B7 family of immune modulators, is upregulated in a variety of tumor cell types and negatively regulates T-cell immune responses.
  • Altiratinib - An orally bioavailable inhibitor of c-Met/hepatocyte growth factor receptor (HGFR), vascular endothelial growth factor receptor type 2 (VEGFR2), Tie2 receptor tyrosine kinase (TIE2), and tropomyosin receptor kinase (Trk), with potential antiangiogenic and antineoplastic activities. Upon administration, altiratinib selectively binds to c-Met, VEGFR2, Tie2 and Trk tyrosine kinases, which may lead to the inhibition of endothelial cell migration, proliferation and survival. This also results in both an inhibition of tumor cell proliferation and increased tumor cell death in c-Met/VEGFR2/Tie2/Trk-expressing cells. These receptor tyrosine kinases (RTKs), frequently overexpressed or mutated by a variety of tumor cell types, play crucial roles in the regulation of angiogenesis, tumor cell growth and survival.
  • Altretamine - A synthetic cytotoxic s-triazine derivative similar in structure to alkylating agent triethylenemelamin with antineoplastic activity. Although the precise mechanism by which altretamine exerts its cytotoxic effect is unknown, N-demethylation of altretamine may produce reactive intermediates which covalently bind to DNA, resulting in DNA damage.
  • Alvac(2) melanoma multi-antigen vaccine - A therapeutic cancer vaccine, based on a replication-defective recombinant canarypox virus (ALVAC) encoding multiple melanoma antigens, with potential immunostimulatory and antineoplastic activities. Vaccination with ALVAC(2) melanoma multi-antigen therapeutic vaccine may stimulate the host immune system to mount an immune response against antigen-expressing melanoma cells, resulting in inhibition of tumor growth and/or metastasis.
  • Alvac(2)-ny-eso-1 (m)/tricom vaccine - A cancer vaccine consisting of a replication-defective recombinant canarypox virus [ALVAC(2)] encoding the cancer-testis antigen NY-ESO and the TRIad of COstimulatory Molecules (B7-1, ICAM-1 and LFA-3; also called TRICOM), with potential immunostimulatory and antineoplastic activities. Upon administration, ALVAC(2)/NY-ESO (M)/TRICOM vaccine may stimulate the host immune system to mount a cytotoxic T lymphocyte (CTL) response against NY-ESO-expressing cancer cells, which may result in the inhibition of tumor cell proliferation. NY-ESO-1, a tumor associated antigen (TAA), is found in normal testis and on the surface of various tumor cells, including bladder, breast, hepatocellular, melanoma, and prostate tumor cells. TRICOM may enhance antigen presentation and activate cytotoxic T-cells. In addition, ALVAC(2) encodes the vaccinia virus (vv) E3L ad K3L genes, which may potentiate the translation of the NY-ESO and TRICOM genes.
  • Alvac-cea b7.1 vaccine - A cancer vaccine that uses a viral vector system derived from the canarypox virus engineered to target the carcinoembryonic antigen (CEA). It causes infected cells to temporarily display CEA and activates the immune system to attack the tumor cells.
  • Alvac-cea vaccine - A cancer vaccine consisting of ALVAC, a highly attenuated poxvirus strain derived from the canarypox virus, encoding for the tumor associated antigen (TAA) carcinoembryonic antigen (CEA), with potential antineoplastic activity. Upon administration, ALVAC-CEA vaccine expresses CEA and may stimulate a host immune response against tumor cells expressing CEA. This may result in the inhibition of tumor growth and/or metastasis. CEA is overexpressed in a variety of tumor cell types.
  • Alvac-eso-1 vaccine - A cancer vaccine consisting of a replication-defective recombinant canarypox virus (ALVAC) encoding the cancer-testis antigen NY-ESO-1, with potential immunostimulatory and antineoplastic activities. Upon administration, ALVAC-ESO-1 vaccine may stimulate the host immune system to mount a cytotoxic T lymphocyte (CTL) response against NY-ESO-1-expressing cancer cells, which may result in the inhibition of tumor cell proliferation. NY-ESO-1, a tumor associated antigen (TAA), is found in normal testis and on the surface of various tumor cells.
  • Alvac-hb7.1 - A vaccine comprise of a canarypox viral vector that carries the gene for human B7.1 (CD80 antigen) with potential use as an autologous therapeutic cancer vaccine. Tumor cells harvested from a patient are infected with ALVAC-hB7 1, thereby producing an autologous cell line that exhibits increased expression of HLA class I and class II, CD54 (ICAM), and CD80. Increased expression of these proteins by this autologous cell line may activate an antitumor T-cell response when the modified cells are administered to the patient.
  • Alvac-mart-1 vaccine - A cancer vaccine containing a replication-defective recombinant canarypox virus (ALVAC), encoding an epitope of MART-1 (melanoma antigen recognized by T-cells), with potential immunostimulatory and antineoplastic activities. Upon administration, the MART-1 epitope is expressed by the ALVAC vector in ALVAC-MART-1 vaccine; a host cytotoxic T lymphocyte (CTL) response against MART-1-expressing tumor cells may follow, resulting in tumor cell lysis and decreased tumor cell proliferation.
  • Alvespimycin - An analogue of the antineoplastic benzoquinone antibiotic geldanamycin. Alvespimycin binds to HSP90, a chaperone protein that aids in the assembly, maturation and folding of proteins. Subsequently, the function of Hsp90 is inhibited, leading to the degradation and depletion of its client proteins such as kinases and transcription factors involved with cell cycle regulation and signal transduction.
  • Alvespimycin hydrochloride - The hydrochloride salt of alvespimycin, an analogue of the antineoplastic benzoquinone antibiotic geldanamycin. Alvespimycin binds to HSP90, a chaperone protein that aids in the assembly, maturation and folding of proteins. Subsequently, the function of Hsp90 is inhibited, leading to the degradation and depletion of its client proteins such as kinases and transcription factors involved with cell cycle regulation and signal transduction.
  • Alvocidib - The free base form of a synthetic N-methylpiperidinyl chlorophenyl flavone compound. As an inhibitor of cyclin-dependent kinase, alvocidib induces cell cycle arrest by preventing phosphorylation of cyclin-dependent kinases (CDKs) and by down-regulating cyclin D1 and D3 expression, resulting in G1 cell cycle arrest and apoptosis. This agent is also a competitive inhibitor of adenosine triphosphate activity.
  • Alvocidib hydrochloride - A synthetic N-methylpiperidinyl chlorophenyl flavone compound. As an inhibitor of cyclin-dependent kinase, alvocidib induces cell cycle arrest by preventing phosphorylation of cyclin-dependent kinases (CDKs) and by down-regulating cyclin D1 and D3 expression, resulting in G1 cell cycle arrest and apoptosis. This agent is also a competitive inhibitor of adenosine triphosphate activity.
  • Alvocidib prodrug tp-1287 - An orally bioavailable, highly soluble phosphate prodrug of alvocidib, a potent inhibitor of cyclin-dependent kinase-9 (CDK9), with potential antineoplastic activity. Upon administration of the phosphate prodrug TP-1287, the prodrug is enzymatically cleaved at the tumor site and the active moiety alvocidib is released. Alvocidib targets and binds to CDK9, thereby reducing the expression of CDK9 target genes such as the anti-apoptotic protein MCL-1, and inducing G1 cell cycle arrest and apoptosis in CDK9-overexpressing cancer cells.
