Antineoplastic agents no

• O6-benzylguanine - A guanine analogue with antineoplastic activity. O6-benzylguanine binds the DNA repair enzyme O(6)-alkylguanine DNA alkyltransferase (AGT), transferring the benzyl moiety to the active-site cysteine and resulting in inhibition of AGT-mediated DNA repair. Co-administration of this agent potentiates the effects of other chemotherapeutic agents that damage DNA.

• Obatoclax mesylate - The mesylate salt of obatoclax, a synthetic small-molecule inhibitor of the bcl-2 family of proteins with potential pro-apoptotic and antineoplastic activities. Obatoclax binds to members of the Bcl-2 protein family, preventing the binding of these anti-apoptotic proteins to the pro-apoptotic proteins Bax and Bak and so promoting the activation of the apoptotic pathway in Bcl-2-overexpressing cells. The Bcl-2 family of proteins (bcl-2, bcl-xl, bcl-w, and Mcl-1) are overexpressed in a wide variety of cancers, including those of the lymphatic system, breast, lung, prostate, and colon.

• Obinutuzumab - A glycoengineered, humanized IgG1 monoclonal antibody with potential antineoplastic activity. Obinutuzumab, a third generation type II anti-CD20 antibody, selectivity binds to the extracellular domain of the human CD20 antigen on malignant human B cells. The Fc region carbohydrates of the antibody, enriched in bisected non-fucosylated glycosylation variants, contribute to its higher binding affinity for human FcgammaRIII receptors compared to non-glycoengineered antibodies, resulting in enhanced antibody-dependent cellular cytotoxicity (ADCC) and caspase-independent apoptosis. In addition, modification of elbow hinge sequences within the antibody variable framework regions may account for the strong apoptosis-inducing activity of R7159 upon binding to CD20 on target cells.

• Oblimersen sodium - The sodium salt of a phosphorothioate antisense oligonucleotide targeted to the initiation codon region of mRNA for the anti-apoptotic gene Bcl-2. Oblimersen inhibits Bcl-2 mRNA translation, which may result in decreased expression of the Bcl-2 protein and tumor cell apoptosis. This agent may enhance the efficacy of standard cytotoxic chemotherapy. The anti-apoptotic bcl-2 protein is an integral outer mitochondrial membrane protein (OMMP) that is overexpressed in some cancer cell types and is linked to tumor drug resistance.

• Ocaratuzumab - An Fc-engineered monoclonal antibody directed against human CD20 with potential antineoplastic activity. Ocaratuzumab specifically binds to CD20 antigen (B1), preventing mitogen-induced B-cell proliferation; inhibiting B-cell differentiation; and promoting antibody-dependent cell-mediated cytotoxicity (ADCC) and apoptosis of B cells expressing CD20. The Fc portion of this monoclonal antibody has been engineered to possess a higher binding affinity for variant Fc receptors on T helper cells, resulting in an augmentation of the anti-tumor immune response. Because of Fc engineering, this agent may be significantly more potent than rituximab in inducing B cell-directed ADCC. CD20 is a non-glycosylated cell surface phosphoprotein that is exclusively expressed on B cells during most stages of B cell development.

• O-chloroacetylcarbamoylfumagillol - A synthetic analog of fumagillin, an antibiotic isolated from the fungus Aspergillus fumigatus fresenius with antineoplastic activity. TNP-470 binds to and irreversibly inactivates methionine aminopeptidase-2 (MetAP2), resulting in endothelial cell cycle arrest late in the G1 phase and inhibition of tumor angiogenesis. This agent may also induce the p53 pathway, thereby stimulating the production of cyclin-dependent kinase inhibitor p21 and inhibiting angiogenesis.

• Ocrelizumab - A Fc-modified, humanized monoclonal antibody directed against the B-cell CD20 cell surface antigen, with immunosuppressive activity. Ocrelizumab binds to CD20 on the surfaces of B-cells, triggering complement-dependent cell lysis (CDCL) and antibody-dependent cell-mediated cytotoxicity (ADCC) of B-cells overexpressing CD20. The CD20 antigen, a non-glycosylated cell surface phosphoprotein that acts as a calcium ion channel, is found on over 90% of B-cells, B-cell lymphomas, and other lymphoid tumor cells of B-cell origin; it plays an important role in B-cell functioning.

• Octreotide - A synthetic long-acting cyclic octapeptide with pharmacologic properties mimicking those of the natural hormone somatostatin. Octreotide is a more potent inhibitor of growth hormone, glucagon, and insulin than somatostatin. Similar to somatostatin, this agent also suppresses the luteinizing hormone response to gonadotropin-releasing hormone, decreases splanchnic blood flow, and inhibits the release of serotonin, gastrin, vasoactive intestinal peptide (VIP), secretin, motilin, pancreatic polypeptide, and thyroid stimulating hormone.

• Octreotide pamoate - A synthetic long-acting octapeptide analogue of endogenous somatostatin. Octreotide pamoate binds to somatostatin receptors expressed by some neuroendocrine and non-neuroendocrine tumor cells, thereby initiating somatostatin receptor-mediated apoptosis. Other possible antineoplastic activities of this agent include suppression of tumor angiogenesis and tumor growth-promoting insulin-like growth factor 1 (IGF-1).

• Odronextamab - A bispecific, human monoclonal antibody with potential antineoplastic activity. Anti-CD20/CD3 monoclonal antibody REGN1979 contains two antigen-recognition sites: one for human CD3, a T cell surface antigen, and one for human CD20, a tumor-associated antigen that is exclusively expressed on B-cells during most stages of B-cell development and is often overexpressed in B-cell malignancies. Upon administration, odronextamab binds to both T-cells and CD20-expressing tumor B-cells, which cross-links the T-cells to tumor cells, and may result in a potent cytotoxic T-lymphocyte (CTL) response against CD20-expressing tumor B-cells.

• Ofatumumab - A fully human, high-affinity IgG1 monoclonal antibody directed against the B cell CD20 cell surface antigen with potential antineoplastic activity. Ofatumumab binds specifically to CD20 on the surfaces of B cells, triggering complement-dependent cell lysis (CDCL) and antibody-dependent cell-mediated cytotoxicity (ADCC) of B cells overexpressing CD20. The CD20 antigen, found on over 90% of B cells, B cell lymphomas, and other B cells of lymphoid tumors of B cell origin, is a non-glycosylated cell surface phosphoprotein that acts as a calcium ion channel; it is exclusively expressed on B cells during most stages of B cell development.

• Ofranergene obadenovec - A non-replicating adenovirus 5 (Ad-5, El-deleted) encoding a human Fas-chimera (Fas-c) transgene under the control of a modified murine pre-proendothelin-1 (PPE-1) promoter, with potential anti-angiogenic activity. Upon the administration of ofranergene obadenovec, the modified murine PPE-1 promoter is specifically activated in PPE-1-expressing angiogenic endothelial cells residing in the tumor microvasculature. Subsequently, the Fas-c pro-apoptotic transgene, containing the human tumor necrosis factor (TNF) receptor 1 (TNFR-1/p55) and the signaling domain of Fas, is expressed in angiogenic endothelial cells. Fas-mediated apoptosis is activated via binding of the TNFR-1 receptor with TNF-alpha, which is more abundant in the tumor microenvironment (TME), enhancing specificity and limiting systemic toxicities.

• Oglufanide disodium - The disodium salt of a synthetic form of a naturally-occurring dipeptide consisting of L-glutamic acid and L-tryptophan with potential antiangiogenic and potential immunomodulating activities. Oglufanide inhibits vascular endothelial growth factor (VEGF), which may inhibit angiogenesis. This agent has also been reported to stimulate the immune response to hepatitic C virus and intracellular bacterial infections.

• Olaparib - A small molecule inhibitor of the nuclear enzyme poly(ADP-ribose) polymerase (PARP) with potential chemosensitizing, radiosensitizing, and antineoplastic activities. Olaparib selectively binds to and inhibits PARP, inhibiting PARP-mediated repair of single strand DNA breaks; PARP inhibition may enhance the cytotoxicity of DNA-damaging agents and may reverse tumor cell chemoresistance and radioresistance. PARP catalyzes post-translational ADP-ribosylation of nuclear proteins and can be activated by single-stranded DNA breaks.

• Olaptesed pegol - A 45-mer L-stereoisomer RNA oligonucleotide linked to a 40 kDa polyethyleneglycol that targets the small chemokine stromal cell-derived factor 1 (SDF-1 or CXCL12) with potential antineoplastic and hematopoietic stem cell-mobilization activities. SDF-1 targeted agent NOX-A12 specifically binds to SDF-1 thereby preventing the binding of SDF-1 to its receptors CXCR4 and CXCR7 blocking the subsequent receptor activation. This may prevent angiogenesis, tumor cell proliferation, invasion and metastasis and could sensitize tumor cells to chemotherapy. In addition, inhibition of SDF-1/CXCR4 interaction may induce mobilization of hematopoietic cells from the bone marrow into blood. The unique mirror-image configuration of this agent renders it resistant to hydrolysis and does not hybridize with native nucleic acids. Furthermore, this agent does not induce the innate immune response and has shown a favorable immunogenicity profile.

• Olaratumab - A fully human IgG1 monoclonal antibody directed against the platelet-derived growth factor receptor alpha (PDGFR alpha) with potential antineoplastic activity. Anti-PDGFR alpha monoclonal antibody IMC-3G3 selectively binds to PDGFR alpha, .blocking the binding of its ligand, PDGF; signal transduction downstream of PDGFR through the MAPK and PI3K pathways is inhibited, which may result in inhibition of angiogenesis and tumor cell proliferation. Overexpressed by various cancer cell types, PDGFR is a transmembrane protein tyrosine kinase receptor, consisting of isoforms A and B that is important in regulating cellular growth and differentiation and angiogenesis.

