Antineoplastic agents b

• B16alphagal melanoma vaccine - A whole cell melanoma cancer vaccine with potential immunostimulating and antineoplastic activities. B16alphaGal melanoma vaccine contains three types of human melanoma cell lines that are genetically engineered to express the alpha(1,3)-galactosyl (alphaGal) epitope on cell surfaces. The agent stimulates a hyperacute rejection of whole melanoma cancer cells expressing alphaGal epitopes, initiated by opsonization by anti-alphaGal antibodies and followed by antibody-dependent cell-mediated cytotoxicity (ADCC) and cell lysis. This results in the stimulation of a broader cytotoxic T-lymphocyte response (CTL) directed against tumor antigens on melanoma cells that do not express alphaGal. AlphaGal is not normally expressed in humans because alpha(1,3)-galactosyltransferase (Alpha-GT), the enzyme that catalyzes the synthesis of alphaGal epitopes on glycoproteins and glycolipids, is not naturally present in humans and other primates.

• B7 transfected melanoma cell vaccine - An allogenic whole tumor cell vaccine with potential antineoplastic activity. B7 transfected melanoma cell vaccine consists of melanoma cells that have been induced to express the human leukocyte antigen (HLA) B7. Vaccination with these altered cells may elicit an anti-tumor immune response via CD8+ cytotoxic T lymphocytes (CTL).

• Babaodan capsule - An orally available mixed powder of traditional Chinese medicine containing eight constituents including natural calculus bovis, snake gall, antelope horn, pearl, musk, radix notoginseng, and other as of yet not disclosed ingredients, with potential antifibrotic, immunomodulatory, and antineoplastic activities. Upon oral administration, babaodan may ameliorate substance-induced liver injury and fibrosis, and inhibit lipopolysaccharide (LPS)-induced hepatic stellate cell (HSC) activation and proliferation through toll-like receptor 4 (TLR4)/nuclear factor-kappa B and TLR4/extracellular-signal-regulated kinase (ERK) pathways. Babaodan may, through an as of yet not elucidated mechanism, enhance the efficacy of chemotherapeutic drugs and may inhibit the occurrence and development of certain tumor types.

• Bactobolin - A 3-dichloromethylactinobolin antineoplastic antibiotic isolated from various Pseudomonas bacterial species. BN-183 induces apoptosis via a caspase-dependent pathway. This agent also has immunomodulatory properties.

• Baculovirus cea protein vaccine - A vaccine consisting of recombinant carcinoembryonic antigen (CEA) produced by a baculovirus expression system with potential antineoplastic activity. Vaccination with baculovirus CEA protein vaccine may stimulate the host immune system to mount a cytotoxic T lymphocyte (CTL) response against CEA positive cells, resulting in decreased tumor growth. CEA is overexpressed in several cancer cell types, including gastrointestinal, breast, and non-small cell lung cancers.

• Bafetinib - An orally active 2-phenylaminopyrimidine derivative with potential antineoplastic activity. INNO-406 specifically binds to and inhibits the Bcr/Abl fusion protein tyrosine kinase, an abnormal enzyme produced by Philadelphia chromosomal translocation associated with chronic myeloid leukemia (CML). Furthermore, this agent also inhibits the Src-family member Lyn tyrosine kinase, upregulated in imatinib-resistant CML cells and in a variety of solid cancer cell types. The inhibitory effect of INNO-406 on these specific tyrosine kinases decreases cellular proliferation and induces apoptosis. A high percentage of CML patients are refractory to imatinib, which sometimes results from point mutations occurring in the kinase domain of the Bcr/Abl fusion product. Due to its dual inhibitory activity, INNO-406 has been shown to overcome this particular drug resistance and to be a potent and effective agent in the treatment of imatinib-resistant CML.

• Balixafortide - An orally bioavailable inhibitor of CXC chemokine receptor 4 (CXCR4) with receptor binding and hematopoietic stem cell-mobilization activities. Balixafortide binds to the chemokine receptor CXCR4, thereby preventing the binding of stromal derived factor-1 (SDF-1 or CXCL12) to the CXCR4 receptor and subsequent receptor activation. This may induce the mobilization of hematopoietic stem and progenitor cells from the bone marrow into blood. CXCR4, a chemokine receptor belonging to the G protein-coupled receptor (GPCR) gene family, plays an important role in chemotaxis and angiogenesis and is upregulated in several tumor cell types; CXCL12/CXCR4 interaction induces retention of hematopoietic cells in the bone marrow.

• Baloramotide - A genetically engineered synthetic protein, Recombinant NY-ESO-1 Protein (Cancer-Testis Tumor Antigen Family) elicits strong humoral and cellular immune responses to NY-ESO-1-expressing cancers and is used to produce specific vaccines to increase the immune response against tumors. NY-ESO-1 epitopes presented by human HLA are recognized by CD4(+) T lymphocytes in patients with NY-ESO-1-expressing melanoma.

• Balstilimab - A monoclonal antibody directed against the negative immunoregulatory human cell surface receptor programmed cell death 1 (PD-1, PCD-1; PDCD1) protein, with potential immune checkpoint inhibitory and antineoplastic activities. Upon administration, balstilimab binds to PD-1, and thereby blocks its binding to the PD-1 ligand programmed cell death-1 ligand 1 (PD-L1), and prevents the activation of its downstream signaling pathways. This may restore immune function through the activation of cytotoxic T-cells. PD-1, a transmembrane protein in the immunoglobulin superfamily expressed on activated T-cells, negatively regulates T-cell activation and effector function when activated by its ligand; it plays an important role in tumor evasion from host immunity.

• Baltaleucel-t - A preparation of autologous Epstein-Barr virus (EBV)-specific cytotoxic T-lymphocytes (CTLs), which have specific reactivity to the EBV antigens, latent membrane proteins (LMP) 1 (LMP1) and 2 (LMP2), EBV nuclear antigen (EBNA) and BamHI-A rightward frame-1 (BARF1), with potential immunomodulating and antineoplastic activities. Upon administration, baltaleucel-T targets and binds to EBV-expressing cancer cells specifically expressing the targeted antigens. This may kill LMP1/LMP2/EBNA/BARF1-expressing EBV-associated cancer cells. LMP1, LMP2, EBNA and BARF1 are tumor-associated antigens (TAAs) that are specifically associated with EBV infection, and play key roles in the proliferation of a variety of tumors.

• Banoxantrone - A bioreductive, alkylaminoanthraquinone prodrug with antineoplastic activity. Under hypoxic conditions, often seen in solid tumors, banoxantrone (AQ4N) is converted and activated by cytochrome P450 enzymes, which are upregulated in certain tumors, to the cytotoxic DNA-binding agent AQ4. Banoxantrone intercalates into and crosslinks DNA, and inhibits topoisomerase II. This results in an inhibition of DNA replication and repair in tumor cells. Combined with conventional therapeutic agents, both oxygenic and hypoxic regions of tumors can be targeted.

• Barasertib - An orally bioavailable, small-molecule, dihydrogen phosphate prodrug of the pyrazoloquinazoline Aurora kinase inhibitor AZD1152-hydroxyquinazoline pyrazol anilide (AZD1152-HQPA) with potential antineoplastic activity. Upon administration and rapid conversion from the prodrug form in plasma, AZD1152-HQPA specifically binds to and inhibits Aurora kinase B, which results in the disruption of spindle checkpoint functions and chromosome alignment and, so, the disruption of chromosome segregation and cytokinesis. Consequently, cell division and cell proliferation are inhibited and apoptosis is induced in Aurora kinase B-overexpressing tumor cells. Aurora kinase B, a serine/threonine protein kinase that functions in the attachment of the mitotic spindle to the centromere, is overexpressed in a wide variety of cancer cell types.

• Bardoxolone - A synthetic triterpenoid compound with potential antineoplastic and anti-inflammatory activities. Bardoxolone blocks the synthesis of inducible nitric oxide synthase (iNOS) and inducible cyclooxygenase (COX-2), two enzymes involved in inflammation and carcinogenesis. This agent also inhibits the interleukin-1 (IL-1)-induced expression of the pro-inflammatory proteins matrix metalloproteinase-1 (MMP-1) and matrix metalloproteinase-13 (MMP-13) and the expression of Bcl-3; Bcl-3 is an IL-1-responsive gene that preferentially contributes to MMP-1 gene expression.

• Bardoxolone methyl - The methyl ester form of bardoxolone, a synthetic triterpenoid compound with potential antineoplastic and anti-inflammatory activities. Bardoxolone blocks the synthesis of inducible nitric oxide synthase (iNOS) and inducible cyclooxygenase (COX-2), two enzymes involved in inflammation and carcinogenesis. This agent also inhibits the interleukin-1 (IL-1)-induced expression of the pro-inflammatory proteins matrix metalloproteinase-1 (MMP-1) and matrix metalloproteinase-13 (MMP-13) and the expression of Bcl-3; Bcl-3 is an IL-1-responsive gene that preferentially contributes to MMP-1 gene expression.

• Baricitinib - An orally bioavailable inhibitor of Janus kinases 1 and 2 (JAK1/2), with potential anti-inflammatory, immunomodulating and antineoplastic activities. Upon administration, baricitinib binds to JAK1/2, which inhibits JAK1/2 activation and leads to the inhibition of the JAK-signal transducers and activators of transcription (STAT) signaling pathway. This decreases the production of inflammatory cytokines and may prevent an inflammatory response. In addition, baricitinib may induce apoptosis and reduce proliferation of JAK1/2-expressing tumor cells. JAK kinases are intracellular enzymes involved in cytokine signaling, inflammation, immune function and hematopoiesis; they are also upregulated and/or mutated in various tumor cell types.

• Batabulin - A synthetic pentafluorophenylsulfonamide with potential antineoplastic activity. Batabulin covalently binds to beta tubulin, resulting in a disruption of microtubule polymerization, collapse of the cytoskeleton, cell cycle arrest, and tumor cell apoptosis.