  • Amatuximab - A chimeric IgG1 monoclonal antibody against human mesothelin with potential anti-tumor activity. Amatuximab specifically targets mesothelin, a cell surface glycoprotein involved in cell adhesion and overexpressed on many epithelial-derived cancer cells. Upon binding to the mesothelin antigen, amatuximab triggers an antibody dependent cellular cytotoxicity (ADCC)-mediated host immune response against mesothelin-expressing cells, resulting in cell lysis.
  • Ambamustine - A tripeptidic nitrogen mustard compound and bifunctional alkylating agent with antineoplastic activity.
  • Ambazone - An antiseptic agent with potential antibacterial and antileukemic activity. Although the exact mechanism of action remains to be fully elucidated, ambazone appears to interfere with the membrane-bound nucleotide system by increasing the intracellular concentration of cAMP in leukemia cells and macrophages, which potentially contributes to this agent's antineoplastic activity. Furthermore, this agent's affinity for various cellular targets, i.e. membranes, nucleic acids and proteins, may contribute to the overall antibacterial effect.
  • Amblyomin-x - A recombinant form of a toxic protein derived from the salivary glands of the Amblyomma cajennense tick that inhibits Factor Xa and induces apoptosis, with potential antithrombotic and antineoplastic activities. Upon administration, amblyomin-X promotes endoplasmic reticulum (ER) stress, mitochondrial dysfunction, cytochrome-c release, poly(ADP-ribose) polymerase (PARP) cleavage, and activation of caspase. Additionally, this agent selectively induces apoptosis in tumor cells. It also affects endothelial cell functions, such as adhesion, and may inhibit angiogenesis. Amblyomin-X targets and binds to factor Xa, inhibits its activity and interrupts the blood coagulation cascade, thereby preventing thrombin formation and thrombus development. As cancer is associated with thrombosis, amblyomin-X could potentially exert its antineoplastic and antithrombotic effects in the cancer patient at the same time.
  • Amcasertib - An orally available cancer cell stemness kinase inhibitor with potential antineoplastic activity. Even though the exact target has not been fully elucidated, amcasertib targets and inhibits one or more pathways involved in cancer stem cell survival. As a result, cancer stem cell (CSC) growth as well as heterogeneous cancer cell growth is inhibited. CSCs, self-replicating cells able to differentiate into heterogeneous cancer cells, appear to be responsible for both tumor relapse and metastasis.
  • Ametantrone - A topoisomerase II inhibitor of the anthrapyrazole family that causes covalent cross-links in DNA of tumor cells.
  • Amifostine - The trihydrate form of a phosphorylated aminosulfhydryl compound. After dephosphorylation of amifostine by alkaline phosphatase to an active free sulfhydryl (thiol) metabolite, the thiol metabolite binds to and detoxifies cytotoxic platinum-containing metabolites of cisplatin and scavenges free radicals induced by cisplatin and ionizing radiation. The elevated activity of this agent in normal tissues results from both the relative abundance of alkaline phosphatase in normal tissues and the greater vascularity of normal tissues compared to tumor tissues.
  • Aminocamptothecin - A water-insoluble camptothecin derivative. Aminocamptothecin binds to the nuclear enzyme topoisomerase I, thereby inhibiting repair of single-strand DNA breakages. Because the terminal lactone ring of aminocamptothecin required for the agent's antitumor activity spontaneously opens under physiological conditions to an inactive carboxy form, the drug must be administered over an extended period of time to achieve effective cytotoxicity.
  • Aminocamptothecin colloidal dispersion - A colloidal dispersion formulation of 9-Aminocamptothecin, a water-insoluble camptothecin derivative. Aminocamptothecin binds to the nuclear enzyme topoisomerase I, thereby inhibiting repair of single-strand DNA breakages. Because the terminal lactone ring of aminocamptothecin required for the agent's antitumor activity spontaneously opens under physiological conditions to an inactive carboxy form, the drug must be administered over an extended period of time to achieve effective cytotoxicity.
  • Aminoflavone prodrug afp464 - A synthetic lysyl prodrug of the amino-substituted flavone derivate aminoflavone with antiproliferative and antineoplastic activities. AFP464 is rapidly converted to aminoflavone in plasma. Aminoflavone activates the aryl hydrocarbon receptor (AhR) signaling pathway leading to an increase in cytochrome P450 1A1 (CYP1A1) and cytochrome P450 1A2 (CYP1A2) expression and, to a lesser extent, an increase in cytochrome P450 1B1 (CYP1B1) expression. Subsequently, aminoflavone is metabolized to toxic metabolites by the cytochromome P450 enzymes that it induces; these toxic metabolites covalently bind to DNA, resulting in the phosphorylation of p53, the induction of the p53 downstream target p21Waf1/Cip1, and apoptosis. Pulmonary toxicity may be dose-limiting.
  • Aminopterin - A synthetic derivative of pterins with antineoplastic and immunosuppressive properties. As a folate analogue, aminopterin competes for the folate binding site of the enzyme dihydrofolate reductase, thereby blocking tetrahydrofolate synthesis, and resulting in depletion of nucleotide precursors and inhibition of DNA, RNA and protein synthesis.
  • Aminopterin sodium - The sodium salt of a pterin derivative with antineoplastic and immunosuppressive properties. As a folate analogue, aminopterin competes for the folate binding site of the enzyme dihydrofolate reductase, thereby blocking tetrahydrofolate synthesis, and resulting in depletion of nucleotide precursors and inhibition of DNA, RNA and protein synthesis.
  • Amivantamab - A human bispecific antibody targeting both epidermal growth factor receptor EGFR and hepatocyte growth factor receptor (HGFR; cMet), with potential antineoplastic activity. Upon administration, amivantamab simultaneously targets and binds to wild-type or certain mutant forms of both EGFR and cMet expressed on cancer cells, thereby preventing receptor phosphorylation. This prevents the activation of both EGFR- and cMet-mediated signaling pathways. In addition, binding results in receptor degradation, which further inhibits EGFR- and cMet-mediated signaling. JNJ-61186372 also causes antibody-dependent cellular cytotoxicity (ADCC). Altogether, this results in the inhibition of tumor cell proliferation. EGFR and cMet, both upregulated or mutated in a variety of tumor cell types, play key roles in tumor cell proliferation.
  • Aml mrna positive lysate loaded autologous dendritic cell vaccine - A cancer vaccine consisting of autologous dendritic cells loaded with separate preparations of acute myelogenous leukemia (AML) cell lysate and AML-specific messenger RNA (mRNA) with potential immunostimulatory and antineoplastic activities. Upon administration, AML mRNA plus lysate loaded autologous dendritic cell vaccine may elicit a potent cytotoxic T-cell (CTL) response against AML cells, resulting in tumor cell death. Autologous dendritic cells doubly-loaded with AML cell lysate and AML-specific mRNA may elicit superior primary, recall, and effector lytic immune responses compared to autologous dendritic cells loaded with tumor lysate or tumor mRNA alone.