• Oleandrin - A lipid soluble cardiac glycoside with potential antineoplastic activity. Upon administration, oleandrin specifically binds to and inhibits the alpha3 subunit of the Na/K-ATPase pump in human cancer cells. This may inhibit the phosphorylation of Akt, upregulate MAPK, inhibit NF-kb activation and inhibit FGF-2 export and may downregulate mTOR thereby inhibiting p70S6K and S6 protein expression. All of this may lead to an induction of apoptosis. As cancer cells with relatively higher expression of the alpha3 subunit and with limited expression of the alpha1 subunit are more sensitive to oleandrin, one may predict the tumor response to treatment with lipid-soluble cardiac glycosides such as oleandrin based on the tumors Na/K-ATPase pump protein subunit expression. Overexpression of the alpha3 subunit in tumor cells correlates with tumor proliferation.

• Oleclumab - A monoclonal antibody against the ectoenzyme CD73 (cluster of differentiation 73), also known as 5'-nucleotidase (5'-NT; ecto-5'-nucleotidase) with potential antineoplastic activity. Upon administration, oleclumab targets and binds to CD73, leading to clustering of and internalization of CD73. This prevents CD73-mediated conversion of adenosine monophosphate (AMP) to adenosine and decreases the amount of free adenosine. This prevents adenosine-mediated lymphocyte suppression and increases the activity of CD8-positive effector cells. This also activates macrophages, and reduces both myeloid-derived suppressor cells (MDSCs) and regulatory T-lymphocytes. By abrogating the inhibitory effect on the immune system and enhancing the cytotoxic T-cell-mediated immune response against cancer cells, tumor cell growth decreases. In addition, clustering and internalization of CD73 decreases the migration of cancer cells and prevents metastasis. CD73, a plasma membrane protein upregulated on a number of cancer cell types, catalyzes the conversion of extracellular nucleotides, such as AMP, to membrane-permeable nucleosides, such as adenosine; it plays a key role in adenosine-mediated immunosuppression within the tumor microenvironment.

• Oligo-fucoidan - A sulfated polysaccharide low-molecular-weight fucoidan, with potential antioxidant, anti-inflammatory, antiproliferative, anti-angiogenic and pro-apoptotic activities. Upon administration of oligo-fucoidan, this agent seems to exert numerous effects through various mechanisms of action, some of which remain to be fully elucidated. Oligo-fucoidan induces cell cycle arrest, activates caspases, induces apoptosis, and inhibits tumor cell proliferation in susceptible tumor cells. It also increases the expression of tumor suppressors, such as p53, while decreasing levels of certain tumor promoters. Oligo-fucoidan also promotes the degradation of transforming growth factor-beta (TGFb) receptor and the inhibition of epithelial-mesenchymal transition (EMT). It prevents tumor progression, alters tumor microenvironment (TME) and decreases the tumor-promoting M2 macrophages in the TME. Oligo-fucoidan has anti-inflammatory effects that suppress the expression of nitric oxide synthase (iNOS), cyclooxygenase (COX)-2 and monocyte chemoattractant protein-1 (MCP-1/CCL2), and decrease the production of certain pro-inflammatory cytokines, such as interleukin-1beta (IL-1b) and tumor necrosis factor (TNF)-alpha (TNFa). This agent may also suppress angiogenic activity by inhibiting vascular endothelial growth factor (VEGF) receptor expression and VEGF-induced endothelial cell proliferation. As an antioxidant, this agent protects cells against oxidative stress by scavenging superoxide radicals and induces the expression of the anti-oxidant nuclear factor erythroid-2-related factor 2 and that of its target gene, superoxide dismutase; and prevents reactive oxidative species (ROS) generation in cancer cells and ROS release into the TME. Fucoidan also has immune-modulatory effects and enhances the proliferation of natural killer (NKs) cells and cytotoxic T-cells (CTLs).

• Oligomeric procyanidin complex - A preparation containing plant-derived polyphenolic bioflavonoids composed of multimers (dimers, trimers, or higher order polymers) of the flavan-3-ol-based monomers catechin and epicatechin, which are extracted from sources rich in these chemicals, such as grape seeds, grape skin and pine bark, with potential anti-oxidant, anti-inflammatory, anti-microbial, anti-cancer and protective activities. Upon oral administration of oligomeric procyanidin complex (OPC), the polyphenols exert anti-oxidant activity by scavenging free radicals, which prevents both the formation of reactive oxygen species (ROS), particularly nitrous oxide (NO), and DNA damage. OPC also inhibits chemical-induced lipid peroxidation. In addition, OPC reduces the production advanced glycation end-products (AGE), decreases AGE accumulation in tissues, and inhibits the progression of AGE/receptor for AGE (RAGE)-mediated inflammatory transduction pathways, which inhibits the activation of pro-inflammatory transcriptional regulators and prevents the secretion of pro-inflammatory cytokines/chemokines. This ultimately prevents inflammatory-driven damage to end organs and may reduce inflammation-induced cancer formation and progression. In addition, OPC inhibits the activity of a variety of enzymes, including xanthine oxidase, collagenase, elastase hyaluronidase and beta-glucuronidase.

• Oligonucleotide spc2996 - A synthetic antisense oligonucleotide against Bcl-2 messenger RNA with potential antitumor activity. Oligonucleotide SPC2996 binds to and inactivates Bcl-2 mRNA, thereby inhibiting the expression of Bcl-2 protein, promoting tumor cell apoptosis, and potentially enhancing the efficacy of standard cytotoxic chemotherapy. Linked to tumor drug resistance, the antiapoptotic protein Bcl-2 is upregulated in several types of cancers.

• Olinvacimab - A fully human monoclonal antibody targeting the vascular endothelial growth factor receptor 2 (VEGFR2), with potential antiangiogenic activity. Upon administration, olinvacimab specifically binds to VEGFR2, thereby preventing the binding of its ligand VEGF. This may result in the inhibition of tumor angiogenesis and a decrease in tumor nutrient supply. VEGFR2 is a pro-angiogenic growth factor receptor tyrosine kinase expressed by endothelial cells, while VEGF is overexpressed in many tumors and is correlated to tumor progression.

• Olive oil extract/curcumin-based capsule - A capsule containing an extract of olive oil, rich in polyphenols, and curcumin, the polyphenol derived from the plant Curcuma longa, also known as turmeric, with potential anti-neoplastic, -angiogenic, -inflammatory, -oxidant and chemopreventive activities. The olive oil extract/curcumin-based capsule is rich in phytonutrients, especially polyphenols. Upon oral administration, the polyphenols, and other active ingredients in this supplement may exert anti-inflammatory activity by decreasing the production of inflammation mediators, such as TNF-alpha, interleukin (IL) 1-beta, IL-6, IL-10, interferon gamma, thromboxane B2, and leukotriene B4. They also inhibit a variety of pro-inflammatory enzymes, such as cyclooxygenase 1 (COX-1) and COX-2, block the formation of reactive-oxygen species and neutralize free radicals. In addition, curcumin and some other polyphenols disrupt cell signal transduction pathways involved in carcinogenesis. Specifically, curcumin inhibits cell invasion by inhibiting matrix metalloproteinase-9 (MMP-9) expression by suppressing NF-kB and AP-1 activation.

• Olive oil/soya oil/egg lecithin-based emulsion - An injectable, isotonic, nutritional lipid emulsion composed of approximately 80% refined olive oil and 20% refined soybean oil, used for parenteral nutrition. The olive oil/soya oil/egg lecithin emulsion provides about 15% of saturated fatty acids (SFA), 65% of mono-unsaturated fatty acids (MUFA) and 20% of essential poly-unsaturated fatty acids (EPUFA). Upon parenteral administration, the emulsion supplies calories, for energy, and essential fatty acids that can be incorporated into cell membranes. The fatty acids may decrease the production of certain pro-inflammatory cytokines, including interleukin 1 (IL-1), IL-6 and tumor necrosis factor (TNF). In addition to olive oil and soya oil, this lipid emulsion contains egg lecithin and provides phosphorus and choline, which are needed to maintain cell membrane integrity.

• Olivomycin - A preparation containing a mixture of glycosidic antibiotics isolated from Streptomyces olivoreticuli with fluorescent microscopy applications and potential antineoplastic activities. Olivomycin preferentially binds to DNA and can be utilized as a fluorescent marker during the characterization of heterochromatin. Additionally, binding to DNA inhibits both RNA transcription and RNA elongation by RNA polymerase; therefore protein synthesis is inhibited. In addition, olivomycin antibiotics are able to induce apoptosis in tumor cells through a mechanism that has not yet been fully elucidated.

• Olmutinib - An orally available small molecule, mutant-selective inhibitor of epidermal growth factor receptor (EGFR) with potential antineoplastic activity. Olmutinib binds to and inhibits mutant forms of EGFR, thereby leading to cell death of EGFR-expressing tumor cells. As this agent is selective towards mutant forms of EGFR, its toxicity profile may be reduced as compared to non-selective EGFR inhibitors which also inhibit the EGFR wild type form.