• Batabulin sodium - The sodium salt form of batabulin, a synthetic pentafluorophenylsulfonamide with potential antineoplastic activity. Batabulin covalently binds to and selectively modifies the beta 1, beta 2, beta 3, and beta 4 isotypes of beta tubulin at a conserved cysteine residue, resulting in disruption of microtubule polymerization, collapse of the cytoskeleton, an increase in chromosomal ploidy, cell cycle arrest, and tumor cell apoptosis.

• Batimastat - A synthetic hydroxamate with potential antineoplastic activity. Batimastat binds covalently to the zinc ion in the active site of matrix metalloproteinases (MMPs), thereby inhibiting the action of MMPs, inducing extracellular matrix degradation, and inhibiting angiogenesis, tumor growth and invasion, and metastasis.

• Bavituximab - A chimeric, IgG1 monoclonal antibody directed against anionic phospholipids with potential antineoplastic activity. Bavituximab binds to anionic phospholipids in a beta 2-glycoprotein I-dependent manner, inhibiting tumor growth by stimulating antibody-dependent cellular cytotoxicity (ADCC) to tumor vessels.

• Bazedoxifene - An indole derivative and third-generation selective estrogen receptor modulator (SERM) with potential antineoplastic activity. Upon administration, bazedoxifene specifically binds to estrogen receptors in responsive tissues, including liver, bone, breast, and endometrium. The resulting ligand-receptor complex is translocated to the nucleus where, depending on the tissue type, it either promotes or suppresses the transcription of estrogen-regulated genes. Bazedoxifene acts as an estrogen antagonist in uterine and breast tissue, thereby blocking the proliferative effects of estrogen-binding to ER-positive cells in these tissues. Bazedoxifene functions as an estrogen agonist in lipid metabolism, thereby decreasing total and LDL cholesterol levels. In bone, it decreases bone resorption and bone turnover and increases bone mineral density.

• Bazlitoran - An oligonucleotide targeted to the mRNA of MYD88 L265P, a mutant form of the linker protein MYD88, with potential antitumor activity. Bazlitoran binds to and inhibits the translation of mutated MYD88 L265P mRNA. This prevents overactivation of signaling pathways mediated by toll-like receptors (TLRs) 7, 8, and 9, nuclear factor-kappa B (NF-kB) activity, Janus-associated kinases-signal transducer and activator of transcription (JAK-STAT) signaling and the production of various cytokines. Together, this leads to an induction of apoptosis and an inhibition of tumor cell proliferation in MYD88 L265P-expressing tumor cells. MYD88, a key adaptor protein in the TLR signaling pathway, is mutated in a variety of B-cell lymphomas, including Waldenstrom's macroglobulinemia (WM) and activated B-cell-like diffuse large B-cell lymphoma (ABC-DLBCL).

• Bc-819 plasmid/polyethylenimine complex - A plasmid DNA encoding for the A fragment of Diphtheria Toxin (DTA) under the control of the H19 gene promoter (BC-819 or DTA-H19) and mixed with the transfectant polyethylenimine (PEI), with potential antineoplastic activity. Upon administration, the PEI moiety enhances the entry of the agent into rapidly dividing cells. Upon cell entry, activation of the H19 gene promoter-containing plasmids and DTA expression are limited to tumor cells, as high levels of H19 expression are only found in tumor cells. DTA disrupts protein synthesis. Tumor-cell selective expression of this toxin leads to the selective destruction of the tumor while sparing healthy, normal cells. H19, an oncofetal, regulatory RNA, is overexpressed in certain cancer cells while its expression in normal cells is minimal or absent; it plays a key role in cancer progression, angiogenesis and metastasis.

• Bcg solution - A solution containing an attenuated, live culture preparation of the Bacillus Calmette Guerin (BCG) strain of Mycobacterium bovis with potential immunostimulating activity. Although the precise mechanism of action is unknown, upon intravesical administration, attenuated, live BCG bacteria in the solution come into direct contact with the bladder wall, inciting an antitumor granulomatous inflammatory reaction.

• Bcg tokyo-172 strain solution - A solution containing an attenuated, live culture preparation of the bacillus Calmette-Guerin (BCG) strain of Mycobacterium bovis obtained from the Pasteur Institute in 1924, with potential immunostimulating and antineoplastic activities. Although the precise mechanism of action is unknown, upon intravesical instillation through a catheter, the attenuated, live BCG bacteria in the BCG Tokyo-172 strain solution come into direct contact with the bladder wall and elicits a local, multifaceted immune response against the BCG antigens, which kills the bladder cancer cells. Previous vaccination with a systemic BCG vaccine may enhance the immune system's response against the BCG antigens.

• Bcg vaccine - A vaccine containing bacillus Calmette-Guerin (BCG), an attenuated strain of Mycobacterium bovis, with non-specific immunoadjuvant and immunotherapeutic activities. Although the mechanism of its anti-tumor activity is unclear, immunization with BCG vaccine likely activates a Th1 cytokine response that includes the induction of interferon. Vaccination with BCG vaccine may be immunoprotective against infection with Mycobacterium tuberculosis.

• Bcl-2 inhibitor apg 2575 - An orally bioavailable and selective inhibitor of the anti-apoptotic protein B-cell lymphoma 2 (Bcl-2), with potential pro-apoptotic and antineoplastic activities. Upon oral administration, Bcl-2 inhibitor APG 2575 targets, binds to and inhibits the activity of Bcl-2. This restores apoptotic processes in tumor cells. Bcl-2 is overexpressed in many cancers and plays an important role in the negative regulation of apoptosis; its expression is associated with increased drug resistance and tumor cell survival.

• Bcl-2 inhibitor bcl201 - A selective inhibitor of the anti-apoptotic protein B-cell lymphoma 2 (Bcl-2), with potential pro-apoptotic and antineoplastic activities. Upon administration, Bcl-2 inhibitor BCL201 binds to and inhibits the activity of Bcl-2. This restores apoptotic processes in tumor cells. Bcl-2 protein is overexpressed in many cancers and plays an important role in the negative regulation of apoptosis; its expression is associated with increased drug resistance and tumor cell survival.

• Bcl-2 inhibitor bgb-11417 - An orally bioavailable inhibitor of the anti-apoptotic protein B-cell lymphoma 2 (Bcl-2), with potential pro-apoptotic and antineoplastic activities. Upon oral administration, Bcl-2 inhibitor BGB-11417 specifically binds to and inhibits the activity of the pro-survival protein Bcl-2. This restores apoptotic processes and inhibits cell proliferation in Bcl-2-overexpressing tumor cells. Bcl-2, a protein that belongs to the Bcl-2 family, is overexpressed in various tumor cell types and plays an important role in the negative regulation of apoptosis. Its tumor expression is associated with increased drug resistance and cancer cell survival.

• Bcl-2 inhibitor lp-108 - An orally bioavailable inhibitor of the anti-apoptotic protein B-cell lymphoma 2 (Bcl-2), with potential pro-apoptotic and antineoplastic activities. Upon oral administration, Bcl-2 inhibitor LP-108 targets, binds to and inhibits the activity of Bcl-2. This restores apoptotic processes in tumor cells. Bcl-2 is overexpressed in many cancers and plays an important role in the negative regulation of apoptosis; its expression is associated with increased drug resistance and tumor cell survival.

• Bcl-2 inhibitor s65487 - An inhibitor of the anti-apoptotic protein B-cell lymphoma 2 (Bcl-2), with potential pro-apoptotic and antineoplastic activities. Upon intravenous administration, Bcl-2 inhibitor S65487 binds to and inhibits the activity of Bcl-2, thereby restoring apoptotic processes in tumor cells. Bcl-2 protein is overexpressed in many cancer types and plays an important role in the negative regulation of apoptosis; its expression is associated with increased drug resistance and tumor cell survival.

• Bcl-xs adenovirus vaccine - A vaccine consisting of replication-defective recombinant adenovirus that encodes for Bcl-Xs with potential antineoplastic activity. Vaccination with Bcl-Xs adenovirus vaccine induces apoptosis in Bcl-2 and Bcl-XL positive cancer cells, resulting in decreased tumor growth while leaving normal cells unaffected. Bcl-Xs block the function of the protooncogenes Bcl-2 and Bcl-XL which are overexpressed in a variety of solid tumors and promote cancer cell survival by inhibiting apoptosis.

• Bcma cart cells secreting mutant pd-1fc fusion protein - A preparation of T-lymphocytes that have been genetically modified to express a chimeric antigen receptor (CAR) targeting the tumor-associated antigen (TAA) B-cell maturation antigen (BCMA; TNFRSF17) and secrete a fusion protein composed of programmed death 1 (PD-1; PDCD1; CD279; programmed cell death-1) and a human immunoglobulin Fc region, with potential immunomodulating and antineoplastic activities. Upon administration of the BCMA CART cells secreting mutant PD-1Fc fusion protein, these T-cells target and bind to tumor cells expressing BCMA and induce selective cytotoxicity in those tumor cells. The expressed PD-1-Fc fusion protein targets and binds to programmed death ligand 1 (PD-L1; cluster of differentiation 274; CD274; programmed cell death-1 ligand 1) expressed on tumor cells, thereby halting PD-1/PD-L1-mediated signaling. This may decrease T-cell exhaustion and may enhance T-cell activity against the PD-L1-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. PD-1, an immune checkpoint receptor expressed on T-cells, plays a key role in tumor immune evasion by binding to its ligand PD-L1 expressed on tumor cells.

• Bcma x cd3 t-cell engaging antibody cc-93269 - A bispecific T-cell engager (BiTE) antibody composed of two single-chain variable fragments (scFv), one directed against the tumor-associated antigen (TAA) human B-cell maturation antigen (BCMA; TNFRSF17), and one that is directed against the CD3 antigen found on T-lymphocytes, with potential immunostimulating and antineoplastic activities. Upon administration of anti-BCMA/CD3 T-cell engaging antibody CC-93269, 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 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.