  • Amolimogene bepiplasmid - A plasmid DNA-based vaccine consisting of small biodegradable poly(lactide-co-glicolide) polymer microparticles encapsulating plasmid-DNA vector encoding a chimeric protein comprising epitopes derived from the E6 and E7 oncoproteins of the human papillomavirus (HPV) types 16 and 18, with potential antineoplastic activity. Upon intramuscular vaccination, amolimogene bepiplasmid may elicit the host immune system to mount a cytotoxic T-lymphocyte (CTL) response against tumor cells positive for HPV-16 and -18 E6 and E7 and may result in a reduction in tumor cell growth. HPV types 16 and 18 oncoproteins E6 and E7 are most commonly involved in cervical cancer.
  • Amonafide l-malate - The malate salt of amonafide, an imide derivative of naphthalic acid, with potential antineoplastic activity. Amonafide intercalates into DNA and inhibits topoisomerase II, resulting in DNA double-strand breaks (DSB) and inhibition of DNA replication and RNA synthesis.
  • Amrubicin - A synthetic 9-amino-anthracycline with antineoplastic activity. Amrubicin intercalates into DNA and inhibits the activity of topoisomerase II, resulting in inhibition of DNA replication, and RNA and protein synthesis, followed by cell growth inhibition and cell death. This agent has demonstrated a higher level of anti-tumor activity than conventional anthracycline drugs without exhibiting any indication of the cumulative cardiac toxicity common to this class of compounds.
  • Amrubicin hydrochloride - The hydrochloride salt of a third-generation synthetic 9-amino-anthracycline with antineoplastic activity. Amrubicin intercalates into DNA and inhibits the activity of topoisomerase II, resulting in inhibition of DNA replication, and RNA and protein synthesis, followed by cell growth inhibition and cell death. This agent has demonstrated a higher level of anti-tumor activity than conventional anthracycline drugs without exhibiting any indication of the cumulative cardiac toxicity common to this class of compounds.
  • Amsacrine - An aminoacridine derivative with potential antineoplastic activity. Although its mechanism of action is incompletely defined, amsacrine may intercalate into DNA and inhibit topoisomerase II, resulting in DNA double-strand breaks, arrest of the S/G2 phase of the cell cycle, and cell death. This agent's cytotoxicity is maximal during the S phase of the cell cycle when topoisomerase levels are greatest. In addition, amsacrine may induce transcription of tumor promoter p53 protein and block p53 ubiquitination and proteasomal degradation, resulting in p53-dependent tumor cell apoptosis.
  • Amsacrine lactate - The lactate form of amsacrine, an aminoacridine analog and topoisomerase II inhibitor, with antineoplastic activity. Although the exact relationship between DNA binding and its activity has yet to be fully elucidated, amsacrine intercalates DNA through its acridine moiety, and its nonintercalative headgroup impedes topoisomerase II activity, augmenting enzyme-mediated DNA cleavage and resulting in DNA double-strand breaks. This ultimately induces programmed cell death.
  • Amsilarotene - A retinobenzoic acid with potential antineoplastic activity. Amsilarotene inhibits retinoblastoma-gene product (RB) phosphorylation and increases the presence of 2 cyclin-dependent kinase (CDK) inhibitors, resulting in cell cycle arrest. This agent also causes a cytotoxic decline in cyclin A and thymidylate synthase expression.
  • Amustaline - A quinacrine mustard compound with potential antineoplastic activity. Amustaline binds to, intercalates and crosslinks DNA and RNA. This agent is mainly used for ex vivo purposes, specifically for the inactivation of pathogens such as viruses, protozoa and bacteria in red blood cells (RBCs).
  • Amustaline dihydrochloride - The hydrochloride salt form of amustaline, a quinacrine mustard compound with potential antineoplastic activity. Amustaline binds to, intercalates and crosslinks DNA and RNA. This agent is mainly used for ex vivo purposes, specifically for the inactivation of pathogens such as viruses, protozoa and bacteria in red blood cells (RBCs).
  • Amuvatinib - An orally bioavailable synthetic carbothioamide with potential antineoplastic activity. Multitargeted receptor tyrosine kinase inhibitor MP470 binds to mutant forms of the stem cell factor receptor (c-Kit; SCFR), inhibiting clinically relevant mutants of this receptor tyrosine kinase that may be associated with resistance to therapy. In addition, MP470 inhibits activities of other receptor tyrosine kinases, such as c-Met, Ret oncoprotein, and mutant forms of Flt3 and PDGFR alpha, which are frequently dysregulated in variety of tumors. This agent also suppresses the induction of DNA repair protein Rad51, thereby potentiating the activities of DNA damage-inducing agents. Mutant forms of c-Kit are often associated with tumor chemoresistance.
  • Amuvatinib hydrochloride - The hydrochloride salt of an orally bioavailable synthetic carbothioamide with potential antineoplastic activity. Multitargeted receptor tyrosine kinase inhibitor MP470 binds to mutant forms of the stem cell factor receptor (c-Kit; SCFR), inhibiting clinically relevant mutants of this receptor tyrosine kinase that may be associated with resistance to therapy. In addition, MP470 inhibits activities of other receptor tyrosine kinases, such as c-Met, Ret oncoprotein, and mutant forms of Flt3 and PDGFR alpha, which are frequently dysregulated in variety of tumors. This agent also suppresses the induction of DNA repair protein Rad51, thereby potentiating the activities of DNA damage-inducing agents. Mutant forms of c-Kit are often associated with tumor chemoresistance.
  • Anakinra - A recombinant human nonglycosylated interleukin-1 (IL-1) receptor antagonist with potential antineoplastic activity. Anakinra binds to the IL-1 receptor, thereby blocking the binding of the IL-1 to and activation of its receptor. Blockade of IL-1 activity may inhibit the cascade of downstream pro-angiogenic factors such as vascular endothelial cell growth factor, tumor necrosis factor-alpha, and IL-6, resulting in inhibition of tumor angiogenesis.
  • Anastrozole - A nonsteroidal inhibitor of estrogen synthesis that resembles paclitaxel in chemical structure. As a third-generation aromatase inhibitor, anastrozole selectively binds to and reversibly inhibits aromatase, a cytochrome P-450 enzyme complex found in many tissues including those of the premenopausal ovary, liver, and breast; aromatase catalyzes the aromatization of androstenedione and testosterone into estrone and estradiol, the final step in estrogen biosynthesis. In estrogen-dependent breast cancers, ananstrozole may inhibit tumor growth.
  • Anaxirone - A synthetic triepoxide alkylating agent with potential antineoplastic activity. Anaxirone alkylates DNA via actual or derived epoxide groups, resulting in inhibition of DNA synthesis. This agent has been shown to exhibit a broad spectrum of antineoplastic activity against experimental tumors, including those resistant to other alkylating agents.