• Oltipraz - A synthetic dithiolethione with potential chemopreventive and anti-angiogenic properties. Oltipraz induces phase II detoxification enzymes, such as glutathione S transferase (GST) and NAD(P)H:quinone oxidoreductase 1 (NQO1). The induction of detoxification enzymes enhances the detoxification of certain cancer-causing agents, thereby enhancing their elimination and preventing carcinogen-induced DNA damages. Although the exact mechanism through which the anti-angiogenesis effect remains to be fully elucidated, oltipraz maybe able to modulate the expression of a number of angiogenic factors, thereby blocking the sustained and focal neovascularization in multiple tumor cell types.

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

• Olvimulogene nanivacirepvec - An attenuated oncolytic vaccinia virus encoding the light-emitting fusion protein Renilla luciferase-Aequorea green fluorescent protein (RUC-GFP) with potential bioluminescent and antineoplastic activities. Upon administration, light-emitting oncolytic vaccinia virus GL-ONC1 specifically enters tumor cells due to the permeable nature of the tumor vasculature. Once inside the cell, the virus replicates, resulting in tumor cell lysis and the release of mature viral particles into the tumor microenvironment. Released viral particles may then infect and destroy neighboring tumor cells. In addition, the release of tumor-associated antigens (TAAs) by lysed tumor cells into the bloodstream may activate the immune system to mount a cytotoxic T lymphocyte (CTL) response against the tumor. The expression of RUC-GFP by this agent allows for both detection and monitoring of virally infected tumor cells in vivo and vitro with luciferase-mediated bioluminescence imaging and fluorescence imaging techniques.

• Omacetaxine mepesuccinate - A semisynthetic formulation of the cytotoxic plant alkaloid homoharringtonine isolated from the evergreen tree Cephalotaxus with potential antineoplastic activity. Omacetaxine mepesuccinate binds to the 80S ribosome in eukaryotic cells and inhibits protein synthesis by interfering with chain elongation. This agent also induces differentiation and apoptosis in some cancer cell types.

• Ombrabulin - A synthetic water-soluble analogue of combretastatin A4, derived from the South African willow bush (Combretum caffrum), with potential vascular-disrupting and antineoplastic activities. Ombrabulin binds to the colchicine binding site of endothelial cell tubulin, inhibiting tubulin polymerization and inducing mitotic arrest and apoptosis in endothelial cells. As apoptotic endothelial cells detach from their substrata, tumor blood vessels collapse; the acute disruption of tumor blood flow may result in tumor necrosis.

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

• Onalespib - A synthetic, orally bioavailable, small-molecule inhibitor of heat shock protein 90 (Hsp90) with potential antineoplastic activity. Onalespib selectively binds to Hsp90, thereby inhibiting its chaperone function and promoting the degradation of oncogenic signaling proteins involved in tumor cell proliferation and survival. Hsp90, a chaperone protein upregulated in a variety of tumor cells, regulates the folding, stability and degradation of many oncogenic signaling proteins.

• Onalespib lactate - The lactate form of onalespib, a synthetic, orally bioavailable, small-molecule inhibitor of heat shock protein 90 (Hsp90) with potential antineoplastic activity. Onalespib selectively binds to Hsp90, thereby inhibiting its chaperone function and promoting the degradation of oncogenic signaling proteins involved in tumor cell proliferation and survival. Hsp90, a chaperone protein upregulated in a variety of tumor cells, regulates the folding, stability and degradation of many oncogenic signaling proteins.

• Onartuzumab - A humanized monovalent monoclonal antibody directed against the hepatocyte growth factor receptor (c-Met) with potential antineoplastic activity. Anti-MET monoclonal antibody MetMAb binds to the extracellular domain of c-Met, preventing the binding of its ligand, hepatocyte growth factor (HGF); the activation of the c-Met signaling pathway is thus inhibited, which may result in cell death in c-Met-expressing tumor cells. c-Met, a receptor tyrosine kinase, is overexpressed on the cell surfaces of a variety of cancer cell types and may play a key role in their proliferation, invasion and survival.

• Onatasertib - An orally available inhibitor of the mammalian target of rapamycin (mTOR) with potential antineoplastic activity. Onatasertib inhibits the activity of mTOR, which may result in the induction of tumor cell apoptosis and a decrease in tumor cell proliferation. mTOR, a serine/threonine kinase that is upregulated in a variety of tumors, plays an important role downstream in the PI3K/AKT/mTOR signaling pathway, which is frequently dysregulated in human cancers.

• Oncolytic adenovirus cadvec - A genetically modified oncolytic viral strain of human adenovirus (Ad) with potential immunostimulating and antineoplastic activities. Upon intratumoral administration, the oncolytic adenovirus CAdVEC selectively infects and replicates in tumor cells, leading to tumor cell lysis. Additionally, CAdVEC has been genetically modified to express currently undisclosed immunomodulatory molecules that may enhance the anti-tumor effects of endogenous T-lymphocytes as well as adoptively transferred chimeric antigen receptor (CAR) T-cells.

• Oncolytic adenovirus encoding gm-csf - A recombinant oncolytic adenovirus encoding the immunohematopoietic cytokine granulocyte-macrophage colony stimulating factor (GM-CSF) with potential antineoplastic activity. Upon administration, the oncolytic adenovirus selectively infects and replicates in tumor cells, which may result in tumor cells lysis. Synergistically, GM-CSF (sargramostim) expressed by the oncolytic adenovirus may promote a cytotoxic T cell response against tumor cells harboring the oncolytic adenovirus, resulting in an immune-mediated tumor cell death.

• Oncolytic adenovirus icovir5-infected autologous mesenchymal stem cells - Bone marrow-derived autologous mesenchymal stem cells (MSCs) infected with the oncolytic, replication-competent adenovirus ICOVIR5, with potential antineoplastic activity. Upon infusion of the oncolytic adenovirus ICOVIR5-infected autologous MSCs, these cells target the adenovirus to tumors. The oncolytic virus then selectively transfects and replicates in the tumor cells causing a direct cytotoxic effect and lysis of the tumor cells. In addition, the viral infection may stimulate an immune response against the virally-infected tumor cells. This may lead to an inhibition of cancer cell proliferation. ICOVIR-5, a virus derived from wild-type human adenovirus serotype 5 (Had5), has been modified to selectively replicate in tumor cells that have a deregulated retinoblastoma/E2F pathway.

• Oncolytic adenovirus orca-010 - A replication competent, oncolytic adenovirus serotype 5 (Ad5) that has been modified with a delta24 (d24) deletion, an incorporation of an RGD-4C motif in the Ad fiber protein, and an insertion of the T1 mutation in E3/19K gene, with potential oncolytic activity. Upon administration, oncolytic adenovirus ORCA-010 binds to specific Ad3 receptors that are highly expressed on certain tumor cells. This results in the replication of oncolytic adenovirus Ad5/3-delta24 in tumor cells and induces tumor cell lysis which may potentially result in the activation of a systemic immune response against tumor-associated antigens (TAAs). The Ad5/3-delta24 has a 24 base pair deletion in constant region 2 of the E1A gene which allows for selective replication in cells that are defective in the retinoblastoma gene (Rb) or cyclin-dependent kinase inhibitor-2A (CDKN2A or p16INK4a). As most tumor cells are defective in the Rb/p16 pathway, this virus selectively replicates in these cells. The RGD-4C motif is a 9-amino acid peptide that binds to various and enhances viral-cell receptor binding by allowing for a Coxsackie-adenovirus receptor (CAR)-independent infection of tumor cells, which is the natural route of viral binding, as CAR expression is often deficient on cancer cells. As integrins are often overexpressed on tumor cell surfaces, integrin receptor binding enhances tumor cells binding and infection by the Ad. The T1 mutation enhances the Ad5 release from tumor cells and promotes spreading throughout the tumor, thereby enhancing anti-tumor activity. The T1 mutation, a single Adenine insertion at position 445 of the nucleotide sequence of the E3/19K gene of Adenovirus, creates a truncated E3/19K protein that is relocated to the plasma membrane due to the disruption of its ER retention signal. This increases plasma membrane permeability and enhances the release of Ad5.

• Oncolytic herpes simplex virus-1 oncr-177 - A recombinant, genetically modified, microRNA (miRNA)-attenuated oncolytic viral strain of the herpes simplex type 1 (HSV-1) virus, with potential oncolytic, immunostimulating and antineoplastic activities. In ONCR-177, a dual bidirectional promoter enables the expression of five different transgenes: the natural killer (NK) cell and T-cell activating cytokine interleuin-12 (IL-12), the chemokines C-C motif chemokine 4 (CCL4) and the extracellular domain of the Fms-related tyrosine kinase 3 ligand (FLT3LG), to allow for expansion and recruitment of classical dendritic cells (DCs), and antagonists to the immune checkpoints programmed cell death protein-1 (PD-1) and cytotoxic T-lymphocyte-associated antigen 4 (CTLA-4) to counter T cell exhaustion. Upon intra-tumoral administration, the oncolytic HSV-1 ONCR-177 specifically targets, infects and selectively replicates in tumor cells only while not infecting normal, healthy cells. This induces tumor cell lysis. The released virus particles then infect and replicate in neighboring tumor cells, thereby further killing tumor cells. The released tumor-associated antigens (TAAs) from the tumor cells activate the immune system to exert an anti-tumor immune response against the tumor cells, thereby further killing the tumor cells. In addition, the expressed transgenes that are released upon tumor cell lysis induce a systemic tumor-specific immune response and activate NKs, DCs and cytotoxic T-lymphocytes (CTLs) while inhibiting regulatory T-cells (Tregs). This further kills nearby non-infected tumor cells. In ONCR-177, the neurovirulence gene ICP34.5 allows for potent oncolysis, even in the presence of host cell antiviral responses. To ensure selective replication and oncolysis in cancer cells while attenuating replication in healthy tissue, tissue specific miRNA-binding cassettes (miR-T) are inserted into early genes essential for viral replication. In addition, UL37 mutation suppresses latent infection.