• Bcma/cd3e tri-specific t-cell activating construct hpn217 - A recombinant antibody derivative composed of tri-specific T-cell activating construct (TriTAC) directed against the human tumor-associated antigen (TAA) B-cell maturation antigen (BCMA; TNFRSF17), the epsilon domain of CD3 antigen (CD3e) found on T-lymphocytes, and albumin, with potential immunostimulating and antineoplastic activities. Upon administration, BCMA/CD3e TriTAC HPN217 targets and binds to BCMA on tumor cells and CD3e on cytotoxic T-lymphocytes (CTLs), thereby bringing BCMA-expressing tumor cells and CTLs together, which results in the CTL-mediated cell death of BCMA-expressing tumor cells. The albumin-binding domain targets and binds to serum albumin, thereby extending the serum half-life of HPN217. BCMA, a member of the tumor necrosis factor receptor superfamily (TNFRSF), is overexpressed on malignant plasma cells and plays a key role in plasma cell survival.

• Bcma-cd19 compound car t cells - A preparation of T-lymphocytes transduced with a lentiviral vector expressing a compound chimeric antigen receptor (cCAR) containing two distinct units of CARs, one specific for the tumor-associated antigen (TAA) B-cell maturation antigen (BCMA; tumor necrosis factor receptor superfamily member 17; TNFRSF17) and one specific for the TAA CD19, with potential immunomodulating and antineoplastic activities. Upon administration, the BCMA-CD19 cCAR T cells specifically and simultaneously target and bind to tumor cells expressing BCMA and/or CD19. This induces selective toxicity in tumor cells that express BCMA and/or CD19. 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 the survival of B-lymphocytes and plasma cells. BCMA is found on the surfaces of B-cells and is overexpressed on malignant plasma cells. CD19 is a B-cell-specific cell surface antigen overexpressed in B-cell lineage malignancies. Targeting two different antigens may improve coverage and protect against antigen escape and relapse as it is less likely for tumor cells to lose both antigens.

• Bcr-abl (b2a2)-derived peptide vaccine - A peptide vaccine consisting of the bcr-abl b2a2 fusion oncoprotein, frequently expressed in chronic myelogenous leukemia (CML), with potential antineoplastic activity. Vaccination with the bcr-abl (b2a2)-derived peptide vaccine may stimulate the host immune system to mount a cytotoxic T lymphocyte (CTL) response against tumor cells that express the bcr-abl b2a2 fusion protein. Fusion genes in CML typically result from the fusion of either BCR exon b2 or BCR exon b3 to ABL exon a2, a 'b3a2' or a 'b2a2' fusion.

• Bcr-abl (b3a2)-derived peptide vaccine - A peptide vaccine consisting of the bcr-abl b3a2 fusion oncoprotein, frequently expressed in chronic myelogenous leukemia (CML), with potential antineoplastic activity. Vaccination with the bcr-abl (b3a2)-derived peptide vaccine may stimulate the host immune system to mount a cytotoxic T lymphocyte (CTL) response against tumor cells that express the bcr-abl b3a2 fusion protein. Fusion genes in CML typically result from the fusion of either BCR exon b2 or BCR exon b3 to ABL exon a2, a 'b3a2' or a 'b2a2' fusion.

• Bcr-abl kinase inhibitor k0706 - An orally bioavailable, Bcr-Abl tyrosine kinase inhibitor (TKI), with potential antineoplastic activity. Upon administration, Bcr-Abl kinase inhibitor K0706 selectively targets and binds to the Bcr-Abl fusion oncoprotein, including various Bcr-Abl mutant forms, such as those with the 'gatekeeper' resistance mutation T315I. This inhibits proliferation of Bcr-Abl-expressing tumor cells. The Bcr-Abl fusion protein is an aberrantly activated tyrosine kinase produced by certain leukemia cells. T315I, an amino acid substitution where threonine (T) has been mutated to isoleucine (I) at position 315 in the tyrosine-protein kinase ABL1 portion of the Bcr-Abl fusion protein, plays a key role in resistance to certain chemotherapeutic agents and its expression is associated with poor prognosis.

• Bcr-abl kinase inhibitor pf-114 - An orally bioavailable, Bcr-Abl tyrosine kinase inhibitor, with potential antineoplastic activity. Designed to overcome resistance of tumor cells to second generation Bcr-Abl inhibitors, PF-114 targets and binds to the Bcr-Abl fusion oncoprotein, including those fusion proteins with the 'gatekeeper' resistance mutation T315I, an amino acid substitution at position 315 in Bcr-Abl from a threonine (T) to an isoleucine (I). This inhibits Bcr-Abl-mediated proliferation of, and enhances apoptosis in, Philadelphia chromosome-positive (Ph+) hematologic malignancies. The Bcr-Abl fusion protein is an aberrantly activated tyrosine kinase produced by leukemia cells that contain the Philadelphia chromosome.

• Bcr-abl p210-b3a2 breakpoint-derived pentapeptide vaccine - A multipeptide vaccine consisting of five peptides derived from the bcr-abl p210-b3a2 breakpoint fusion protein with potential antineoplastic activity. Vaccination with bcr-abl p210-b3a2 breakpoint-derived multipeptide vaccine may stimulate the host immune system to mount a cytotoxic T lymphocyte (CTL) response against tumor cells that express the bcr-abl p210-b3a2 breakpoint fusion protein. In chronic myelogenous leukemia (CML), fusion genes typically result from the fusion of either bcr exon b2 or exon b3 to abl exon a2, resulting in either a b3a2 or a b2a2 gene fusion product.

• Bcr-abl peptide vaccine - A multivalent antineoplastic vaccine comprised of the bcr-abl oncogene breakpoint fusion peptide that elicits a bcr-abl specific T-cell immune response.

• Bcr-abl/kit/akt/erk inhibitor hqp1351 - An orally bioavailable inhibitor of a variety of kinases, including the Bcr-Abl tyrosine kinase, the mast/stem cell growth factor receptor Kit (c-Kit), the serine/threonine protein kinase Akt (protein kinase B), and the extracellular signal-regulated kinase (ERK) with antineoplastic activity. Upon administration, HQP1351 targets, binds to and inhibits the kinase activities of Bcr-Abl, AKT, c-Kit and ERK. This inhibits their mediated signaling pathways and inhibits proliferation of tumor cells in which these kinases are overexpressed and/or mutated. Bcr-Abl, c-Kit, AKT and ERK play key roles in the proliferation, differentiation and survival of tumor cells.

• Beauvericin - A cyclic hexadepsipeptide antibiotic and mycotoxin isolated from the fungus Beauveria bassiana and various Fusarium fungal species. As a potassium-specific ionophore, beauvericin A increases intracellular calcium concentrations and triggers DNA fragmentation and apoptosis through a calcium dependent caspase 3-sensitive pathway. This agent has been studied as a potential antineoplastic agent.

• Becatecarin - A synthetic diethylaminoethyl analogue of the indolocarbazole glycoside antineoplastic antibiotic rebeccamycin. Becatecarin intercalates into DNA and stabilizes the DNA-topoisomerase I complex, thereby interfering with the topoisomerase I-catalyzed DNA breakage-reunion reaction and initiating DNA cleavage and apoptosis.

• Belagenpumatucel-l - A transforming growth factor beta2 (TGF-beta2) antisense gene-modified allogeneic tumor cell vaccine with potential immunostimulatory and antineoplastic activities. Belagenpumatucel-L is prepared by transfecting allogeneic non-small cell lung cancer (NSCLC) cells with a plasmid containing a TGF-beta2 antisense transgene, expanding the cells, and then irradiating and freezing them. Upon administration, this agent may elicit a cytotoxic T lymphocyte (CTL) response against host NSCLC cells, resulting in decreased tumor cell proliferation; vaccine immunogenicity may be potentiated by suppression of tumor TGF-beta2 production by antisense RNA expressed by the vaccine plasmid TGF-beta2 antisense transgene. Elevated levels of TGF-beta2 are frequently linked to immunosuppression in cancer patients and may be inversely correlated with prognosis in patients with NSCLC.

• Belantamab mafodotin - An antibody-drug conjugate (ADC) consisting of belantamab, an afucosylated, humanized monoclonal antibody, directed against the B-cell maturation antigen (BCMA), conjugated to mafodotin, an auristatin analogue and microtubule inhibitor monomethyl auristatin phenylalanine (MMAF), with potential antineoplastic activity. Upon administration of belantamab mafodotin, the anti-BCMA antibody moiety selectively binds to BCMA on tumor cell surfaces. Upon internalization, the MMAF moiety binds to tubulin and inhibits its polymerization, which results in G2/M phase arrest and induces tumor cell apoptosis. In addition, belantamab mafodotin induces antibody-dependent cellular cytotoxicity (ADCC). Altogether, this results in the inhibition of cellular proliferation in tumor cells that overexpress BCMA. BCMA, a receptor for a proliferation-inducing ligand and B-cell activating factor, is a member of the tumor necrosis factor (TNF) receptor superfamily and plays a key role in plasma cell survival; it is found on the surfaces of plasma cells and overexpressed on malignant plasma cells. Afucosylation of the antibody moiety increases ADCC.

• Belapectin - A carbohydrate-based galectin inhibitor, with potential antineoplastic activity. Belapectin binds to the carbohydrate-binding domain of galectins, especially galectin-3, and may result in an induction of apoptosis mediated through activation of both mitochondria and caspases. This may reduce tumor growth in galectin-overexpressing tumor cells. Galectins, often overexpressed on tumor cells, play a key role in cancer cell proliferation, apoptosis, tumor angiogenesis and evasion of immune responses.

• Belimumab - A fully human IgG1 monoclonal antibody directed against B-Lymphocyte stimulator protein (BlyS or TNFSF13B) with potential immunomodulating activity. Belimumab specifically recognizes and inhibits the biological activity of BlyS, thereby preventing the binding of BlyS to B-lymphocytes. This inhibits the maturation of B-lymphocytes and may induce apoptosis in B-lymphocytes. In addition, it may decrease B-lymphocyte proliferation and/or survival. BlyS, a member of TNF family supporting B-lymphocyte maturation and survival, has been implicated in the pathogenesis of autoimmune diseases and B-lymphocyte malignancies.