  • Ancitabine - A cytarabine congener prodrug with antineoplastic activity. Upon administration, ancitabine is slowly hydrolyzed into cytarabine, which is converted to the active triphosphate form and competes with deoxycytidine triphosphate 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 and RNA polymerases, resulting in a decrease in cell growth. Compared to cytarabine, a more prolonged, consistent cytarabine-mediated therapeutic effect may be achieved with ancitabine because of the slow hydrolytic conversion of ancitabine to cytarabine.
  • Ancitabine hydrochloride - The hydrochloride salt of a cytarabine congener prodrug with antineoplastic activity. Upon administration, ancitabine is slowly hydrolyzed into cytarabine. Subsequently, 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. Cytarabine agent also inhibits DNA polymerase, resulting in a decrease in DNA replication and repair. Compared to cytarabine, a more prolonged, consistent cytarabine-mediated therapeutic effect may be achieved with ancitabine because of the slow hydrolytic conversion of ancitabine to cytarabine.
  • Andecaliximab - A humanized monoclonal antibody against matrix metalloproteinase 9 (MMP-9), with potential antineoplastic activity. Upon administration, andecaliximab binds to MMP-9 and inhibits its enzymatic activity. This results in an inhibition of extracellular matrix protein degradation and, potentially, the inhibition of angiogenesis, tumor growth, invasion, and metastasis. MMP-9, a protein belonging to the MMP family, plays a key role in the degradation of collagens and proteoglycans; increased activity of MMP-9 has been associated with increased invasion and metastasis of cancer.
  • Androgen antagonist apc-100 - An orally available, vitamin E derivative and androgen receptor (AR) antagonist with potential anti-oxidant, chemopreventative and antineoplastic activity. APC-100 binds to ARs in target tissues thereby inhibiting androgen-induced receptor activation and facilitating the formation of inactive complexes that cannot be translocated to the nucleus. By inhibiting the formation of the complex between androgen activated AR- and the AP1 transcription factor JunD, the expression of androgen-responsive genes are blocked. One of such gene is spermidine/spermine N1-acetyl transferase gene (SSAT) that is responsible for the breakdown of polyamines, which are produced in high levels by prostatic epithelial cells, into reactive oxygen species (ROS) that cause cellular damage. APC-100 may ultimately lead to an inhibition of growth in both AR-dependent and AR-independent prostate tumor cells.
  • Androgen receptor antagonist bay 1161116 - An orally bioavailable antagonist of the androgen receptor (AR), with potential antineoplastic activity. Upon oral administration, AR antagonist BAY 1161116 specifically binds to AR, inhibits AR activation, and prevents AR-mediated signaling. This inhibits cell growth in AR-overexpressing tumor cells. AR is overexpressed in prostate cancers and is involved in proliferation, survival and chemoresistance of tumor cells.
  • Androgen receptor antagonist shr3680 - An orally bioavailable androgen receptor (AR) antagonist with potential antineoplastic activity. Upon administration, SHR3680 competitively binds to AR in target tissues, which both prevents androgen-induced receptor activation and facilitates the formation of inactive complexes that cannot be translocated to the nucleus. This prevents binding to and transcription of AR-responsive genes, inhibits the expression of genes that regulate prostate cancer cell proliferation, and may lead to an inhibition of cell growth of AR-expressing tumor cells. ARs are overexpressed in prostate cancer and play a key role in prostate cancer cell proliferation.
  • Androgen receptor antagonist tas3681 - An orally bioavailable inhibitor of the androgen receptor (AR), with potential antineoplastic activity. Upon oral administration, AR inhibitor TAS3681 specifically binds to AR. This prevents AR activation, downregulates AR and prevents AR-mediated signaling. This inhibits cell growth in AR-overexpressing tumor cells. AR is overexpressed in prostate cancers and is involved in proliferation, survival and chemoresistance of tumor cells.
  • Androgen receptor antagonist trc253 - An orally bioavailable androgen receptor (AR) antagonist, with potential antineoplastic activity. Upon oral administration, AR antagonist TRC253 specifically binds to both wild-type and certain mutant forms of AR, thereby preventing androgen-induced receptor activation and facilitating the formation of inactive complexes that cannot translocate to the nucleus. This prevents binding to and transcription of AR-responsive genes, inhibits the expression of genes that regulate prostate cancer cell proliferation, and may lead to an inhibition of growth of tumor cells in which AR is overexpressed and/or mutated. AR is often overexpressed and/or mutated in prostate cancers and plays a key role in proliferation, survival and chemoresistance of tumor cells.
  • Androgen receptor antisense oligonucleotide azd5312 - An antisense oligonucleotide targeting the androgen receptor (AR) mRNA, with potential antineoplastic activity. Upon intravenous administration, AZD5312 hybridizes with AR mRNA, which blocks translation of the AR protein. This both inhibits AR-induced tumor cell growth and promotes apoptosis in AR-overexpressing tumor cells. AR is overexpressed in certain breast and prostate cancers and is involved in tumor cell proliferation and survival.
  • Androgen receptor antisense oligonucleotide ezn-4176 - A locked nucleic acid (LNA)-based antisense oligonucleotide targeting the androgen receptor (AR) mRNA, with potential antineoplastic activity. Upon administration, EZN-4176 is hybridized and releases the complementary sequences of AR mRNA, thereby blocking translation of the AR protein and inhibiting AR-induced tumor cell growth and promoting tumor cell apoptosis in AR-overexpressing tumor cells. AR is overexpressed in certain breast and prostate cancers and is involved in tumor cell proliferation and survival. LNAs contain a methylene bridge linking 2'-oxygen and 4'-carbon of ribose sugar rings, thereby increasing their thermal stability and decreasing degradation.
  • Androgen receptor degrader arv-110 - An orally available selective androgen receptor (AR)-targeted protein degrader, using the proteolysis targeting chimera (PROTAC) technology, with potential antineoplastic activity. ARV-110 is composed of an AR ligand attached to an E3 ligase recognition moiety. Upon oral administration, ARV-110 targets and binds to the AR ligand binding domain. E3 ligase is recruited to the AR by the E3 ligase recognition moiety and the AR target protein is tagged by ubiquitin. This causes ubiquitination and degradation of AR by the proteasome. This prevents the expression of AR target genes and halts AR-mediated signaling. This results in an inhibition of proliferation in AR-overexpressing tumor cells. In addition, the degradation of the AR protein releases the ARV-110 is released and can bind to additional AR target proteins. AR plays a key role in the proliferation of castration-resistant prostate cancer cells (CRPC).
  • Androgen receptor degrader cc-94676 - An orally bioavailable androgen receptor (AR) degrader, with potential antineoplastic activity. Upon administration, AR degrader CC-94676 causes degradation of AR, prevents AR-mediated signaling and inhibits the proliferation of AR-overexpressing tumor cells. AR plays a key role in tumor cell proliferation in castration-resistant prostate cancer (CRPC).
  • Androgen receptor downregulator azd3514 - An orally available selective androgen receptor (AR) downregulator (SARD), with potential antineoplastic activity. Upon oral administration, AZD3514 binds to the AR ligand binding domain and inhibits the binding of androgen, thereby preventing androgen-dependent AR signaling. AZD3514 also causes downregulation of AR expression, which further prevents AR-mediated signaling. This results in an inhibition of proliferation in AR-overexpressing tumor cells. AR plays a key role in the proliferation of castration-resistant prostate cancer cells.