• Oncolytic herpes simplex virus-1-encoding gm-csf - An ICP34.5-, ICP47-deleted, oncolytic herpes simplex type-1 virus (HSV-1) isolated from the mouth of an HSV-1-infected patient of Chinese Han ethnicity, and encoding the immunostimulating factor cytokine granulocyte-macrophage colony stimulating factor (GM-CSF) with potential immunostimulating and antineoplastic activities. Upon administration, the recombinant human GM-CSF HSV-1 selectively infects and replicates in tumor cells, thereby inducing tumor cell lysis. In addition, GM-CSF attracts dendritic cells (DCs) and may stimulate a cytotoxic T cell response against tumor cells, which results in immune-mediated tumor cell death. Deletion of the gene encoding for ICP34.5 provides tumor selectivity and prevents replication in healthy cells. As ICP47 blocks antigen presentation in HSV-infected cells, deletion of this gene may induce a more potent antitumor immune response in the tumor cells. Additionally, deletion of ICP47 causes increased expression of the HSV US11 gene and allows US11 to be expressed as an immediate early and not a late gene. This further enhances the degree of viral replication and oncolysis of tumor cells. Interruption of the ICP6 gene, which encodes the large subunit of the viral ribonucleotide reductase, in the viral vector also enhances selective replication in tumor cells.

• Oncolytic hsv-1 c134 - A neurovirulent, oncolytic second-generation, replication-competent, recombinant and genetically-engineered herpes simplex virus type 1 (HSV-1) where the gene for ICP34.5 has been deleted and the gene encoding the human cytomegalovirus (HCMV), protein kinase R (PKR) evasion protein IRS1, with potential oncolytic and immunostimulating activities. Upon intratumoral administration, oncolytic HSV-1 C134 specifically infects and replicates within the rapidly dividing, glioma cells, thereby directly lysing tumor cells. The released virus particles, in turn, infect and replicate in neighboring tumor cells, thereby further killing tumor cells. Tumor antigens released from the lysed tumor cells also activate the immune system to induce a tumor-specific systemic immune and cytotoxic T-lymphocyte (CTL) response, thereby killing nearby non-infected tumor cells. Deletion of the gene encoding for ICP34.5 imparts tumor selectivity by preventing replication in healthy cells. IRS1 expression allows the virus to replicate within tumors but limits viral spread.

• Oncolytic hsv-1 expressing il-12 and anti-pd-1 antibody t3011 - A genetically engineered oncolytic herpes simplex virus type 1 (oHSV-1) expressing the human immunostimulating cytokine interleukin-12 (IL-12) and an antibody directed against the negative immunoregulatory human cell receptor programmed cell death protein 1 (PD-1; PDCD1; CD279), with potential immune checkpoint inhibitory and antineoplastic activities. Upon intratumoral administration, oHSV-1 expressing IL-12 and anti-PD-1 antibody T3011 infects and replicates in tumor cells causing viral-mediated tumor cell lysis. The released virus particles, in turn, infect and replicate in neighboring tumor cells. Tumor antigens released from the lysed tumor cells also activate the immune system to induce a tumor-specific systemic immune and cytotoxic T-lymphocyte (CTL) response, thereby killing nearby non-infected tumor cells. In addition, oHSV-1 expressing IL-12 and anti-PD-1 antibody T3011 promotes the secretion of IL-12 and anti-PD-1 antibody by the tumor cells. IL-12 promotes the activation of natural killer cells, which induces both the secretion of interferon-gamma and a cytotoxic T-lymphocyte (CTL) response against the tumor cells. This results in both immune-mediated tumor cell death and further inhibition of tumor cell proliferation. Anti-PD-1 antibody targets, binds to and inhibits PD-1 and its downstream signaling pathways. This may restore immune function through the activation of T-cells and T-cell-mediated immune responses against tumor cells. PD-1, a transmembrane protein in the immunoglobulin superfamily (IgSF) expressed on T-cells, functions as an immune checkpoint that negatively regulates T-cell activation and effector function when activated by its ligands programmed cell death-1 ligand 1 (PD-L1) or 2 (PD-L2); it plays an important role in tumor evasion from host immunity.

• Oncolytic hsv-1 g207 - A neuroattenuated, replication-competent, recombinant herpes simplex virus-1 (HSV-1) with potential oncolytic activity. Upon intracerebral administration, oncolytic HSV-1 G207 preferentially replicates within glioma cells, which may elicit tumor-specific systemic immune and cytotoxic T lymphocyte (CTL) responses in addition to direct cytopathic effects. Derived from wild-type HSV-1 strain F, this agent has been neuroattenuated by deletions in both copies of the gamma34.5 gene, the major determinant of HSV neurovirulence. In addition, the HSV-1 gene UL39, encoding the viral ribonucleotide reductase large subunit infected cell protein 6 (ICP6), has been inactivated through the insertion of the Escherichia coli lacZ gene. By inactivating UL39, viral ribonucleotide reductase activity is disrupted, resulting in the inhibition of nucleotide metabolism and viral DNA synthesis in nondividing cells but not in dividing cells.

• Oncolytic hsv-1 nv1020 - A genetically engineered oncolytic virus with potential antineoplastic property. NV1020 is constructed from the herpes simplex virus 1 (HSV-1) by the deletion of a single copy of the gamma (1)34.5 gene and the substitution of the UL23 region of the thymidine kinase (tk) gene with a DNA fragment from HSV-2, thereby resulting in a replication-competent, attenuated virus. This modified virus preferentially transfects rapidly dividing cells, which causes cell lysis in tumor cells. NV1020 has shown reduced virulence against normal tissues and a decreased neurovirulence in comparison with some other modified HSV strains.

• Oncolytic hsv-1 rqnestin34.5v.2 - A neuroattenuated, replication-competent, recombinant and genetically-engineered herpes simplex virus type 1 (HSV-1), with potential oncolytic and immunostimulating activities. In rQNestin34.5v.2, the UL39 gene encoding for the viral ribonucleotide reductase large subunit infected cell protein 6 (ICP6) and both endogenous copies of the gamma34.5 gene that encodes for the RL1 neurovirulence protein infected cell protein 34.5 (ICP34.5), which is needed for robust viral growth in an infected cell, are deleted, and one copy of the gamma34.5 gene is reinserted under control of a nestin promoter, which is selectively activated in gliomas. Upon intratumoral administration, oncolytic HSV-1 rQNestin34.5v.2 preferentially infects and replicates within the rapidly dividing, glioma cells, thereby directly lysing tumor cells. The released virus particles, in turn, infect and replicate in neighboring tumor cells, thereby further killing tumor cells. rQNestin34.5v.2 also elicits a tumor-specific systemic immune and cytotoxic T-lymphocyte (CTL) response, thereby killing nearby non-infected tumor cells. By inactivating UL39, viral ribonucleotide reductase activity is disrupted, resulting in the inhibition of nucleotide metabolism and viral DNA synthesis in non-dividing, healthy cells but not in dividing cells. Glioma-selective expression of ICP34.5 imparts tumor selectivity by preventing replication in healthy cells.

• Oncolytic hsv-1 rrp450 - A gene therapy agent containing an attenuated, replication-competent, genetically engineered mutant form of the Herpes simplex virus 1 (HSV-1) strain KOS with potential antineoplastic activity. Upon infusion into the hepatic artery, oncolytic HSV-1 rRp450 replicates in hepatocellular carcinoma (HCC) cells and exerts direct cytotoxic effects eventually disrupting cancer cell membranes and liberating progeny virions thereby infecting adjacent tumor cells. In addition, rRp450 expresses the cytochrome P450 transgene that activates oxazaphosphorines, such as cyclophosphamide (CPA). Therefore, CPA can become activated in the presence of rRp450 and exert its antineoplastic effect. rRp450 is deleted for the HSV-1 gene UL39, encoding the viral ribonucleotide reductase large subunit infected cell protein 6 (ICP6), thereby disrupting the activity of viral ribonucleotide reductase and resulting in the inhibition of nucleotide metabolism and viral DNA synthesis in nondividing cells but not in dividing cells. UL39 is replaced by the rat CYP2B1 gene, encoding a cytochrome P450 enzyme that activates oxazaphosphorines. rRp450 also expresses viral thymidine kinase, which activates the cancer prodrug ganciclovir.

• Oncolytic hsv1716 - A neuroattenuated, replication-restricted, ICP34.5 deleted (RL1 gene)-mutant herpes simplex virus (HSV) type I, constructed from wild-type strain 17, with potential oncolytic activity. Upon intratumoral injection, oncolytic HSV1716 transfects, replicates in, and lyses rapidly dividing cells such as tumor cells. Because the RL1 gene is deleted, HSV1716 is unable to replicate in non-dividing cells.