• Belinostat - A novel hydroxamic acid-type histone deacetylase (HDAC) inhibitor with antineoplastic activity. Belinostat targets HDAC enzymes, thereby inhibiting tumor cell proliferation, inducing apoptosis, promoting cellular differentiation, and inhibiting angiogenesis. This agent may sensitize drug-resistant tumor cells to other antineoplastic agents, possibly through a mechanism involving the down-regulation of thymidylate synthase.

• Belotecan hydrochloride - The hydrochloride salt of the semi-synthetic camptothecin analogue belotecan with potential antitumor activity. Belotecan binds to and inhibits the activity of topoisomerase I, stabilizing the cleavable complex of topoisomerase I-DNA, which inhibits the religation of single-stranded DNA breaks generated by topoisomerase I; lethal double-stranded DNA breaks occur when the topoisomerase I-DNA complex is encountered by the DNA replication machinery, DNA replication is disrupted, and the tumor cell undergoes apoptosis. Topoisomerase I is an enzyme that mediates reversible single-strand breaks in DNA during DNA replication.

• Belvarafenib - An orally available inhibitor of members of the Raf family of serine/threonine protein kinases, with potential antineoplastic activity. Upon administration, belvarafenib binds to and inhibits the B-Raf mutant V600E and C-Raf. This inhibits B-Raf V600E- and C-Raf-mediated signal transduction pathways, thereby inhibiting tumor cell growth of susceptible tumor cells. In addition, belvarafenib may also inhibit mutated Ras proteins. Raf protein kinases play a key role in the Raf/mitogen-activated protein kinase kinase (MEK)/extracellular signal-related kinase (ERK) signaling pathway, which is often dysregulated in human cancers and plays a key role in tumor cell proliferation and survival. The Raf mutation B-Raf V600E, where the valine at residue 600 is substituted for glutamic acid, is frequently overexpressed in a variety of human tumors and results in the constitutive activation of the Raf/MEK/ERK signaling pathway.

• Belzutifan - An orally active, small molecule inhibitor of hypoxia inducible factor (HIF)-2alpha (HIF-2a), with potential antineoplastic activity. Upon oral administration, belzutifan binds to and blocks the function of HIF-2alpha, thereby preventing HIF-2alpha heterodimerization and its subsequent binding to DNA. This results in decreased transcription and expression of HIF-2alpha downstream target genes, many of which regulate hypoxic signaling. This inhibits cell growth and survival of HIF-2alpha-expressing tumor cells. HIF-2alpha, the alpha subunit for the heterodimeric transcription factor HIF-2, is overexpressed in many cancers and promotes tumorigenesis.

• Bemarituzumab - A glycoengineered, humanized monoclonal antibody directed against the fibroblast growth factor receptor type 2b (FGFR2b), with potential antineoplastic activity. Upon administration, bemarituzumab specifically binds to and inhibits FGFR2b on tumor cell surfaces, which prevents FGFR2 from binding to its ligands, FGFR2b activation and the activation of FGFR2b-mediated signal transduction pathways. The binding of FPA144 to FGFR2b protein also induces antibody-dependent cell-mediated cytotoxicity (ADCC) against FGFR2b-expressing tumor cells. This results in the inhibition of cell proliferation and the induction of cell death of FGFR2-expressing tumor cells. FGFR2b, a specific isoform of the receptor tyrosine kinase FGFR2 upregulated in many tumor cell types, is essential to tumor proliferation, differentiation and survival. Glycoengineering enhances the FPA144-mediated ADCC.

• Bemcentinib - An orally available and selective inhibitor of the AXL receptor tyrosine kinase (UFO), with potential antineoplastic activity. Upon administration, bemcentinib targets and binds to the intracellular catalytic kinase domain of AXL and prevents its activity. This blocks AXL-mediated signal transduction pathways and inhibits the epithelial-mesenchymal transition (EMT), which, in turn, inhibits tumor cell proliferation and migration. In addition, bemcentinib enhances chemo-sensitivity. AXL, a member of the TAM (TYRO3, AXL and MER) family of receptor tyrosine kinases overexpressed by many tumor cell types, plays a key role in tumor cell proliferation, survival, invasion and metastasis; its expression is associated with drug resistance and poor prognosis.

• Bempegaldesleukin - A recombinant form of the endogenous cytokine interleukin-2 (IL-2) conjugated to six releasable polyethylene glycol (PEG) chains, with potential immunostimulating activity. Upon administration of bempegaldesleukin, the IL-2 moiety binds to the IL-2 receptor beta subunit (IL2Rb; IL2Rbeta; CD122). The binding of IL-2 to IL2Rb activates IL2Rb-mediated signaling, which activates cytotoxic T-lymphocytes (CTLs) and natural killer (NK) cells, and induces expression of certain cytotoxic cytokines, such as interferon-gamma (IFNg) and transforming growth factor-beta (TGFb). The specific induction of T-cell-mediated cytotoxic immune responses against tumor cells primarily causes tumor cell destruction. IL2Rb plays a key role in the proliferation and activation of effector T-cells. PEG conjugation prevents IL-2 binding to the IL2Ralpha subunit (IL2Ra) because signaling through IL2Ra activates CD4-positive regulatory, immunosuppressive T-cells (Tregs), which would suppress tumor cell killing.

• Benaxibine - A cyclophosphamide synergizer with antineoplastic, antidiabetic, antihypertensive and immunopotentiating activity. Benaxibine is active against integrin alph-4 precursor.

• Bendamustine - A bifunctional mechlorethamine derivative with alkylating and antimetabolite activities. Although the exact mechanism of action of bendamustine is unknown, this agent appears to alkylate and crosslink macromolecules, resulting in DNA, RNA and protein synthesis inhibition, and eventually the induction of apoptosis.

• Bendamustine hydrochloride - The hydrochloride salt of bendamustine, a bifunctional mechlorethamine derivative with alkylator and antimetabolite activities. Bendamustine possesses three active moieties: an alkylating group; a benzimidazole ring, which may act as a purine analogue; and a butyric acid side chain. Although its exact mechanism of action is unknown this agent appears to act primarily as an alkylator. Bendamustine metabolites alkylate and crosslink macromolecules, resulting in DNA, RNA and protein synthesis inhibition, and, subsequently, apoptosis. Bendamustine may differ from other alkylators in that it may be more potent in activating p53-dependent stress pathways and inducing apoptosis; it may induce mitotic catastrophe; and it may activate a base excision DNA repair pathway rather than an alkyltransferase DNA repair mechanism. Accordingly, this agent may be more efficacious and less susceptible to drug resistance than other alkylators.

• Bendamustine-containing nanoparticle-based formulation rxdx-107 - A nanoparticle-based formulation containing the alkyl ester of bendamustine, a bifunctional mechlorethamine derivative, encapsulated in human serum albumin (HSA), with potential alkylating and antineoplastic activities. Upon administration of the alkyl ester bendamustine-containing nanoparticle formulation RXDX-107, the nanoparticle formulation permits high concentrations of the alkyl ester of bendamustine be localized at the tumor site. The modified bendamustine alkylates and crosslinks macromolecules, resulting in DNA, RNA and protein synthesis inhibition, and, subsequently, apoptosis.

• Benzaldehyde dimethane sulfonate - A dimethane sulfonate derivative and alkylating agent with a structure similar to other alkylating agents such as chlorambucil, busulfan and melphalan, with potential antineoplastic activity. Although the exact mechanism of action has yet to be fully elucidated, benzaldehyde dimethane sulfonate alkylates DNA, which results in DNA double strand breaks, inhibition of DNA replication, cell cycle arrest and cell death. In addition, this agent is metabolized by the enzyme aldehyde dehydrogenase (ALDH) into the active carboxylic acid metabolite benzoic acid dimethane sulfonate (BA), which further contributes to its alkylating activity. Unlike other alkylating agents, benzaldehyde dimethane sulfonate has demonstrated antitumor activity in renal cell carcinoma.

• Benzoylphenylurea - A low molecular weight agent with antineoplastic activity. Benzoylphenylurea binds to the colchicine binding site on tubulin, thereby blocking tubulin polymerization and disrupting mitotic function. This agent also inhibits DNA polymerase, and has been shown to arrest leukemia cells in the G1-S transition phase of the cell cycle.

• Berberine chloride - The orally bioavailable, hydrochloride salt form of berberine, a quaternary ammonium salt of an isoquinoline alkaloid and active component of various Chinese herbs, with potential antineoplastic, radiosensitizing, anti-inflammatory, anti-lipidemic and antidiabetic activities. Although the mechanisms of action through which berberine exerts its effects are not yet fully elucidated, upon administration this agent appears to suppress the activation of various proteins and/or modulate the expression of a variety of genes involved in tumorigenesis and inflammation, including, but not limited to transcription factor nuclear factor-kappa B (NF-kB), myeloid cell leukemia 1 (Mcl-1), B-cell lymphoma 2 (Bcl-2), B-cell lymphoma-extra large (Bcl-xl), cyclooxygenase (COX)-2, tumor necrosis factor (TNF), interleukin (IL)-6, IL-12, inducible nitric oxide synthase (iNOS), intercellular adhesion molecule-1 (ICAM-1), E-selectin, monocyte chemoattractant protein-1 (MCP-1), C-X-C motif chemokine 2 (CXCL2), cyclin D1, activator protein (AP-1), hypoxia-inducible factor 1 (HIF-1), signal transducer and activator of transcription 3 (STAT3), peroxisome proliferator-activated receptor (PPAR), arylamine N-acetyltransferase (NAT), and DNA topoisomerase I and II. The modulation of gene expression may induce cell cycle arrest and apoptosis, and inhibit cancer cell proliferation. In addition, berberine modulates lipid and glucose metabolism.