  • Androgen receptor inhibitor epi-7386 - An orally bioavailable, second-generation inhibitor of the N-terminal domain (NTD) of androgen receptor (AR), with potential antineoplastic activity. Upon oral administration, AR inhibitor EPI-7386 specifically binds to the NTD of AR, thereby inhibiting both AR activation and the AR-mediated signaling pathway. This may inhibit cell growth in AR-overexpressing tumor cells. AR is overexpressed in prostate cancers and is involved in the proliferation, survival and chemoresistance of tumor cells. EPI-7386 may be more active and metabolically stable than first-generation AR NTD inhibitors.
  • Androgen receptor ligand-binding domain-encoding plasmid dna vaccine mvi-118 - A cancer vaccine containing pTVG4 plasmid DNA encoding the human androgen receptor (AR) ligand-binding domain (LBD) (pTVG-AR), with potential immunostimulating and antineoplastic activities. Upon intradermal administration of AR LBD-encoding plasmid DNA vaccine MVI-118, the plasmid DNA vaccine expresses AR LBD and may stimulate the host immune system to generate a cytotoxic T-lymphocyte (CTL) response against AR LBD-expressing prostate cancer cells. This reduces proliferation of AR-expressing tumor cells. AR, a tumor-associated antigen (TAA) overexpressed in prostate cancer cells, plays a key role in the development and progression of prostate cancer; its expression is correlated with poor prognosis.
  • Androgen receptor/glucocorticoid receptor antagonist cb-03-10 - An orally bioavailable steroidal cortexolone derivative and antagonist of the androgen receptor (AR) and glucocorticoid receptor (GR), with potential antineoplastic activity. Upon oral administration, AR/GR antagonist CB-03-10 specifically binds to AR and GR, inhibits AR and GR activation, and prevents AR- and GR-mediated signaling. This leads to an induction of both extrinsic and intrinsic apoptotic pathways and inhibits cell growth in AR- and GR-overexpressing tumor cells. AR and GR are overexpressed in certain types of cancer cells and are involved in proliferation, survival and chemoresistance of tumor cells.
  • Andrographolide - A labdane diterpenoid that is produced by the Andrographis paniculata plant, which has a broad range of therapeutic applications including anti-inflammatory and anti-platelet aggregation activities and potential antineoplastic properties. Since andrographolide has multiple therapeutic activities there are several proposed mechanisms of action for this agent. The anti-inflammatory effects of this agent appear to be related to the inhibition of nitric oxide (NO) production by macrophages. This agent may activate the NO/cyclic GMP pathway and inhibit both the phospholipase C gamma 2 (PLC gamma2)/protein kinase C (PKC) and PI3K/AKT-MAPK signaling pathways in activated platelets to inhibit platelet aggregation. In activated platelets, these three signaling pathways are downstream of integrin activation mediated by collagen binding and influence the association of fibrinogen with its receptors. Additionally, andrographolide may exert its anti-cancer activity through the induction of cell cycle arrest at G0/G1 phase and the stimulation of lymphocyte proliferation and activation. These processes could result in decreased proliferation of and increased immunocytotoxicity against tumor cells.
  • Androstane steroid he3235 - An orally bioavailable adrenal steroid analogue with potential antineoplastic activity. Androstane steroid HE3235 appears to bind the androgen receptor (AR), down-regulating anti-apoptotic genes, such as Bcl-2, while increasing the expression of pro-apoptotic genes, such as caspases. In vitro and in vivo studies indicate that this agent inhibits androstenediol-dependent LNCaP cell tumor growth. In addition, HE3235 may potentiate chemotherapeutic agents by down-regulating ABCG2, the gene encoding the multi-drug resistant (MDR) protein MDR2.
  • Anetumab ravtansine - A fully human IgG1 monoclonal antibody directed against the cell surface glycoprotein mesothelin and conjugated to the maytansinoid DM4 with potential antineoplastic activity. The monoclonal antibody moiety of anetumab ravtansine targets and binds to the tumor associated antigen mesothelin; upon internalization, the DM4 moiety binds to tubulin and disrupts microtubule assembly/disassembly dynamics, resulting in inhibition of cell division and cell growth of mesothelin-expressing tumor cells. Mesothelin is overexpressed on all mesotheliomas as well as many ovarian and pancreatic cancers while minimally expressed on normal tissue.
  • Ang2/vegf-binding peptides-antibody fusion protein cvx-241 - A fusion protein containing angiopoietin-2 (Ang2) and vascular endothelial growth factor (VEGF) derived peptides covalently attached, via a proprietary diketone linker, to a proprietary humanized catalytic aldolase monoclonal antibody, with potential antiangiogenic and antineoplastic activities. The Ang2/VEGF peptide moieties of Ang2/VEGF-binding peptides-antibody fusion protein CVX-241 bind to Ang2 and VEGF receptors, which may inhibit tumor angiogenesis and tumor cell proliferation. The proprietary humanized catalytic IgG1 monoclonal aldolase antibody contains reactive lysine residues in its binding sites, which react covalently with compounds having a diketone function; the Ang2 and VEGFR peptide moieties are then covalently attached to the diketone linkers via a proprietary spacer. Both VEGF and Ang2 are upregulated in a variety of cancer cell types and play a crucial role in angiogenesis. This agent possesses an enhanced half-life compared to the naked peptides.
  • Angelica sinensis root extract - An herbal extract derived from the root of the plant Angelica sinensis with possible antiinflammatory, antispasmodic, vasodilatory, estrogenic, and antitumor activities. Angelica sinensis contains volatile oils, including safrole, isosafrole, and n-butylphthalide; coumarin derivatives, including psoralens, bergapten, osthol, imperatorin, and oxypeucedanin; and ferulic acid. The coumarin derivatives in this agent may vasodilate and relax smooth muscle and may exhibit additive anticoagulant effects. Ferulic acid, a phenolic phytochemical present in plant cell walls, may neutralize free radicals such as reactive oxygen species. In addition, Angelica sinensis extract has been shown to inhibit the growth and induce apoptosis of glioblastoma mutltiforme brain tumor cells through p53-dependent and p53-independent pathways.
  • Angiogenesis inhibitor ji-101 - An orally active inhibitor of vascular endothelial growth factor receptor 2 (VEGFR2), platelet-derived growth factor receptor beta (PDGFRb), and the ephrin B4 receptor B4 (EphB4) with potential antiangiogenic and antineoplastic activities. Angiogenesis inhibitor JI-101 binds to and inhibits VEGFR2, PDGFRb and EphB4, which may inhibit tumor angiogenesis and, so, cellular proliferation in tumor cells overexpressing VEGFR2, PDGFRb and EphB4. The receptor tyrosine kinases VEGFR2, PDGFRb and EphB4 may be overexpressed in a number of different cancer cell types and may play crucial roles in tumor angiogenesis.