• Oncolytic measles virus encoding helicobacter pylori neutrophil-activating protein - An attenuated oncolytic Edmonston (Ed) strain of measles virus (MV) encoding the N-terminus of the human lambda immunoglobulin light chain containing the Helicobacter pylori neutrophil-activating protein (NAP), with potential immunostimulating and antineoplastic activities. Upon administration, the oncolytic measles virus encoding H. pylori NAP selectively infects and replicates in tumor cells, leading to syncytia formation and tumor cell lysis. The expressed NAP, a toll-like receptor-2 (TLR2) agonist, may stimulate the secretion of proinflammatory cytokines such as tumor necrosis factor-alpha (TNF-a), interleukin (IL)-1 and IL-6, leading to local inflammatory reaction in the tumor microenvironment (TME). H. pylori NAP, a bacterial antigen and potent immunomodulator, may enhance the antitumor effect of oncolytic MV.

• Oncolytic measles virus encoding thyroidal sodium iodide symporter - An attenuated oncolytic Edmonston (Ed) strain of measles virus encoding the human thyroidal sodium iodide symporter (MV-NIS) with potential antineoplastic activity. The cellular receptor of MV is human CD46 antigen, a type 1 integral membrane glycoprotein found on nearly all human tissues and overexpressed on many cancer cell types. After attachment to and fusion of host cell membranes, MV-NIS induces syncytia and cell lysis. When combined with radioiodine 123 (I-123), expressed NIS facilitates uptake of I-123 into MV-infected cells, thereby allowing for noninvasive imaging of viral gene expression. MV-NIS also enhances the oncolytic activity of MV against radiosensitive tumor cells by additional destruction of the MV-infected cells when using iodine-131.

• Oncolytic newcastle disease virus medi5395 - An oncolytic viral agent containing the oncolytic, live-attenuated, replication-competent strain of the avian paramyxovirus Newcastle disease virus (NDV) that has been engineered to include a transgene encoding granulocyte-macrophage colony-stimulating factor (GM-CSF), with potential antineoplastic and immunostimulating activities. Upon administration, MEDI5395 specifically infects and replicates in cancer cells. This may result in a direct cytotoxic effect involving the lysis of tumor cells via apoptotic mechanisms and may eventually lead to an inhibition of cancer cell proliferation through the increased production and secretion of pro-inflammatory cytokines and chemokines which are able to recruit mediators of both the innate and adaptive immune responses. Additionally, the inclusion of the GM-CSF transgene in the viral construct leads to expression of GM-CSF, which may potentiate and strengthen the anti-tumor immune response.

• Oncolytic newcastle disease virus mth-68h - An oncolytic viral agent containing the oncolytic, live-attenuated strain of the paramyxovirus Newcastle disease virus (NDV), with potential antineoplastic activity. Upon administration, NDV MTH-68H specifically infects and replicates in cancer cells. This may result in a direct cytotoxic effect involving the lysis of tumor cells via apoptotic mechanisms and may eventually lead to an inhibition of cancer cell proliferation.

• Oncolytic newcastle disease virus strain pv701 - An attenuated, replication-competent, oncolytic strain of Newcastle disease virus. PV701 selectively lyses tumor cells. The selectivity of this agent is related to defects in the interferon-mediated antiviral response found in tumor cells.

• Oncolytic type 2 herpes simplex virus expressing granulocyte macrophage colony-stimulating factor oh2 - A genetically engineered, ICP34.5- and ICP47-deleted oncolytic human herpes simplex type-2 virus (HSV-2), derived from the HG52 strain, encoding the immunostimulating factor cytokine granulocyte-macrophage colony stimulating factor (GM-CSF), with potential immunostimulating and antineoplastic activities. Upon administration, the oncolytic HSV-2 expressing GM-CSF OH2 selectively infects and replicates in tumor cells, thereby inducing tumor cell lysis. In addition, GM-CSF attracts dendritic cells (DCs) and may stimulate a cytotoxic T cell response against tumor cells, which results in immune-mediated tumor cell death. Deletion of the gene encoding for ICP34.5 provides tumor selectivity and prevents replication in healthy cells. As ICP47 blocks antigen presentation in HSV-infected cells, deletion of this gene may induce a more potent antitumor immune response in the tumor cells. Additionally, deletion of ICP47 causes increased expression of the HSV US11 gene and allows US11 to be expressed as an immediate early and not a late gene. This further enhances the degree of viral replication and oncolysis of tumor cells. Mutation of the ICP6 gene, which encodes the large subunit of the viral ribonucleotide reductase, in the viral vector also enhances selective replication in tumor cells.

• Oncolytic virus asp9801 - An engineered oncolytic virus with potential antineoplastic and immunomodulating activities. Upon intratumoral injection of ASP-9801, the oncolytic virus selectively targets and replicates in cancer cells without being able to infect and replicate in normal, healthy cells. This induces selective oncolytic virus-mediated cytotoxicity in cancer cells, which leads to cancer cell lysis. Following the lysis of infected cells, the replicated virus is released and can infect adjacent tumor cells, which both induces further tumor cell oncolysis and may activate the immune system to exert an anti-tumor immune response against the tumor cells.

• Oncolytic virus rp1 - A genetically modified oncolytic viral strain of the herpes simplex type 1 (HSV-1) virus, with potential oncolytic, immunostimulating and antineoplastic activities. Upon administration, the oncolytic virus RP1 specifically targets, infects and replicates in tumor cells only while not infecting normal, healthy cells. This induces tumor cell lysis. The released virus particles, infect and replicate in neighboring tumor cells, thereby further killing tumor cells. The released tumor-associated antigens (TAAs) from the tumor cells activate the immune system to exert an anti-tumor immune response against the tumor cells, thereby further killing the tumor cells. The virus itself also elicits a tumor-specific systemic immune and cytotoxic T-lymphocyte (CTL) response, thereby killing nearby non-infected tumor cells. In RP1, ICP34.5 and 47 proteins of the HSV1 strain have been deleted; RP1 expresses a fusogenic protein for optimal tumor cell infection and killing.

• Ontorpacept - A soluble recombinant antibody-like fusion protein composed of the N-terminal CD47 binding domain of human signal-regulatory protein alpha (SIRPa) linked to the Fc domain of human immunoglobulin G1 (IgG1), with potential immune checkpoint inhibitory and antineoplastic activities. Upon administration, ontorpacept selectively targets and binds to CD47 expressed on tumor cells and blocks the interaction of CD47 with endogenous SIRPa, a cell surface protein expressed on macrophages. This prevents CD47/SIRPa-mediated signaling and abrogates the CD47/SIRPa-mediated inhibition of macrophage activation and phagocytosis of cancer cells. This induces pro-phagocytic signaling mediated by the binding of calreticulin (CRT), which is specifically expressed on the surface of tumor cells, to low-density lipoprotein (LDL) receptor-related protein-1 (LRP-1), expressed on macrophages, and results in macrophage activation and the specific phagocytosis of tumor cells. CD47, also called integrin-associated protein (IAP), is a tumor-associated antigen (TAA) expressed on normal, healthy hematopoietic stem cells (HSC) and overexpressed on the surface of a variety of cancer cells. Expression of CD47, and its interaction with SIRPa, leads to the inhibition of macrophage activation and protects cancer cells from phagocytosis, thereby allowing cancer cells to proliferate.

• Ontuxizumab - A humanized IgG1 monoclonal antibody directed against human endosialin/TEM1 (tumor endothelial marker;CD248) with potential anti-angiogenic and antineoplastic activities. Ontuxizumab binds to and inhibits the activity of cell surface protein endosialin/TEM1, which may result in the inhibition of angiogenesis, tumor cell proliferation and metastasis. Endosialin/TEM1 plays a key role in angiogenesis and may be overexpressed on tumor stromal cells and endothelial cells.

• Onvansertib - An orally bioavailable, adenosine triphosphate (ATP) competitive inhibitor of polo-like kinase 1 (PLK1; PLK-1; STPK13), with potential antineoplastic activity. Upon administration, onvansertib selectively binds to and inhibits PLK1, which disrupts mitosis and induces selective G2/M cell-cycle arrest followed by apoptosis in PLK1-overexpressing tumor cells. PLK1, named after the polo gene of Drosophila melanogaster, is a serine/threonine kinase that is crucial for the regulation of mitosis, and plays a key role in tumor cell proliferation. PLK1 expression is upregulated in a variety of tumor cell types and high expression is associated with increased aggressiveness and poor prognosis.

• Onvatilimab - A human monoclonal antibody against the protein V-domain immunoglobulin (Ig) suppressor of T-cell activation (VISTA; programmed death 1 homolog; PD1H; PD-1H), with potential negative checkpoint regulatory and antineoplastic activities. Upon administration, onvatilimab targets and binds to VISTA. This inhibits VISTA signaling, abrogates the VISTA-induced suppression of T-lymphocyte-mediated immune responses, enhances cytotoxic T-cell responses against tumor cells and inhibits tumor cell growth. VISTA, mainly expressed on hematopoietic cells, plays a key role in immunosuppression.

• Opaganib - An orally available, aryladamantane compound and selective inhibitor of sphingosine kinase-2 (SK2) with potential antineoplastic activity. Upon administration, opaganib competitively binds to and inhibits SK2, thereby preventing the phosphorylation of the pro-apoptotic amino alcohol sphingosine to sphingosine 1-phosphate (S1P), the lipid mediator that is pro-survival and critical for immunomodulation. This may eventually lead to the induction of apoptosis and may result in an inhibition of cell proliferation in cancer cells overexpressing SK2. SK2 and its isoenzyme SK1 are overexpressed in numerous cancer cell types.