• Bermekimab - A "true human" (cloned from human B lymphocytes) monoclonal antibody directed against interleukin-1 alpha (IL1a) with potential antineoplastic activity. Bermekimab binds to IL1a and may block the activity of IL1a. IL1a, an inflammatory mediator, plays a key role in interleukin-mediated tumor cell activity such as angiogenesis, tissue matrix remodeling, metastasis and tumor cell invasion.

• Bersanlimab - A fully human IgG1 monoclonal antibody directed against intercellular adhesion molecule-1 (ICAM-1 or CD54), with potential antineoplastic activity. Bersanlimab selectively binds to the adhesion protein ICAM-1, which may result in antibody-dependent cellular cytotoxicity (ADCC), hyper-cross-linking-induced apoptosis, and a decrease in cellular proliferation of ICAM-1-expressing tumor cells. ICAM-1, normally expressed on leukocytes and endothelial cells, may be overexpressed in a variety of cancers.

• Berubicin hydrochloride - The hydrochloride salt of the anthracycline derivative berubicin with potential antineoplastic activity. Berubicin intercalates into DNA and interrupts topoisomerase II activity, resulting in the inhibition of DNA replication and repair, and RNA and protein synthesis. Unlike other anthracycline derivatives, this agent crosses the blood-brain barrier (BBB).

• Berzosertib - An inhibitor of ataxia telangiectasia and rad3-related (ATR) kinase, a DNA damage response kinase, with potential antineoplastic activity. Upon administration, berzosertib selectively binds to and inhibits ATR kinase activity and prevents ATR-mediated signaling in the ATR-checkpoint kinase 1 (Chk1) signaling pathway. This prevents DNA damage checkpoint activation, disrupts DNA damage repair, and induces tumor cell apoptosis. ATR, a serine/threonine protein kinase upregulated in a variety of cancer cell types, plays a key role in DNA repair, cell cycle progression, and survival; it is activated by DNA damage caused during DNA replication-associated stress.

• Bet bromodomain inhibitor zen-3694 - An orally bioavailable inhibitor of the bromodomain and extra-terminal (BET) family of proteins, with potential antineoplastic activity. Upon oral administration, the BET inhibitor ZEN-3694 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.

• Bet inhibitor abbv-744 - An orally bioavailable inhibitor of the Bromodomain and Extra-Terminal (BET) family of proteins, with potential antineoplastic activity. Upon oral administration, the BET inhibitor ABBV-744 preferentially binds to the second bromodomain (BD2) 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 contain two homologous bromodomains, the BD1 and BD2 domains. They play an important role during development and cellular growth.

• Bet inhibitor bay1238097 - An inhibitor of the Bromodomain (BRD) and Extra-Terminal domain (BET) family of proteins, with potential antineoplastic activity. Upon administration, the BET inhibitor BAY1238097 binds to the acetylated lysine recognition motifs on the BRD of BET proteins, thereby preventing the interaction between BET proteins and histones. This disrupts chromatin remodeling and prevents the expression of certain growth-promoting genes. This leads to an inhibition of tumor cell growth. BET proteins (BRD2, BRD3, BRD4 and BRDT) are transcriptional regulators that bind to acetylated lysines on the tails of histones H3 and H4, and regulate chromatin structure and function; they play an important role in the modulation of gene expression during development and cellular growth.

• Bet inhibitor bi 894999 - An orally bioavailable inhibitor of the bromodomain and extra-terminal (BET) family of proteins with potential antineoplastic activity. Upon oral administration, BET inhibitor BI 894999 binds to bromodomain-containing proteins 2, 3, and 4 (BRD2, BRD3, and BRD4) as well as bromodomain testis-specific protein (BRDT), thereby preventing the interaction between BET proteins and acetylated histones. This disrupts chromatin remodeling and suppresses the expression of certain oncogenes, including Myc and other transcriptional regulators. Preventing the expression of certain growth-promoting genes may lead to an inhibition of tumor cell growth. Characterized by a tandem repeat of bromodomains at the N-terminus, BET proteins, comprised of BRD2, BRD3, BRD4 and BRDT, are transcriptional regulators that play an important role during cellular development and growth.

• Bet inhibitor bms-986158 - An inhibitor of the Bromodomain (BRD) and Extra-Terminal domain (BET) family of proteins, with potential antineoplastic activity. Upon administration, the BET inhibitor BMS-986158 binds to the acetyl-lysine binding site in the BRD of BET proteins, thereby preventing the interaction between BET proteins and acetylated histones. This disrupts chromatin remodeling and prevents the expression of certain growth-promoting genes, resulting in an inhibition of tumor cell growth. BET proteins (BRD2, BRD3, BRD4 and BRDT) are transcriptional regulators that bind to acetylated lysines on the tails of histones H3 and H4, and regulate chromatin structure and function; they play an important role in the modulation of gene expression during development and cellular growth.

• Bet inhibitor cc-90010 - An orally bioavailable inhibitor of the Bromodomain and Extra-Terminal (BET) family of proteins, with potential antineoplastic activity. Upon oral administration, the BET inhibitor CC-90010 preferentially binds to the second bromodomain (BD2) 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 (BRD2, BRD3, BRD4 and BRDT) are transcriptional regulators that contain two homologous bromodomains, the BD1 and BD2 domains. They play an important role during development and cellular growth.

• Bet inhibitor ft-1101 - An orally bioavailable inhibitor of the Bromodomain and Extra-Terminal (BET) family of proteins, with potential antineoplastic activity. Upon administration, the BET inhibitor FT-1101 binds to the acetylated lysine recognition motifs in the bromodomain sites 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 the inhibition of tumor cell growth. BET proteins, comprised of BRD2, BRD3, BRD4 and BRDT, are transcriptional regulators that play an important role during development and cellular growth.

• Bet inhibitor gsk2820151 - An orally bioavailable inhibitor of the Bromodomain and Extra-Terminal (BET) family of proteins, with potential antineoplastic activity. Upon oral administration, the BET inhibitor GSK2820151 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 tumor cell growth. BET proteins, comprised of BRD2, BRD3, BRD4 and BRDT, are transcriptional regulators that play an important role during development and cellular growth.

• Bet inhibitor incb054329 - An inhibitor of the Bromodomain and Extra-Terminal (BET) family of bromodomain-containing proteins with potential antineoplastic activity. Upon administration, the BET inhibitor INCB054329 binds to the acetylated lysine recognition motifs on the bromodomain 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 tumor cell growth. Characterized by a tandem repeat of bromodomain at the N-terminus, BET proteins, BRD2, BRD3, BRD4 and BRDT, are transcriptional regulators that play an important role during cellular growth.

• Bet inhibitor incb057643 - An inhibitor of the Bromodomain (BRD) and Extra-Terminal (BET) family of BRD-containing proteins, with potential antineoplastic activity. Upon administration, the BET inhibitor INCB057643 binds to the acetylated lysine recognition motifs found in the BRD of BET proteins, thereby preventing the interaction between the BET proteins and acetylated lysines on histones. This disrupts chromatin remodeling and gene expression. Prevention of the expression of certain growth-promoting genes, such as c-Myc-dependent target genes, may lead to an inhibition of tumor cell growth. BET proteins are transcriptional regulators that are overexpressed in certain tumor cells and play an important role in cellular growth.

• Bet inhibitor ro6870810 - A small molecule inhibitor of the BET (Bromodomain and Extra-Terminal) family of bromodomain-containing proteins with potential antineoplastic activity. Upon administration, the BET inhibitor RO6870810 binds to the acetylated lysine recognition motifs found in the bromodomain of BET proteins, which prevents the interaction between BET proteins and acetylated histones. This interaction disrupts chromatin remodeling and gene expression. Prevention of the expression of certain growth-promoting genes may lead to an inhibition of tumor cell growth. Characterized by a tandem repeat of bromodomains at the N-terminus, BET proteins, comprised of BRD2, BRD3, BRD4 and BRDT, are transcriptional regulators that play an important role during cellular development and growth.

• Beta alethine - A disulfide agent that stimulates T and B-cell functions and exhibits anti-tumor and immunostimulant activity. (NCI)

• Beta-carotene - A naturally-occurring retinol (vitamin A) precursor obtained from certain fruits and vegetables with potential antineoplastic and chemopreventive activities. As an anti-oxidant, beta carotene inhibits free-radical damage to DNA. This agent also induces cell differentiation and apoptosis of some tumor cell types, particularly in early stages of tumorigenesis, and enhances immune system activity by stimulating the release of natural killer cells, lymphocytes, and monocytes.

• Beta-elemene - One of the isomers of elemene, a lipid soluble sesquiterpene and the active component isolated from the Chinese medicinal herb Rhizoma zedoariae with potential antineoplastic and chemopreventive activities. Although the exact mechanism of action through which beta-elemene exerts its effect has yet to be fully elucidated, this agent appears to induce apoptosis through different mechanisms of action and induces cell cycle arrest at different stages based on the tumor cell type involved. Beta-elemene may sensitize cancer cells to other chemotherapeutic agents.

• Beta-glucan - A polysaccharide isolated from the cell walls of bacteria, plants, and fungi with immunostimulant and antineoplastic activities. In a solubilized form, beta-glucan binds to a lectin site within complement receptor 3 (CR3) on leukocytes, priming the receptor to trigger cytotoxic degranulation of leukocytes when leukocyte CR3 binds to complement 3 (iC3b)-coated tumors. Thus, the attachment of beta-glucan to CR3 of circulating leukocytes simulates leukocytes to kill iC3b-coated tumor cells in the same way as they kill iC3b-coated yeast.

• Beta-glucan mm-10-001 - A powder formulation containing a triple helix beta-glucan, isolated from the cell walls of the shiitake mushroom (Lentinula edodes), with potential immunostimulating activity. The beta-glucan in beta-glucan MM-10-001 binds to a lectin site within the complement receptor 3 (CR3 or iC3b receptor) on leukocytes, priming the receptor to trigger cytotoxic degranulation of leukocytes when leukocyte CR3 binds to iC3b-opsonized tumor cells. iC3b is the proteolyticly inactive product of the complement cleavage fragment C3b.