  • Angiopoietin-2-specific fusion protein pf-04856884 - A humanized monoclonal antibody fused to two peptides that bind to angiopoietin 2 (Ang2; ANGPT2), with potential anti-angiogenic and antineoplastic activities. Upon intravenous administration, Ang2-targeting PF-04856884 CovX body specifically binds to Ang2 and prevents the binding of Ang2 to its receptor Tie2 expressed on endothelial cells. This inhibits Tie2-mediated signaling, prevents angiogenesis and inhibits tumor cell proliferation. Ang2, a proangiogenic cytokine and ligand for the Tie2 receptor, plays a key role in the regulation of tumor angiogenesis and tumor cell proliferation; its expression is upregulated by tumor endothelial cells.
  • Anhydrous enol-oxaloacetate - The anhydrous form of enol-oxaloacetate, a small molecule blood glutamate scavenger, that can be used to lower glutamate plasma levels, and has potential neuroprotective activity. Upon administration, enol-oxaloacetate targets and binds to glutamate in the bloodstream. This lowers glutamate plasma levels and lowers the free glutamate available to be picked up by cells, such as tumor brain cells, thereby preventing glutamate metabolism and glutamate-mediated signaling. This prevents the proliferation of rapidly growing cells, such as brain tumor cells. And by lowering glutamate plasma levels, a molecular imbalance is formed and glutamate is excreted across the blood-brain barrier, resulting in lower free brain glutamate. This may help protect the brain from excitotoxicity in conditions where there is a surge of glutamate production, such as traumatic brain injury, thereby protecting neuronal cells. Glutamate, a non-essential amino acid and the major excitatory neurotransmitter in the central nervous system (CNS), provides energy and generates building blocks for the production of macromolecules, which are needed for cellular growth and survival.
  • Anhydrovinblastine - A semisynthetic derivative of the vinca alkaloid vinblastine, with potential antineoplastic activity. Like vinblastine, anhydrovinblastine targets and binds to tubulin and inhibits microtubule formation, resulting in disruption of mitotic spindle assembly and causing tumor cell cycle arrest in the M phase.
  • Aniline mustard - An alkylating mustard with antineoplastic activity. Aniline mustard forms covalent linkages with nucleophilic centers, resulting in depurination, base miscoding and strand scission, and crosslinking of DNA strands, all of which contribute to its cytotoxicity.
  • Anlotinib hydrochloride - The hydrochloride salt form of anlotinib, a receptor tyrosine kinase (RTK) inhibitor with potential antineoplastic and anti-angiogenic activities. Upon administration, anlotininib targets multiple RTKs, including vascular endothelial growth factor receptor type 2 (VEGFR2) and type 3 (VEGFR3). This agent may both inhibit angiogenesis and halt tumor cell growth.
  • Annamycin - A lipophilic, anthracycline antineoplastic antibiotic. Annamycin intercalates into DNA and inhibits topoisomerase II, thereby inhibiting DNA replication and repair as well as inhibiting RNA and protein synthesis. This agent appears to not be a substrate for the p-glycoprotein associated multidrug-resistance (MDR) transporter; therefore, overcoming the resistance pattern seen with other anthracycline compounds.
  • Annamycin liposomal - A liposome-encapsulated form of the semi-synthetic doxorubicin analogue annamycin with antineoplastic activity. Annamycin intercalates into DNA and inhibits topoisomerase II, resulting in the inhibition of DNA replication and repair and RNA and protein synthesis. This agent circumvents multidrug-resistance (MDR) transporters, including P-glycoprotein (P-gp). Liposomal annamycin is less toxic and shows improved antitumor activity compared to annamycin.
  • Annonaceous acetogenins - A family of naturally occurring polyketides that consist of C32 or C34 long chain fatty acids and combined with a propan-2-ol unit at C-2 to form a gamma-lactone, which are isolated from various species of the plant family Annonaceae, with potential antineoplastic and antimicrobial activity. Annonaceous acetogenins bind to the ubiquinone catalytic site(s) within the mitochondrial NADH:ubiquinone oxidoreductase (complex I), and block the electron transport chain in mitochondria. In addition, the acetogenins bind to and block the activity of ubiquinone-linked NADH oxidase, an enzyme overexpressed in the plasma membranes of cancer cells. This inhibits adenosine triphosphate (ATP) production, decreases intracellular ATP levels, and induces tumor cell apoptosis. Compared to normal cells, cancer cells have higher ATP demands. The Annonaceous acetogenins also inhibit microbial glucose dehydrogenase 6.
  • Ansamitomicin p-3 - An ansamacrolide and maytansine analogue originally isolated from the Ethiopian shrub Maytenus serrata with antineoplastic activity. Ansamitomicin P-3 binds to tubulin at the maytansine-binding site, thereby inhibiting microtubule assembly, inducing microtubule disassembly, and disrupting mitosis.
  • Anthocyanin-rich corn extract - A corn-based, water-soluble extract rich in the polyphenol anthocyanin, with potential antioxidant, anti-inflammatory and chemoprotective activities. Upon administration of the anthocyanin-rich corn extract, the anthocyanins scavenge reactive oxygen species (ROS), which protects healthy cells from radiation-induced oxidative stress and DNA damage. In addition, anthocyanins modulate the expression of various genes and proteins involved in inflammation, tumor cell proliferation, angiogenesis, tumor cell invasion and differentiation. This agent also chelates metals and induces the expression of enzymes involved in Phase II antioxidant and detoxification pathways, which may further protect cells against oxidative stress induced by toxins and carcinogens.
  • Anthramycin - A pyrrolo(1,4)benzodiazepine antineoplastic antibiotic isolated from the bacterium Streptomyces refuineus var. thermotolerans. Anthramycin binds covalently to guanine in the minor groove of DNA, thereby inhibiting DNA replication and RNA and protein synthesis.
  • Anthrapyrazole - An antineoplastic antibiotic that intercalates into DNA and interacts with topoisomerase II, thereby inhibiting DNA replication and repair and RNA and protein synthesis. Anthrapyrazoles may also block cell cycle division. In the presence of electron donors, some anthrapyrazole antibiotics cause single-strand breaks in DNA via photosensitization by visible light. These agents are less cardiotoxic than doxorubicin.
  • Anti c-kit antibody-drug conjugate lop628 - An antibody-drug conjugate (ADC) consisting of a humanized monoclonal antibody against the stem cell factor receptor c-Kit (SCFR) and conjugated, via a non-cleavable linker, to the cytotoxic agent maytansine, with potential antineoplastic activity. The monoclonal antibody moiety of anti c-KIT ADC LOP628 targets and binds to the cell surface antigen c-Kit. After antibody-antigen interaction followed by internalization, the maytansine moiety binds to tubulin, inhibits microtubule assembly, and induces microtubule disassembly. This leads to a disruption of mitosis and the inhibition of cell proliferation in cancer cells expressing c-Kit. c-Kit, a transmembrane protein and receptor tyrosine kinase, is overexpressed in solid tumors and hematological malignancies; it plays a key role in the regulation of cell differentiation and proliferation.