• Opcs/green tea/spirullina/curcumin/antrodia camphorate/fermented soymilk extract capsule - A capsule containing a fermented soymilk extract and oligomeric proanthocyanidins (OPCs), green tea, spirullina, curcumin and antrodia camphorate powder, with potential antioxidant, immunomodulating, anti-infective and anti-cancer activities. OPCs/green tea/spirullina/curcumin/antrodia camphorate/fermented soymilk extract capsule may boost the immune system and may alleviate fatigue and poor appetite in cancer chemotherapy patients.

• Opioid growth factor - An endogenous pentapeptide with potential antineoplastic and antiangiogenic activities. Opioid growth factor (OGF) binds to and activates the OGF receptor, present on some tumor cells and vascular cells, thereby inhibiting tumor cell proliferation and angiogenesis. (NCI05)

• Opolimogene capmilisbac - A proprietary, live-attenuated, double-deleted (LADD) strain of the Gram-positive bacterium Listeria monocytogenes (Lm) encoding multiple, as of yet undisclosed, tumor-associated antigens (TAAs), with potential immunostimulatory and antineoplastic activities. Upon intravenous administration, opolimogene capmilisbac is taken up by antigen-presenting cells (APCs), including dendritic cells (DCs). The TAAs are subsequently expressed by the APCs and then processed and presented to the immune system by both major histocompatibility complex (MHC) class I and II molecules. This activates the immune system and leads to the recruitment and activation of cytotoxic T-lymphocytes (CTLs) against the TAA-expressing tumor cells, eventually resulting in tumor cell lysis. Two genes contributing to the virulence of Lm have been removed to minimize the risk of infection.

• Oportuzumab monatox - A fusion protein immunotoxin consisting of a humanized, single-chain monoclonal antibody fragment specific for the epithelial cell adhesion molecule (EpCAM) conjugated with a truncated form of Pseudomonas exotoxin A with potential antineoplastic activity. Oportuzumab monatox binds to Ep-CAM-positive tumor cells, thereby delivering the Pseudomonas exotoxin A moiety specifically; the Pseudomonas exotoxin A moiety then inactivates elongation factor 2 (EF-2) through ADP ribosylation, resulting in inhibition of protein synthesis in target cells. EpCAM, a cell surface protein, is expressed by a variety of tumor cells and is frequently found in head and neck cancers.

• Oprozomib - An orally bioavailable proteasome inhibitor with potential antineoplastic activity. Proteasome inhibitor ONX 0912 inhibits the activity of the proteasome, thereby blocking the targeted proteolysis normally performed by the proteasome; this may result in an accumulation of unwanted or misfolded proteins. Disruption of various cell signaling pathways may follow, eventually leading to the induction of apoptosis and inhibition of tumor growth. Proteasomes are large protease complexes that degrade unneeded or damaged proteins that have been ubiquitinated.

• Opucolimab - A recombinant human monoclonal antibody directed against the immunosuppressive ligand programmed cell death-1 ligand 1 (PD-L1; cluster of differentiation 274; CD274), with potential immune checkpoint inhibitory and antineoplastic activities. Upon administration, opucolimab specifically targets and binds to PD-L1, blocking its binding to and activation of its receptor programmed cell death 1 (PD-1; cluster of differentiation 279; CD279). This reverses T-cell inactivation caused by PD-1/PD-L1 signaling and enhances the cytotoxic T-lymphocyte (CTL)-mediated anti-tumor immune response against PD-L1-expressing tumor cells. PD-L1 is overexpressed by many human cancer cell types. PD-L1 binding to PD-1 on T-cells suppresses the immune system and results in immune evasion. PD-1, a transmembrane protein belonging to the immunoglobulin superfamily (IgSF) expressed on activated T-cells, is a negative regulator of the immune system that limits the expansion and survival of CD8-positive T-cells.

• Oral aminolevulinic acid hydrochloride - A powder for an oral solution comprised of the hydrochloride salt of 5-aminolevulinic acid (ALA) with a potential application for photodynamic therapy. After oral administration, ALA is converted intracellularly into the photosensitizer protoporphyrin IX (PpIX). Upon exposure to light of appropriate wavelength (violet to blue range), excited PpIX emits a characteristic red fluorescence which could facilitate guided resection, and generates excited singlet oxygen molecules that could kill cells when appropriate laser dosage is applied. ALA is preferentially taken up by and accumulates in many types of cancer cells compared to normal, healthy cells. Consequently, cancer cells can be visualized and can be distinguished from normal, healthy cells.

• Oral azacitidine - An orally bioavailable formulation of azacitidine, a pyrimidine nucleoside analogue of cytidine, with antineoplastic activity. Upon oral administration, azacitidine is taken up by cells and metabolized to 5-azadeoxycitidine triphosphate. The incorporation of 5-azadeoxycitidine triphosphate into DNA reversibly inhibits DNA methyltransferase, and blocks DNA methylation. Hypomethylation of DNA by azacitidine may re-activate tumor suppressor genes previously silenced by hypermethylation, resulting in an antitumor effect. In addition, the incorporation of 5-azacitidine triphosphate into RNA disrupts normal RNA function and impairs tRNA (cytosine-5)-methyltransferase activity, resulting in an inhibition of RNA and protein synthesis.

• Oral cancer vaccine v3-ova - An orally available cancer vaccine composed of autologous ovarian cancer antigens obtained from hydrolyzed, inactivated blood and tumor tissue of patients with ovarian cancer, with potential immunostimulatory and antineoplastic activities. Upon oral administration of the oral cancer vaccine V3-OVA, the ovarian cancer antigens stimulate the immune system and activate a cytotoxic T-lymphocyte (CTL) immune response against ovarian cancer cells.

• Oral docetaxel - An oral proprietary P-glycoprotein (P-gp) pump inhibitor-based formulation containing the taxane docetaxel, a semisynthetic analogue of paclitaxel, and a P-gp pump inhibitor, with potential antineoplastic activity. Upon administration of oral docetaxel, the P-gp pump inhibitor moiety, which is not absorbed, binds to the P-gp pump in the gastrointestinal (GI) tract and prevents the P-gp pump-mediated efflux of docetaxel from cells the docetaxel has been internalized by back into the GI tract. This decreases P-gp-mediated excretion and enhances absorption of docetaxel. Upon absorption, docetaxel binds specifically to the beta-tubulin subunit of the microtubule, stabilizes tubulin and inhibits microtubule disassembly, which results in cell-cycle arrest at the G2/M phase and cell death. The P-gp pump inhibitor enhances the bioavailability of certain poorly bioavailable agents and thereby allows oral administration of those agents. P-gp, an efflux membrane transporter, plays a key role in active drug export, and prevents cellular uptake and accumulation of certain substances.

• Oral fludarabine phosphate - An oral formulation of the phosphate salt of fludarabine, a synthetic purine nucleoside analogue antimetabolite with antineoplastic activity. Fudarabine is preferentially transported into malignant cells and metabolized by deoxycytidine kinase to its active form, 2-fluoro-ara-ATP; 2-fluoro-ara-ATP competes directly with deoxyadenosine triphosphate (dATP) and inhibits alpha DNA polymerase, RNA reductase, and DNA primase, which may result in inhibition of DNA synthesis and cell death.

• Oral hsp90 inhibitor ipi-493 - An orally bioavailable formulation of the ansamycin derivative 17-amino-17-demethoxygeldanamycin (17-AG) with potential antineoplastic activity. Oral Hsp90 inhibitor IPI-493 binds to and inhibits Hsp90, which may result the in growth inhibition in sensitive tumor cell populations. Hsp90, a 90 kDa molecular chaperone, may be highly expressed in tumor cells, playing a key role in the conformational maturation, stability and function of other substrate or "client" proteins within the cell; many of these client proteins are involved in signal transduction, cell cycle regulation and apoptosis, and may include kinases, transcription factors and hormone receptors.

• Oral ixabepilone - An enteric-coated formulation of ixabepilone, a semisynthetic analogue of epothilone B and a non-taxane tubulin inhibitor, with antineoplastic activity. Ixabepilone binds to and stabilizes tubulin molecules, thereby interfering with the dynamics of microtubule assembly/disassembly. This results in cell cycle arrest at the G2-M phase and leads to apoptosis within fast growing tumor cells. This agent demonstrates antineoplastic activity against taxane-resistant cell lines. Compared to intravenously administered ixabepilone, the oral formulation provides a more manageable way to administer this agent.

• Oral microencapsulated diindolylmethane - An orally bioavailable microencapsulated formulation of diindolylmethane, an indole phytonutrient found in cruciferous vegetables, with estrogen-modulating, antiandrogenic, and potential antineoplastic activities. As a dimer of indole-3-carbinol, diindolylmethane (DIM) modulates estrogen balance by reducing the levels of 16-hydroxy estrogen metabolites and increasing the formation of beneficial 2-hydroxy estrogen metabolites. DIM also antagonizes androgen receptor activity, which may result in diminished cell proliferation and apoptosis in susceptible tumor cell populations. Pure DIM, which is relatively hydrophobic, is poorly absorbed after oral administration. This oral formulation, which consists of DIM, d-alpha-tocopheryl acid succinate, phosphatidylcholine, and silica microencapsulated in starch, significantly improves the gastrointestinal absorption of DIM.

• Oral myoma vaccine v3-myoma - An orally available therapeutic myoma vaccine containing pooled antigens derived from hydrolyzed, inactivated blood and tumor tissue samples from patients with uterine myoma, with potential antineoplastic and immunomodulatory activities. Upon oral administration, V3-myoma may stimulate the immune system to mount a cytotoxic T-lymphocyte-mediated response against cells expressing myoma-associated antigens. This may reduce the myoma growth and improve myoma-related symptoms.