• Betaglucin gel - A soluble gel containing the beta-glucan betaglucin, with potential immunostimulating activity. Upon topical administration of the betaglucin gel, betaglucin is able to increase the number of macrophages and natural killer (NK) cells. NK cells and macrophages may kill a variety of tumor cells, and virally infected cells. This may treat human papillomavirus (HPV)-related anogenital warts.

• Beta-lapachone prodrug arq 761 - A synthetic, soluble prodrug of beta-lapachone, a poorly soluble, ortho-naphthoquinone with potential antineoplastic and radiosensitizing activity. ARQ 761 is converted to beta-lapachone (b-lap) in vivo. When b-lap is activated by NAD(P)H:quinone oxidoreductase-1 (NQO1) this agent creates a futile oxidoreduction, generating highly reactive oxygen species (ROS) that results in DNA damage. The activation of b-lap also causes hyperactivation of poly (ADP-ribose) polymerase-1 (PARP-1), an enzyme that facilitates DNA repair, accompanied by rapid depletion of NAD+/ATP nucleotide levels. As a result, a caspase-independent and endoplasmic reticulum (ER) stress-induced mu-calpain-mediated cell death occurs in NQO1-overexpressing tumor cells. In addition, b-lap induces expression of the checkpoints activator E2F transcription factor 1 (E2F1) and thereby activates the E2F1-mediated checkpoint pathway that directly triggers apoptosis. As ARQ 761 is soluble and requires less solvent, this formulation may cause less hemolytic anemia associated with administration of the synthetic b-lap ARQ 501.

• Beta-thioguanine deoxyriboside - A thiopurine nucleoside derivative with antineoplastic activity. After conversion to the triphosphate, beta-thioguanine deoxyriboside is incorporated into DNA, resulting in inhibition of DNA replication. This agent is cytotoxic against leukemia cell lines and has demonstrated some activity against leukemia cells in vivo. Beta-thioguanine deoxyriboside demonstrates antineoplastic activity against 6-thioguanine-resistant tumor cells.

• Bet-bromodomain inhibitor odm-207 - An orally bioavailable inhibitor of the Bromodomain and Extra-Terminal (BET) family of proteins, with potential antineoplastic activity. Upon oral administration, the BET inhibitor ODM-207 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 of oncogenic drivers that are important for cell proliferation and survival. 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 bind to acetylated lysine residues in histones and play an important role during development and cellular growth. In tumor cells, BET proteins play a key role in the regulation of oncogene transcription and tumor cell proliferation.

• Betulinic acid - A pentacyclic lupane-type triterpene derivative of betulin (isolated from the bark of Betula alba, the common white birch) with antiinflammatory, anti-HIV and antineoplastic activities. Betulinic acid induces apoptosis through induction of changes in mitochondrial membrane potential, production of reactive oxygen species, and opening of mitochondrial permeability transition pores, resulting in the release of mitochondrial apogenic factors, activation of caspases, and DNA fragmentation. Although originally thought to exhibit specific cytotoxicity against melanoma cells, this agent has been found to be cytotoxic against non-melanoma tumor cell types including neuroectodermal and brain tumor cells.

• Bevacizumab - A recombinant humanized monoclonal antibody directed against the vascular endothelial growth factor (VEGF), a pro-angiogenic cytokine. Bevacizumab binds to VEGF and inhibits VEGF receptor binding, thereby preventing the growth and maintenance of tumor blood vessels.

• Bevacizumab-irdye 800cw - An immunoconjugate and a fluorescent tracer consisting of the recombinant humanized anti-vascular endothelial growth factor (VEGF) monoclonal antibody bevacizumab conjugated to the N-hydroxysuccinamide (NHS) ester form of the near-infrared (NIR) fluorescent dye IRDye 800CW, that may be used for VEGF-specific tumor imaging. Upon administration, the bevacizumab moiety of bevacizumab-IRDye 800CW binds to VEGF and the fluorescent signal can be visualized using NIR fluorescence imaging (700-1,000 nm).

• Bexarotene - A synthetic retinoic acid agent with potential antineoplastic, chemopreventive, teratogenic and embryotoxic properties. Bexarotene selectively binds to and activates retinoid X receptors (RXRs), thereby inducing changes in gene expression that lead to cell differentiation, decreased cell proliferation, apoptosis of some cancer cell types, and tumor regression.

• Bexmarilimab - A monoclonal antibody directed against common lymphatic endothelial and vascular endothelial receptor-1 (CLEVER-1; stabilin-1; FEEL-1), with potential immunomodulatory and antineoplastic activities. Upon administration, bexmarilimab targets and binds to CLEVER-1 that is expressed on tumor endothelial cells. This prevents the recruitment, infiltration and attachment of tumor-associated macrophages (TAMs) at the tumor site. By preventing the binding of TAMs to tumor cells, the infiltration of activated T-regulatory cells (Tregs) to the tumor and the TAM-mediated immune suppression is abrogated, leading to the polarization of TAM from the immunosuppressive M2 macrophages to the anti-inflammatory and immunostimulatory M1 macrophages. This leads to the activation of the immune system, resulting in a cytotoxic T-lymphocyte (CTL)-mediated immune response and inhibition of tumor cell growth and metastasis. CLEVER-1 is an endothelial cell surface molecule involved in immune suppression, cancer growth and metastasis.

• Bf-200 gel formulation - A topical nanoemulsion-based gel formulation containing 5-aminolevulinic acid (ALA), a metabolic precursor of the photosensitizer protoporphyrin IX, with a potential application for enhanced photodynamic therapy (PDT) for various precancerous and malignant skin lesions. After topical administration of a thick layer of the ALA-based BF-200 gel formulation to the affected area, ALA penetrates the skin and is intracellularly converted to protoporphyrin IX (PpIX). Exposure of PpIX to the proper excitation wavelength of light generates singlet oxygen molecules, resulting in a local cytotoxic effect.

• Bh3 mimetic abt-737 - An orally bioavailable, selective small molecule B-cell lymphoma 2 (Bcl-2) Homology 3 (BH3) mimetic, with potential pro-apoptotic and antineoplastic activities. ABT-737 binds to the hydrophobic groove of multiple members of the anti-apoptotic Bcl-2 protein family, including Bcl-2, Bcl-xl and Bcl-w. This inhibits the activity of these pro-survival proteins and restores apoptotic processes in tumor cells, via activation of Bak/Bax-mediated apoptosis. The pro-survival Bcl-2 proteins are overexpressed in many cancers and play important roles in the regulation of apoptosis. Their expression is associated with increased drug resistance and tumor cell survival. ABT-737 does not inhibit the pro-survival proteins Mcl-1, Bcl-B, Bfl-1 (A1); therefore, tumors that overexpress these Bcl-2 family proteins are resistant to ABT-737.

• Bicalutamide - A synthetic, nonsteroidal antiandrogen. Bicalutamide competitively binds to cytosolic androgen receptors in target tissues, thereby inhibiting the receptor binding of androgens. This agent does not bind to most mutated forms of androgen receptors.

• Bi-functional alkylating agent val-083 - A bi-functional alkylating agent, with potential antineoplastic activity. Upon administration, VAL-083 crosses the blood brain barrier (BBB) and appears to be selective for tumor cells. This agent alkylates and crosslinks DNA which ultimately leads to a reduction in cancer cell proliferation. In addition, VAL-083 does not show cross-resistance to other conventional chemotherapeutic agents and has a long half-life in the brain.

• Bifunctional expression vector plasmid dna-bi-shrna ews/fli1 type 1 lipoplex - A proprietary plasmid DNA expression vector encoding bi-functional short hairpin RNAs (bi-shRNAs) targeting the identical type 1 translocation junction region of the human fusion oncogene Ewing sarcoma (EWS)/Ets family transcription factor Friend leukemia virus integration 1 (FLI1) and are encapsulated in liposomal delivery vehicle (lipoplex; LPX), with potential antineoplastic activity. pbi-shRNA EWS/FLI1 type 1 contains 2 stem-loop structures encoded by a plasmid vector: one cleavage-dependent unit with perfectly matched passenger- and guide-strand, which is the small interfering RNA (siRNA)-like component, and one cleavage-independent unit composed of a strategically mismatched double strand, which is the microRNA (miRNA)-like component. Upon intratumoral administration and transcription into tumor cells, one shRNA unit with an imperfectly matched sequence causes inhibition of EWS/FLI1 messenger RNA (mRNA) translation (through mRNA sequestration and cleavage-independent degradation) while the other unit with a perfectly matched sequence promotes EWS/FLI1 mRNA degradation (through cleavage-dependent mRNA silencing). This prevents EWS/FLI1 expression in tumor cells, which results in a reduction of tumor cell proliferation. The EWS/FLI1 type 1 fusion gene product is overexpressed in type 1 Ewing's sarcoma and correlates with increased tumor proliferation and poor prognosis.

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

• Binetrakin - A recombinant agent chemically identical to or similar to the endogenous cytokine interleukin-4 (IL-4). Produced primarily by activated T-cells, IL-4 binds to and activates its cell-surface receptor, stimulating the proliferation and differentiation of activated B-cells and enhancing their ability to present antigens to T-cells. As a potential immunotherapeutic agent, binetrakin also augments the effects of other cytokines on dendritic cells (DC), cytotoxic T lymphocytes (CTL), and tumor-infiltrating lymphocytes (TIL).