  • Anti-5t4 antibody-drug conjugate asn004 - An antibody-drug conjugate (ADC) composed of an antibody directed against 5T4 and conjugated, via a non-cleavable linker, to a proprietary polymer carrying multiple auristatin analog molecules via a cleavable linker, with potential antineoplastic activity. Upon administration, the antibody moiety of ASN004 selectively binds to cells expressing the 5T4 oncofetal antigen. After internalization and cleavage within the tumor cell cytosol, free auristatin analog molecules binds to tubulin and inhibits its polymerization, which may result in G2/M phase arrest and tumor cell apoptosis. 5T4, a transmembrane glycoprotein, is overexpressed by a variety of cancer cell types; its expression is correlated with increased invasiveness.
  • Anti-5t4 antibody-drug conjugate pf-06263507 - An antibody-drug conjugate composed of an antibody directed against 5T4 and conjugated, via the stable linker maleimidocaproyl (mc), to the microtubule inhibitor monomethyl auristatin phenylalanine (MMAF), with potential antineoplastic activity. Upon administration, the antibody moiety of PF-06263507 selectively binds to cells expressing the 5T4 oncofetal antigen. After internalization and enzymatic cleavage of the immunoconjugate within the tumor cell cytosol, free MMAF binds to tubulin and inhibits its polymerization, which may result in G2/M phase arrest and tumor cell apoptosis. 5T4, a transmembrane glycoprotein, is overexpressed by a variety of cancer cell types; its expression is correlated with increased invasiveness.
  • Anti-5t4 antibody-drug conjugate syd1875 - An antibody-drug conjugate (ADC) composed of a humanized immunoglobulin G1 (IgG1) monoclonal antibody directed against the oncofetal antigen 5T4 and site-specifically conjugated to a duocarmycin-based linker-drug valine-citrulline-seco-DUocarmycin-hydroxyBenzamide-Azaindole (vc-seco-DUBA), with potential antineoplastic activity. Upon administration, the antibody moiety of SYD1875 selectively binds to cells expressing the 5T4 oncofetal antigen. After internalization and cleavage within the tumor cell by proteases, the free and activated duocarmycin payload binds to the minor groove of DNA and alkylates adenine at the N3 position, which eventually leads to tumor cell apoptosis. 5T4, a transmembrane glycoprotein, is overexpressed by a variety of cancer cell types; its expression is correlated with increased invasiveness.
  • Anti-a33 monoclonal antibody krn330 - A recombinant fully human monoclonal antibody directed against the human A33 antigen, with potential immunomodulatory and antineoplastic activity. Anti-A33 monoclonal antibody KRN330 recognizes and binds to the human A33 antigen, which may stimulate the immune system to mount a cytotoxic T-lymphocyte (CTL) response against A33-positive colorectal cancers. A33 antigen, a 43 kDa transmembrane glycoprotein of the immunoglobulin superfamily, is highly and homogenously expressed in 95% of colorectal cancer cancers with only restricted expression in normal colonic mucosa and small bowel epithelia.
  • Anti-a5b1 integrin monoclonal antibody pf-04605412 - A monoclonal antibody directed against the human alpha5beta1 integrin with potential antiangiogenic and antineoplastic activities. Anti-alpha5beta1 integrin monoclonal antibody PF-04605412 selectively binds to alpha5beta1 integrin, preventing the binding of integrin ligands. This may result in the inhibition of endothelial cell-cell interactions, endothelial cell-matrix interactions, and integrin-mediated tumor angiogenesis and metastasis in alpha5beta1-expressing tumor cells. Alpha5beta1 integrin, a cell adhesion and signaling receptor, is often overexpressed on the surface of tumor vessel endothelial cells and plays a crucial role in endothelial cell adhesion and migration.
  • Anti-actr/4-1bb/cd3zeta-viral vector-transduced autologous t-lymphocytes actr087 - Autologous T-lymphocytes that are genetically modified and transfected with a viral vector expressing the ACTR gene, a proprietary gene encoding for an antibody-coupled T-cell receptor (ATCR), with potential antineoplastic activity. The ACTR contains the extracellular Fc receptor CD16 domain, normally found on certain immune cells, such as natural killer (NK) cells, coupled to the co-immunostimulatory signaling domain 4-1BB, normally expressed on T-cells, and linked to the intracellular CD3 zeta domain (CD3z), which is needed for TCR signaling. Upon reintroduction into the patient and co-administration of a cancer-specific antibody, the co-administered antibody targets and binds to the tumor-associated antigen (TAA) expressed on the tumor cell. In turn, this induces the activation of the ACTR087 cells and destruction of the tumor cells by a) releasing cytotoxins that directly kill cancer cells; b) releasing cytokines that trigger an immune response and recruit other immune-mediated killer cells to kill the tumor cells; b) targeting and killing adjacent tumor cells that are not bound to the antibody; c) inducing T-cell proliferation and thereby further enhancing the T-cell mediated tumor cell attack. CD3 zeta is one of several membrane-bound polypeptides found in the TCR/CD3 complex; it enhances the survival and persistence of T-lymphocytes. The 4-1BB co-stimulatory molecule signaling domain enhances activation and signaling after recognition of the TAA.
  • Anti-ag7 antibody drug conjugate abgn-107 - An antibody drug conjugate (ADC) composed of a monoclonal antibody that targets the tumor-associated antigen (TAA) AG7 and is linked, through a hydrophilic, self-immolative linker, to a proprietary cytotoxic payload, with potential antineoplastic activity. Upon administration of AbGn-107 the antibody moiety targets and binds to the AG7 antigen expressed on a variety of cancer cells. Upon binding and internalization, the linker is cleaved and the payload is released, binds to tubulin, inhibits tubulin polymerization and kills the AG7-expressing tumor cells.
  • Anti-ags-16 monoclonal antibody ags-16m18 - A humanized monoclonal antibody directed against the activator of g-proteins signaling (AGS) cell surface protein AGS-16 with potential antineoplastic activity. Anti-AGS-16 monoclonal antibody AGS-16M18 selectively binds to AGS-16, triggering complement-dependent cell lysis (CDCL) and antibody-dependent cell-mediated cytotoxicity (ADCC) in tumor cells expressing AGS-16. While normally expressed at low levels in the proximal tubules of the kidney, AGS-16 has been found to be overexpressed in more than 95% of kidney and 40% of liver neoplasms.
  • Anti-ags-5 antibody-drug conjugate asg-5me - An antibody drug conjugate (ADC) containing the fully human IgG2k monoclonal antibody targeting an epitope of SLC44A4 (AGS-5) linked, via a valine-citrulline (vc) maleimidocaproyl (mc) linker, to the antimicrotubulin drug monomethyl auristatin E (MMAE), with potential antineoplastic activity. The monoclonal antibody moiety of ASG-5ME selectively binds to AGS-5. After internalization and proteolytic cleavage, MMAE binds to tubulin and inhibits its polymerization, which results in G2/M phase arrest and tumor cell apoptosis. SLC44A4, potentially a sodium-dependent transmembrane transport protein, is overexpressed on more than 80 percent of samples derived from patients with pancreatic, prostate and gastric cancers.