• Oral pancreatic cancer vaccine v3-p - An orally bioavailable, therapeutic cancer vaccine composed of the carbohydrate antigen sialyl-Lewis A (carbohydrate antigen 19-9; CA19.9; CA19-9) that is derived from pooled blood of pancreatic cancer patients, with potential immunomodulating activity. Upon oral administration of the oral pancreatic cancer vaccine V3-P, the CA19.9 antigens may stimulate the host immune system to mount a cytotoxic T-lymphocyte (CTL)-mediated immune response against pancreatic cancer cells expressing the CA19.9 antigen. CA19.9 is overexpressed on a number of different tumor cell types and plays a key role in tumor cell survival and metastasis.

• Oral picoplatin - An oral preparation of picoplatin, a third generation platinum compound with antineoplastic activity. Designed to overcome platinum drug resistance, picoplatin alkylates DNA, forming both inter- and intra-strand cross-linkages, resulting in inhibition of DNA replication and RNA transcription and the induction of apoptosis. Because of the increase in steric bulk around the platinum center, there is a relative reduction in the inactivation of picoplatin by thiol-containing species such as glutathione and metallothionein in comparison to cisplatin.

• Oral sodium phenylbutyrate - An orally active derivative of the short-chain fatty acid butyrate with potential antineoplastic activity. 4-Phenylbutyrate inhibits histone deacetylase, resulting in cell cycle gene expression modulation, reduced cell proliferation, increased cell differentiation, and apoptosis. This agent also initiates fragmentation of genomic DNA, resulting in decreased DNA synthesis and the inhibition of tumor cell migration and invasion.

• Oral topotecan hydrochloride - An oral formulation of the hydrochloride salt of topotecan, a semisynthetic derivative of the quinoline alkaloid camptothecin, with potential antineoplastic activity. Topotecan selectively inhibits topoisomerase I activity by stabilizing topoisomerase I-DNA covalent complexes during the S phase of the cell cycle, thereby inhibiting religation of topoisomerase I-mediated single-strand DNA breaks and producing potentially lethal double-strand DNA breaks when encountered by the DNA replication machinery.

• Orantinib - An orally bioavailable receptor tyrosine kinase inhibitor. SU6668 binds to and inhibits the autophosphorylation of vascular endothelial growth factor receptor 2 (VEGFR2), platelet-derived growth factor receptor (PDGFR), and fibroblast growth factor receptor (FGFR), thereby inhibiting angiogenesis and cell proliferation. SU6668 also inhibits the phosphorylation of the stem cell factor receptor tyrosine kinase c-kit, often expressed in acute myelogenous leukemia cells.

• Oraxol - A combination formulation composed of a capsule containing the taxane compound paclitaxel and a tablet containing the multidrug resistance (MDR) efflux pump P-glycoprotein (P-gp) inhibitor HM30181A, with potential antineoplastic activity. Upon oral administration of oraxol, the HM30181A moiety binds to and inhibits P-gp, which prevents P-gp-mediated efflux of paclitaxel, therefore enhancing its oral bioavailability. In turn, paclitaxel binds to and stabilizes microtubules, preventing their depolymerization, which results in the inhibition of cellular motility, mitosis, and replication. Altogether, this may result in greater intracellular concentration of paclitaxel, and enhanced cytotoxicity against tumor cells, when compared to the administration of paclitaxel alone. P-gp, encoded by the MDR-1 gene, is a member of the ATP-binding cassette (ABC) superfamily of transmembrane transporters; it prevents the intestinal uptake and intracellular accumulation of various cytotoxic agents.

• Oregovomab - A murine monoclonal antibody that attaches to the tumor-associated antigen CA125. Vaccination with monoclonal antibody B43.13 may stimulate a host cytotoxic immune response against tumor cells that express CA125.

• Orelabrutinib - A small molecule inhibitor of Bruton's tyrosine kinase (BTK; Bruton agammaglobulinemia tyrosine kinase) with potential antineoplastic activity. Upon administration, orelabrutinib binds to and inhibits the activity of BTK. This prevents both the activation of the B-cell antigen receptor (BCR) signaling pathway and BTK-mediated activation of downstream survival pathways, inhibiting the growth of malignant B-cells that overexpress BTK. BTK, a member of the Src-related BTK/Tec family of cytoplasmic tyrosine kinases, is overexpressed or mutated in B-cell malignancies; it plays an important role in the development, activation, signaling, proliferation and survival of B-lymphocytes.

• Ormaplatin - A platinum(IV) analogue with antineoplastic activity. Ormaplatin alkylates DNA, forming both inter- and intra-strand platinum-DNA crosslinks, which result in inhibition of DNA replication and transcription and cell-cycle nonspecific cytotoxicity.

• Ortataxel - A semisynthetic, second-generation taxane derivative with potential antineoplastic activity. Ortataxel binds to and stabilizes tubulin molecules, thereby interfering with the dynamics of microtubule assembly/disassembly. This results in the inhibition of cell division and cellular proliferation. As it represents a poor substrate for P-glycoprotein (P-gp), multi-drug resistance protein (MRP-1) and breast cancer resistance protein (BCRP) mediated efflux, ortataxel modulates multi-drug resistance mechanisms and may be useful for treating multi-drug resistant tumors that express Pgp, MRP-1 and BCRP.

• Orteronel - An orally bioavailable non-steroidal androgen synthesis inhibitor of steroid 17alpha-monooxygenase (17,20 lyase) with potential antiandrogen activity. TAK-700 binds to and inhibits the steroid 17alpha-monooxygenase in both the testes and adrenal glands, thereby inhibiting androgen production. This may decrease androgen-dependent growth signaling and may inhibit cell proliferation of androgen-dependent tumor cells. The cytochrome P450 enzyme CYP17A1 (P450C17), localized to the endoplasmic reticulum (ER), exhibits both 17alpha-hydroxylase and 17,20-lyase activities, and plays a key role in the steroidogenic pathway that produces steroidal hormones, such as progestins, mineralocorticoids, glucocorticoids, androgens, and estrogens.

• Orvacabtagene autoleucel - A preparation of autologous CD4- and CD8-positive T-lymphocytes that have been ex vivo transduced with a genetically-engineered lentiviral vector (LV) expressing a chimeric antigen receptor (CAR) containing a single chain variable fragment (scFv) specific for the tumor-associated antigen (TAA) human B-cell maturation antigen (BCMA; tumor necrosis factor receptor superfamily member 17; TNFRSF17) fused to the co-stimulatory domain of 4-1BB (CD137) and the CD3-zeta (CD3z) T-cell signaling domain, with potential immunostimulating and antineoplastic activities. Upon administration, orvacabtagene autoleucel specifically recognize and induce selective toxicity in BCMA-expressing tumor cells. BCMA, a tumor-specific antigen and 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) and plays a key role in plasma cell survival. BCMA is found on the surfaces of plasma cells and overexpressed on malignant plasma cells.

• Osilodrostat - An orally bioavailable inhibitor of both steroid 11beta-hydroxylase (cytochrome P450 (CYP) 11B1) and aldosterone synthase (CYP11B2; steroid 18-hydroxylase), with potential anti-adrenal activity and ability to treat Cushing disease (CD). Upon administration, osilodrostat binds to and inhibits the activity of CYP11B1, the enzyme that catalyzes the final step of cortisol synthesis from the precursor 11-deoxycortisol, and CYP11B2, the enzyme that catalyzes aldosterone synthesis from corticosterone and 11-deoxycorticosterone in the adrenal gland. The inhibition of CYP11B1 prevents the production of excess cortisol, thereby decreasing and normalizing the levels of cortisol. CD is most often caused by an adrenocorticotropic hormone (ACTH)-secreting pituitary tumor.

• Osimertinib - A third-generation, orally available, irreversible, mutant-selective, epidermal growth factor receptor (EGFR) inhibitor, with potential antineoplastic activity. Upon oral administration, osimertinib covalently binds to and inhibits the activity of mutant forms of EGFR, including the T790M EGFR mutant, thereby preventing EGFR-mediated signaling. This may both induce cell death and inhibit tumor growth in EGFR-overexpressing tumor cells. EGFR, a receptor tyrosine kinase mutated in many tumor cell types, plays a key role in tumor cell proliferation and tumor vascularization. AZD9291 preferentially inhibits mutated forms of EGFR including T790M, a secondarily-acquired resistance mutation, and may have enhanced anti-tumor effects in tumors with T790M-mediated resistance when compared to other EGFR tyrosine kinase inhibitors. As this agent is selective towards mutant forms of EGFR, its toxicity profile may be reduced when compared to non-selective EGFR inhibitors which also inhibit wild-type EGFR.

• Otlertuzumab - A recombinant single-chain polypeptide engineered to exhibit the full binding and activity of an anti-CD37 monoclonal antibody with potential immunostimulatory and antineoplastic activities. Otlertuzumab binds to CD37 on B-cells, which may result in antibody-dependent cell-mediated cytotoxicity (ADCC) and apoptosis. CD37 is a transmembrane glycoprotein expressed at high-levels on B cells and to a lesser extent on T cells and myeloid cells. This agent may have a longer half-life in vivo than conventional monoclonal antibodies.

• Ovapuldencel-t - A cancer vaccine consisting of autologous dendritic cells (DCs) loaded with autologous, lethally irradiated cancer cells and mixed with the cytokine granulocyte-macrophage colony stimulating factor (GM-CSF), with potential immunostimulatory and antineoplastic activities. Upon vaccination, ovapuldencel-T may stimulate the immune system to exert a cytotoxic T-lymphocyte (CTL) immune response against the repertoire of tumor associated antigens (TAAs) found in the irradiated cancer cells. GM-CSF enhances the activation of dendritic cells (DCs) and promotes antigen presentation to both B- and T-lymphocytes.