• Binimetinib - An orally available inhibitor of mitogen-activated protein kinase kinase 1 and 2 (MEK1/2) with potential antineoplastic activity. Binimetinib, noncompetitive with ATP, binds to and inhibits the activity of MEK1/2. Inhibition of MEK1/2 prevents the activation of MEK1/2 dependent effector proteins and transcription factors, which may result in the inhibition of growth factor-mediated cell signaling. This may eventually lead to an inhibition of tumor cell proliferation and an inhibition in production of various inflammatory cytokines including interleukin-1, -6 and tumor necrosis factor. MEK1/2 are dual-specificity threonine/tyrosine kinases that play key roles in the activation of the RAS/RAF/MEK/ERK pathway and are often upregulated in a variety of tumor cell types.

• Bintrafusp alfa - A bifunctional fusion protein composed of avelumab, an anti-programmed death ligand 1 (PD-L1) human monoclonal antibody, bound to the soluble extracellular domain of human transforming growth factor beta (TGFbeta) receptor type II (TGFbetaRII), with potential antineoplastic and immune checkpoint modulating activities. Upon administration, the TGFbetaRII moiety of bintrafusp alfa binds to and neutralizes TGFbeta while the avelumab moiety simultaneously binds to PD-L1. This prevents TGFbeta- and PD-L1-mediated signaling, and increases natural killer (NK) cell and cytotoxic T-lymphocyte (CTL) activities. This inhibits tumor cell proliferation in susceptible tumor cells. TGFbeta and PD-L1 are both upregulated in certain types of cancers; their overexpression is associated with increased evasion of immune surveillance and contributes to poor prognosis.

• Birabresib - A synthetic, small molecule inhibitor of the BET (Bromodomain and Extra-Terminal) family of bromodomain-containing proteins 2, 3 and 4 with potential antineoplastic activity. Upon administration, birabresib binds to the acetylated lysine recognition motifs on the bromodomain of BET proteins, thereby preventing the interaction between the BET proteins and acetylated histone peptides. This disrupts chromatin remodeling and gene expression. Prevention of the expression of certain growth-promoting genes, including c-Myc-dependent target genes, may lead to an inhibition of tumor cell growth. Characterized by a tandem repeat of bromodomain at the N-terminus, the BET proteins BRD2, BRD3, BRD4 are transcriptional regulators that play an important role in cellular growth.

• Birinapant - A synthetic small molecule that is both a peptidomimetic of second mitochondrial-derived activator of caspases (SMAC) and inhibitor of IAP (Inhibitor of Apoptosis Protein) family proteins, with potential antineoplastic activity. As a SMAC mimetic and IAP antagonist, birinapant selectively binds to and inhibits the activity of IAPs, such as X chromosome-linked IAP (XIAP) and cellular IAPs 1 (cIAP1) and 2 (cIAP2), with a greater effect on cIAP1 than cIAP2. Since IAPs shield cancer cells from the apoptosis process, this agent may restore and promote the induction of apoptosis through apoptotic signaling pathways in cancer cells and inactivate the nuclear factor-kappa B (NF-kB)-mediated survival pathway. IAPs are overexpressed by many cancer cell types. They are able to suppress apoptosis by binding to, via their baculoviral lAP repeat (BIR) domains, and inhibiting active caspases-3, -7 and -9. IAP overexpression promotes both cancer cell survival and chemotherapy resistance.

• Bisantrene - An anthracenyl bishydrazone with antineoplastic activity. Bisantrene intercalates with and disrupts the configuration of DNA, resulting in DNA single-strand breaks, DNA-protein crosslinking, and inhibition of DNA replication. This agent is similar to doxorubicin in activity, but unlike doxorubicin, does not exhibit cardiotoxicity.

• Bisantrene hydrochloride - The hydrochloride salt of an anthracenyl bishydrazone with antineoplastic activity. Bisantrene intercalates with and disrupts the helical structure of DNA, resulting in DNA single-strand breaks, DNA-protein crosslinking, and inhibition of DNA replication. This agent is similar to doxorubicin in activity, but unlike doxorubicin, does not exhibit cardiotoxicity.

• Bi-shrna-furin/gm-csf-expressing autologous tumor cell vaccine - Autologous tumor cells transfected with a plasmid expressing recombinant human granulocyte macrophage-colony stimulating factor (rhGM-CSF) and bifunctional short hairpin RNA (bi-shRNA) against furin, with potential immunostimulatory and antineoplastic activities. Upon intradermal vaccination of bi-shRNA-furin/GM-CSF-expressing autologous tumor cell vaccine, expressed GM-CSF protein, a potent stimulator of the immune system, recruits immune effectors to the site of injection and promotes antigen presentation. The furin bifunctional shRNA blocks furin protein production. Decreased levels of furin lead to a reduction in the conversion of transforming growth factor (TGF) beta into TGF beta1 and beta2 protein isoforms. In turn, as part of the negative feedback mechanism, reduced furin protein levels inhibit TGFbeta1 and TGFbeta2 gene expression, thereby further decreasing TGF levels. As TGFs are potent immunosuppressive cytokines, reducing their levels may activate the immune system locally and this may eventually cause a cytotoxic T-lymphocyte (CTL) response against the tumor cells.

• Bisnafide - A bis-naphthalimide compound with anticancer activity. Bisnafide selectively intercalates guanine-cytosine (GC) rich regions of DNA, thereby interfering with DNA replication machinery and activity of topoisomerase II. As a result, this agent causes potent cytotoxicity.

• Bisnafide dimesylate - The dimesylate salt form of bisnafide, a bis-naphthalimide compound with anticancer activity. Bisnafide selectively intercalates guanine-cytosine (GC) rich regions of DNA, thereby interfering with DNA replication machinery and activity of topoisomerase II. As a result, this agent causes potent cytotoxicity.

• Bispecific antibody 2b1 - A monoclonal antibody with potential antineoplastic activity. Specific for both the immunoglobulin G (IgG) receptor CD16 and c-erbB-2, bispecific antibody 2B1 may enhance cellular immune responses against c-erbB-2-positive cells, resulting in increased tumor cell lysis.

• Bispecific antibody agen1223 - A bispecific antibody that simultaneously binds to two different and as of yet undisclosed antigens co-expressed specifically on tumor-infiltrating regulatory T-cells (Tregs), with potential immunomodulating and antineoplastic activities. Upon administration, AGEN1223 targets and binds to the two antigens co-expressed specifically on tumor-infiltrating Tregs. This leads to the selective depletion of immunosuppressive Tregs in the tumor microenvironment (TME), while sparing peripheral Tregs and effector T-cells, enhancing the overall antitumor response. AGEN1223 may also co-stimulate antigen-specific effector T-cells, resulting in tumor cell death.

• Bispecific antibody amg 509 - A bispecific antibody that simultaneously binds to two different and as of yet undisclosed antigens, with potential immunomodulating and antineoplastic activities. Upon administration, AMG 509 targets and binds to the two antigens. This may modulate the tumor microenvironment (TME) and may enhance an immune-mediated antitumor response.

• Bispecific antibody gs-1423 - A bispecific antibody that simultaneously binds two different as of yet undisclosed antigens, with potential immunomodulating and antineoplastic activities. Upon administration, GS-1423 targets and binds the two antigens. This may modulate the tumor microenvironment (TME) and may enhance an immune-mediated antitumor response.

• Bispecific antibody mdx447 - An antibody with potential antineoplastic activity. Specific for both the high-affinity immunoglobulin G (IgG) receptor CD64 and epidermal growth factor receptor (EGFR), bispecific antibody MDX447 may enhance cellular immune responses against EGFR positive cells, resulting in increased tumor cell lysis.

• Bispecific antibody mdx-h210 - A humanized bivalent antibody directed against both cytotoxic effector cells expressing Fc gamma receptor type I (Fc gammaRI, or CD64) and HER2/neu-overexpressing tumor cells with potential antineoplastic activity. Bispecific antibody MDX-H210 was constructed by chemically linking Fab' fragments of the anti-HER2/neu-specific monoclonal antibody 520C9 and the Fab' fragments of the anti-Fc gammaRI-specific monoclonal antibody H22. This agent selectively binds to both HER2/neu-expressing tumor cells and Fc gammaRI-expressing cytotoxic effector cells, which may trigger antibody-dependent cell-mediated cytotoxicity (ADCC) and cell lysis of HER2/neu-expressing tumor cells. While HER2/neu is overexpressed in a variety of epithelial malignancies, expression of Fc gammaRI is primarily found in cytotoxic immune cells, including monocytes, macrophages, and cytokine-activated polymorphonuclear (PMN) cells.

• Bisthianostat - An orally bioavailable pan-inhibitor of human histone deacetylase (HDAC), with potential antineoplastic activity. Upon administration, bisthianostat selectively binds to and inhibits HDACs, which inhibits deacetylation of histone proteins and leads to the accumulation of highly acetylated histones. This may result in an induction of chromatin remodeling, the inhibition of tumor oncogene transcription, and the selective transcription of tumor suppressor genes. This prevents cell division, induces cell cycle arrest and apoptosis. This may inhibit the proliferation of susceptible tumor cells. HDACs, upregulated in many tumor cell types, are a family of enzymes that deacetylate histone proteins.

• Bite antibody amg 910 - A half-life extended (HLE), bispecific T-cell engager (BiTE) antibody that simultaneously binds to two different and as of yet undisclosed antigens, with potential immunomodulating and antineoplastic activities. Upon administration, AMG 910 targets and binds to the two antigens. This may modulate the tumor microenvironment (TME) and may enhance an immune-mediated antitumor response.

• Bivalent brd4 inhibitor azd5153 - An orally bioavailable bivalent inhibitor of bromodomain-containing protein 4 (BRD4), with potential antineoplastic activity. Upon oral administration, the BRD4 inhibitor AZD5153 selectively binds to the acetylated lysine recognition motifs in two bromodomains in the BRD4 protein, thereby preventing the binding of BRD4 to acetylated lysines on histones. This disrupts chromatin remodeling and dysregulates expression of target genes, which leads to the downregulation of the expression of certain growth-promoting genes, induces apoptosis and inhibits the proliferation of BRD4-overexpressing tumor cells. BRD4, a member of the human bromodomain and extra-terminal (BET) family of proteins, is a transcriptional regulator that is overexpressed in certain tumor cells and plays an important role in cellular proliferation.