  • Anti-ags-8 monoclonal antibody ags-8m4 - A humanized monoclonal antibody directed against the activator of g-proteins signaling (AGS) cell surface protein AGS-8 with potential antineoplastic activity. Anti-AGS-8 monoclonal antibody AGS-8M4 selectively binds to AGS-8, triggering complement-dependent cell lysis and antibody-dependent cell-mediated cytotoxicity in tumor cells expressing AGS-8. While normally expressed at low levels in the heart in response to ischemia, AGS-8 has been found to be expressed in more than 70% of ovarian neoplasms.
  • Anti-alpha bcma/anti-alpha cd3 t-cell engaging bispecific antibody tnb-383b - A T-cell engaging bispecific antibody (T-BsAb) directed against the tumor-associated antigen (TAA) human alpha B-cell maturation antigen (aBCMA) and against the alphaCD3 (aCD3) antigen found on T-lymphocytes, with potential immunostimulating and antineoplastic activities. TNB-383B is composed of two aBCMA moieties in sequence on one arm, a single aCD3 arm, and a silenced IgG4 Fc. Upon administration of anti-aBCMA/aCD3 T-cell engaging bispecific antibody TNB-383B, this bispecific antibody binds to both CD3 on cytotoxic T-lymphocytes (CTLs) and BCMA found on BCMA-expressing tumor cells. This activates and redirects CTLs to BCMA-expressing tumor cells, which results in the CTL-mediated cell death of BCMA-expressing tumor cells. BCMA, a member of the tumor necrosis factor receptor superfamily that is specifically overexpressed on malignant plasma cells, plays a key role in promoting plasma cell survival. Binding to aCD3 preferentially activates effector over regulatory T-cells and stimulates minimal cytokine release.
  • Anti-alpha5beta1 integrin antibody mint1526a - An antibody directed against the human alpha5beta1 integrin (a5b1) with potential antiangiogenic and antineoplastic activities. Anti-a5b1 antibody MINT1526A selectively binds to a5b1, thereby preventing the binding of integrin ligands. This may result in the inhibition of endothelial cell-cell interactions, endothelial cell-matrix interactions, and integrin-mediated tumor angiogenesis and metastasis in a5b1-expressing tumor cells. a5b1, a cell adhesion and signaling receptor, is often overexpressed on the surface of tumor vessel endothelial cells and plays a crucial role in both endothelial cell adhesion and migration.
  • Anti-ang2 monoclonal antibody medi-3617 - A fully human IgG1 monoclonal antibody against angiopoietin 2 (ANG2), with potential antiangiogenic activity. Anti-ANG2 monoclonal antibody MEDI-3617 binds to Ang2 and interferes with the interaction between Ang2 and its receptor TEK tyrosine kinase (Tie2), thereby resulting in the disruption of vascular remodeling. This may inhibit angiogenesis and may eventually lead to an inhibition of tumor cell proliferation.
  • Antiangiogenic drug combination tl-118 - A proprietary, oral suspension containing a combination of agents comprised of a nonsteroidal anti-inflammatory agent, an alkylating agent, a histamine H2 antagonist and a sulfonamide with potential anti-angiogenic and antineoplastic activities. Antiangiogenic drug combination TL-118 is administrated as a specific dosing regimen and may result in a synergistic effect and reduce angiogenesis and inhibit tumor cell proliferation.
  • Anti-angiopoietin monoclonal antibody amg 780 - An immunoglobulin (Ig) G2 monoclonal antibody targeting the proangiogenic cytokines angiopoietin 1 (Ang1) and 2 (Ang2), with potential anti-angiogenic and antineoplastic activities. Upon administration, anti-angiopoietin monoclonal antibody AMG 780 binds to Ang1 and Ang2. This prevents the binding of the angiopoietin ligands to their receptor Tie2 (TEK), an endothelial cell-specific receptor tyrosine kinase. This prevents Tie2-mediated signaling and results in an inhibition of Tie2-expressing, tumor-stimulated endothelial cell proliferation, which prevents angiogenesis and inhibits tumor cell proliferation.
  • Anti-april monoclonal antibody bion-1301 - A humanized monoclonal antibody targeting a proliferation-inducing ligand (APRIL; tumor necrosis factor ligand superfamily member 13; TNFSF13), with potential antineoplastic and immune checkpoint inhibitory activities. Following administration, anti-APRIL monoclonal antibody BION-1301 binds to APRIL and inhibits its binding to both of its receptors, B-cell maturation antigen (BCMA; tumor necrosis factor receptor superfamily member 17; TNFRSF17) and transmembrane activator and CAML Interactor (TACI; tumor necrosis factor receptor superfamily member 13B; TNFRSF13B). This inhibits the activation of both BCMA and TACI, and their downstream signaling pathways, which prevents tumor growth, tumor cell adhesion to bone marrow cells and immune suppression. Additionally, BION-1301 may reduce APRIL-induced drug resistance which occurs in some tumors. APRIL, an extracellular protein and member of the tumor necrosis factor ligand superfamily (TNFSF), is expressed by bone marrow plasma cells and myeloid cells, and overexpressed in multiple myeloma (MM), chronic lymphocytic leukemia (CLL), and colorectal carcinoma. APRIL induces immune suppression and tumor progression through the activation of BCMA- and TACI-dependent signaling pathways.
  • Anti-axl fusion protein avb-s6-500 - A soluble fusion protein comprised of the extracellular domain of the receptor tyrosine kinase (RTK) AXL (UFO) fused to a human immunoglobulin G1 (IgG1) Fc domain, with potential antineoplastic activity. Upon administration, AXL Fc fusion protein AVB-S6-500 selectively binds to growth arrest-specific protein 6 (GAS6), the endogenous ligand for AXL. This may inhibit GAS6/AXL-mediated signaling, which plays a key role in tumor cell proliferation, survival, invasion and metastasis, as well as immune evasion and resistance to other anticancer agents. AXL, a member of the Tyro3, AXL and Mer (TAM) family of RTKs, is overexpressed by many tumor cell types and its expression is associated with drug resistance and poor prognosis.
  • Anti-axl/pbd antibody-drug conjugate adct-601 - An antibody-drug conjugate (ADC), consisting of a humanized immunoglobulin (Ig) G1 monoclonal antibody directed against AXL receptor tyrosine kinase (AXL; UFO) that is site-specifically conjugated to PL1601, which contains a valine-alanine cleavable linker and SG3199, a cytotoxic pyrrolobenzodiazepine (PBD) dimer, with potential antineoplastic activity. Upon administration, the monoclonal antibody moiety of anti-AXL/PBD antibody-drug conjugate ADCT-60 binds to AXL, which is expressed on the surfaces of a variety of cancer cell types. Upon endocytosis and enzymatic cleavage, free PBD is released and forms highly cytotoxic DNA interstrand cross-links, thereby blocking cell division and killing AXL-expressing cancer cells. AXL, a member of the TAM (TYRO3, AXL and MER) family of receptor tyrosine kinases, is overexpressed by many tumor cell types, and plays a key role in tumor cell proliferation, survival, invasion and metastasis; its expression is associated with drug resistance and poor prognosis.

Alphabetic list of antineoplastic agents - 0-9 - A1 - A2 - A3 - A4 - A5 -A6 - B - C - D - E - F - G - H - I - JK - L - M - NO - PQ - R - S - T - UVW - XYZ

 

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