• Ovarian cancer peptide vaccine - A cancer vaccine comprised of synthetic peptides corresponding to naturally-occurring peptides derived from ovarian cancer cell antigens. Ovarian cancer peptide vaccine may elicit a cytotoxic T-cell response against tumor cells expressing the related ovarian cancer cell antigens. (NCI05)

• Ovarian cancer stem cell/htert/survivin mrnas-loaded autologous dendritic cell vaccine dc-006 - A cancer vaccine containing autologous dendritic cells (DCs) that are transfected with mRNAs extracted from amplified ovarian cancer stem cells, and mRNAs of the universal tumor antigens human telomerase reverse transcriptase (hTERT) and survivin with potential immunostimulatory and antineoplastic activities. Upon administration, ovarian cancer stem cell/hTERT/survivin mRNAs-loaded autologous DC-006 vaccine may elicit a highly specific cytotoxic T-cell (CTL) response against ovarian cancer cells expressing hTERT, survivin, and specific ovarian cancer stem cell antigens. hTERT, the catalytic subunit of human telomerase, and survivin, a member of the inhibitor of apoptosis (IAP) family of proteins, may be upregulated in certain tumor cell types, playing key roles in tumor cell growth and survival. Ovarian cancer stem cells contain a specific range of antigens that are essential for the neoplastic growth and survival of ovarian cancer cells.

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

• Ovine submaxillary mucin - A naturally occurring mucin glycoprotein. Ovine submaxillary mucin (OSM), extracted from an ovine submaxillary gland, provides a rich source of the sialylated Tn antigen (sTn), which is a carbohydrate antigen found on mucins of many epithelial tumors. Vaccination with OSM may result in the production of antibodies as well as elicitation of a cytotoxic T- lymphocyte (CTL) response against tumor cells expressing sTn, thereby results in decreased tumor cell growth.

• Ox40l-expressing oncolytic adenovirus dnx-2440 - A selectively replication competent oncolytic adenovirus that is engineered to express OX40 ligand (OX40L) with potential oncolytic and immunostimulatory activities. Upon administration, OX40L-expressing oncolytic adenovirus DNX-2440, which contains an integrin binding RGD-4C motif, infects tumor cells in a Coxsackievirus-adenovirus receptor-independent manner and selectively replicates in tumor cells that are defective in retinoblastoma gene (Rb) or cyclin-dependent kinase inhibitor-2A (p16). Tumor cell selectivity is achieved through a 24-base pair deletion in the E1A gene, which renders the oncolytic adenovirus unable to replicate in normal cells that maintain a functional Rb pathway, but fully replication competent in Rb/p16 defective tumor cells. Active replication of the OX40L-expressing oncolytic adenovirus DNX-2440 within tumor cells may induce oncolysis and release of OX40L. OX40L may then bind to and activate signaling pathways downstream of its cognate receptor, tumor necrosis factor receptor superfamily member 4 (TNFRSF4; OX40), which is expressed on activated T-cells. OX40L/OX40 binding promotes increased cytokine production, which can induce proliferation of memory and effector T-lymphocytes and promote the killing of nearby tumor cells. OX40L, a cell surface glycoprotein and member of the tumor necrosis factor (TNF) ligand family, provides a co-stimulatory signal for the proliferation and survival of activated T-cells. The Rb gene product and p16 are negative regulators of the cell cycle and are defective in certain tumor types.

• Oxaliplatin - An organoplatinum complex in which the platinum atom is complexed with 1,2-diaminocyclohexane (DACH) and with an oxalate ligand as a 'leaving group.' A 'leaving group' is an atom or a group of atoms that is displaced as a stable species taking with it the bonding electrons. After displacement of the labile oxalate ligand leaving group, active oxaliplatin derivatives, such as monoaquo and diaquo DACH platinum, alkylate macromolecules, forming both inter- and intra-strand platinum-DNA crosslinks, which result in inhibition of DNA replication and transcription and cell-cycle nonspecific cytotoxicity. The DACH side chain appears to inhibit alkylating-agent resistance.

• Oxaliplatin eluting beads - A formulation of drug-eluting beads (DEB) consisting of polymeric microbeads impregnated with the organoplatinum complex and alkylating agent oxaliplatin, with potential antineoplastic activity. The beads consist of polyvinyl alcohol (PVA) microspheres modified with sulfonic acid groups and loaded with oxaliplatin. During transarterial chemoembolization (TACE) in the hepatic artery, the oxaliplatin eluting beads occlude tumor blood vessels that feed the tumor and induce ischemic necrosis of tumor tissue due to mechanical blockage of the tumor vasculature. The beads release cytotoxic oxaliplatin locally, which may result in oxaliplatin-mediated inhibition of tumor cell proliferation through formation of both inter- and intra-strand platinum-DNA crosslinks, and the inhibition of DNA replication.

• Oxaliplatin-encapsulated transferrin-conjugated n-glutaryl phosphatidylethanolamine liposome - A nanoparticle formulation containing N-glutaryl phosphatidylethanolamine (NGPE)-liposomes encapsulating oxaliplatin and conjugated to the human transferrin (Tf) ligand, with potential antineoplastic activity. Upon infusion of oxaliplatin-encapsulated transferrin-conjugated NGPE liposomes, the transferrin moiety targets and binds to the Tf receptor, which is overexpressed on a variety of human cancer cells. Upon binding and internalization, oxaliplatin is released and its active derivatives alkylate macromolecules, forming both inter- and intra-strand platinum-DNA crosslinks, which results in an inhibition of DNA replication and transcription. By extending the circulation time and specifically targeting transferrin receptors, this formulation may improve the efficacy and safety of oxaliplatin therapy, compared to administration of oxaliplatin alone. NGPE, a reactive phospholipid, is used as a linker to attach the Tf ligand, to the liposome.

• Oxeclosporin -

• Oxidative phosphorylation inhibitor iacs-010759 - An orally bioavailable oxidative phosphorylation (OxPhos) inhibitor, with potential antineoplastic activity. Upon administration of the OxPhos inhibitor IACS-010759, this agent binds to and inhibits complex I of the electron transport chain (NADH ubiquinone oxidoreductase), thereby selectively depriving tumor cells of nutrients, and energy, and inhibiting nucleotide and amino acid production, which induces autophagy, causes tumor cell death and inhibits cell proliferation. Mitochondrial complex I, which is hyperactivated in cancer cells to meet their increased demands for energy, plays a key role in the promotion of cancer cell proliferation.

• Oxidative phosphorylation inhibitor im156 - An orally bioavailable biguanide compound and mitochondrial oxidative phosphorylation (OxPhos) inhibitor, with potential antineoplastic activity. Upon administration, IM156 inhibits oxidative phosphorylation, decreases mitochondrial function, prevents tumor cell metabolism and deprives tumor cells of energy, thereby preventing tumor cell proliferation. Mitochondrial OxPhos is overactivated in cancer cells and plays a key role in tumor cell proliferation. Drug resistant tumor cells are very susceptible to decreased mitochondrial OxPhos as they cannot easily compensate for the decrease in mitochondrial function by increasing glycolysis.

• Oxidopamine - An antagonist of the neurotransmitter dopamine with potential antineoplastic activity. 6-Hydroxydopamine (6-HOD) can be taken up by selective adrenergic terminals, thereby causing acute degeneration of adrenergic terminals that leads to depletion of norepinephrine, and of dopamine in the dopamine-sensitive sites. This agent is auto-oxidated at physiological pH that leads to the formation of reactive free radicals, thereby leading to cytotoxicity in neural cells. 6-Hydroxydopamine is often used to induce CNS and sympathetic neural lesions that model aging and various nervous disorders in animal systems.

• Oxphos inhibitor vlx600 - A lipophilic cation-based triazinoindolyl-hydrazone compound and mitochondrial oxidative phosphorylation (OxPhos) inhibitor, with potential antineoplastic activity. Upon infusion, in normal cells and proliferating tumor cells where glucose is readily available, inhibition of OxPhos by VLX600 induces a hypoxia-inducible factor 1-alpha (HIF-1alpha)-dependent shift to, and an increase in glycolysis. Glycolysis alone does not produce enough energy to support the growth of tumor cells in this environment, and the induction of autophagy occurs. In the metabolically compromised tumor microenvironment, the availability of oxygen and glucose is limited due to poor vascularization and perfusion of tumor micro-areas. Tumor cells growing in this environment are thus unable to compensate for decreased mitochondrial function by increasing glycolysis. This leads to nutrient depletion, decreased energy production, induction of autophagy, tumor cell death and an inhibition of cell proliferation in quiescent tumor cells. Mitochondrial OxPhos, which is hyperactivated in cancer cells, plays a key role in the promotion of cancer cell proliferation.

• Ozarelix - A highly modified, fourth generation linear decapeptide with gonadotropin-releasing hormone (GnRH or LHRH) antagonizing properties. Ozarelix competitively binds to and blocks the gonadotropin releasing hormone receptor in the anterior pituitary gland, thereby inhibiting the secretion and release of luteinizing hormone (LH) and follicle stimulating hormone (FSH). In males, the inhibition of LH secretion prevents the release of testosterone. As a result, this may relieve symptoms associated with hormonally dependent disease states such as hormone-dependent prostate cancer.

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