• Bivalent hpv16/18 therapeutic cervical cancer vaccine - A bivalent human papillomavirus (HPV) therapeutic vaccine containing recombinant inactivated adenylate cyclase (CyaA) from Bordetella pertussis carrying a sequence encoding the E7 antigen of both HPV16 and 18, with potential immunostimulatory and antiviral properties. Upon administration of bivalent HPV16/18 therapeutic cervical cancer vaccine, the expressed proteins may activate cell-mediated immunity and induce both cytotoxic CD8+ T cells and CD4+ helper T cells against the target antigens HPV16-E7 and HPV18-E7, which leads to HPV viral clearance. Adenylate cyclase is a virulence factor of Bordetella pertussis. Its ability to bind to CD11b-expressing dendritic cells and deliver antigens directly to the cytosol allows the activation and induction of T-cell immunity. CyaA may also induce a B cell response.

• Bizalimogene ralaplasmid - A DNA vaccine consisting of plasmids encoding the E6 and E7 genes of human papilloma virus (HPV) subtypes 16 and 18, respectively, with potential immunostimulating and antineoplastic activities. Administered via intramuscular electroporation, bizalimogene ralaplasmid expresses E6 and E7 proteins, which may elicit a cytotoxic T-lymphocyte (CTL) response against cervical cancer cells expressing E6 and E7 proteins, resulting in tumor cell lysis. HPV type 16 and HPV type 18 are the most common HPV types involved in cervical carcinogenesis.

• Bizelesin - A synthetic cyclopropylpyrroloindole antineoplastic antibiotic. Bizelesin binds to the minor groove of DNA and induces interstrand cross-linking of DNA, thereby inhibiting DNA replication and RNA synthesis. Bizelesin also enhances p53 and p21 induction and triggers G2/M cell-cycle arrest, resulting in cell senescence without apoptosis.

• Bl22 immunotoxin - A recombinant immunotoxin consisting of the Fv portion of the anti-CD22 antibody RFB4 fused to a fragment of Pseudomonas exotoxin-A with potential antineoplastic activity. BL22 immunotoxin binds to CD22, an antigen expressed in B-cell malignancies, thereby delivering its toxin directly to tumor cells. The toxin moiety induces caspase-mediated apoptosis of tumor cells via a mechanism involving mitochondrial damage; it also blocks translational elongation via binding to elongation factor-2 in eukaryotic cells.

• Black cohosh - A triterpene-containing herb isolated from the roots and rhizomes of the plant Cimicifuga racemosa (also known as Actaea racemosa). While the mechanism of action of black cohosh is not completely understood, it appears to act as a selective estrogen receptor modulator. In vitro, this preparation has been shown to induce cell cycle arrest and caspase-dependent apoptosis of estrogen-sensitive breast cancer cells.

• Black raspberry nectar - A concentrated fruit juice containing black raspberries, with potential antioxidant, pro-apoptotic, anti-angiogenic and chemopreventive activities. In addition to vitamins, minerals and phytosterols, black raspberries are rich in phenolic acids, such as gallic acid, ellagic acid, anthocyanidins, and flavonoids. Upon oral administration, the phytochemicals in the black raspberry nectar inhibit the activation of several signal transduction pathways involved in carcinogenesis and the expression of downstream target genes that are upregulated in a variety of cancer cell types. In addition, the phytochemicals in black raspberry may protect the oral microbiome and may enhance the bacterial defense against pathogens.

• Bleomycin - A mixture of glycopeptide antineoplastic antibiotics isolated from the bacterium Streptomyces verticillus. Bleomycin forms complexes with iron that reduce molecular oxygen to superoxide and hydroxyl radicals which cause single- and double-stranded breaks in DNA; these reactive oxygen species also induce lipid peroxidation, carbohydrate oxidation, and alterations in prostaglandin synthesis and degradation.

• Bleomycin a2 - The primary bleomycin species in bleomycin sulfate, a mixture of the sulfate salts of several basic glycopeptide antineoplastic antibiotics isolated from Streptomyces verticillus. Bleomycin A2 forms complexes with iron that reduce molecular oxygen to superoxide and hydroxyl radicals which cause single- and double-stranded breaks in DNA; these reactive oxygen species also induce lipid peroxidation, carbohydrate oxidation, and alterations in prostaglandin synthesis and degradation.

• Bleomycin b2 - One of the primary bleomycin species in bleomycin sulfate, a mixture of the sulfate salts of glycopeptide bleomycin A2 and B2 isolated from Streptomyces verticillus with potential antineoplastic activity. Bleomycin B2 forms complexes with iron that reduce molecular oxygen to superoxide and hydroxyl radicals which cause single- and double-stranded breaks in DNA; these reactive oxygen species also induce lipid peroxidation, carbohydrate oxidation, and alterations in prostaglandin synthesis and degradation.

• Bleomycin sulfate - A mixture of the sulfate salts of basic glycopeptide antineoplastic antibiotics isolated from Streptomyces verticillus. Bleomycin sulfate forms complexes with iron that reduce molecular oxygen to superoxide and hydroxyl radicals which cause single- and double-stranded breaks in DNA; these reactive oxygen species also induce lipid peroxidation, carbohydrate oxidation, and alterations in prostaglandin synthesis and degradation.

• Blinatumomab - A recombinant, single-chain, anti-CD19/anti-CD3 bispecific monoclonal antibody with potential immunostimulating and antineoplastic activities. Blinatumomab possesses two antigen-recognition sites, one for the CD3 complex, a group of T cell surface glycoproteins that complex with the T cell receptor (TCR), and one for CD19, a tumor-associated antigen (TAA) overexpressed on the surface of B cells. This bispecific monoclonal antibody brings CD19-expressing tumor B-cells and cytotoxic T lymphocytes (CTLs) and helper T lymphocytes (HTLs) together, which may result in the CTL- and HTL-mediated cell death of CD19-expressing B-lymphocytes.

• Blueberry powder supplement - An orally available, dietary supplement consisting of lyophilized blueberry powder, with antioxidant and potential chemopreventive and chemosensitizing activity. In addition to vitamins and minerals, blueberries are rich in phytonutrients, such as proanthocyanidins, anthocyanins (e.g. malvidin, delphinidin, pelargonidin, cyanidin, petunidin, and peonidin), hydroxycinnamic acids, hydroxybenzoic acids, pterostilbene, resveratrol, and flavonols (e.g. kaempferol, quercetin and myricetin). Although the exact mechanism of action through which blueberries may exert their anti-tumor effect has yet to be fully elucidated, the effects of blueberry powder on cancer cells may be attributable to the phytonutrient's antioxidant and pro-apoptotic activities.

• Bmi1 inhibitor ptc596 - An orally active inhibitor of the polycomb ring finger oncogene BMI1 (B-cell-specific Moloney murine leukemia virus integration site 1), with potential antineoplastic activity. Upon oral administration, BMI1 inhibitor PTC596 targets BMI1 expressed by both tumor cells and cancer stem cells (CSCs), and induces hyper-phosphorylation of BMI1 leading to its degradation. This inhibits BMI1-mediated signal transduction pathways and results in a reduction of proliferation of BMI1-expressing tumor cells. BMI1, a key protein in the polycomb repressive complex 1 (PRC1), is overexpressed in certain tumor cell types, and plays a key role in CSC survival, proliferation and resistance to chemotherapeutics; its expression is associated with increased tumor aggressiveness and a poor prognosis.

• Bms-184476 - A 7-methylthiomethyl ether derivative of paclitaxel with antineoplastic activity. BMS-184476 binds to and stabilizes the resulting microtubules, thereby inhibiting microtubule disassembly which results in cell- cycle arrest at the G2/M phase and apoptosis. (NCI)

• Bms-188797 - An analog of paclitaxel with antineoplastic activity. BMS-188797 binds to and stabilizes the resulting microtubules, thereby inhibiting microtubule disassembly which results in cell- cycle arrest at the G2/M phase and apoptosis. (NCI)

• Bms-214662 - A nonsedating benzodiazepine derivative with potential antineoplastic activity. Farnesyltransferase inhibitor BMS-214662 inhibits the enzyme farnesyltransferase and the post-translational farnesylation of number of proteins involved in signal transduction, which may result in the inhibition of Ras function and apoptosis in susceptible tumor cells. This agent may reverse the malignant phenotype of H-Ras-transformed cells and has been shown to be active against tumor cells with and without Ras mutations.

• Bms-275183 - An orally available, C-4 methyl carbonate analog of paclitaxel with potential antineoplastic activity. Like paclitaxel, BMS-275183 binds to tubulin and stabilizes microtubules, thereby inhibiting microtubule disassembly which results in cell-cycle arrest at the G2/M phase and an induction of apoptosis.

• Boanmycin hydrochloride - The hydrochloride salt form of boanmycin (aka bleomycin A6), a component of the antibiotic bleomycin produced by Streptomyces species, with potential antineoplastic activity. Upon administration, boanmycin forms complexes with iron that reduce molecular oxygen to superoxide and hydroxyl radicals. This causes single- and double-stranded DNA breaks which eventually leads to cell death. Compared to bleomycin, boanmycin appears to have a more favorable toxicity profile.

• Bomedemstat - An orally available, irreversible inhibitor of lysine-specific demethylase 1 (LSD1), with potential antineoplastic activity. Upon administration, bomedemstat binds to and inhibits LSD1, a demethylase that suppresses the expression of target genes by converting the di- and mono-methylated forms of lysine at position 4 of histone H3 (H3K4) to mono- and unmethylated H3K4. LSD1 inhibition enhances H3K4 methylation and increases the expression of tumor suppressor genes. In addition, LSD1 demethylates mono- or di-methylated H3K9 which increases gene expression of tumor promoting genes; thus, inhibition of LSD1 also promotes H3K9 methylation and decreases transcription of these genes. Altogether, this may lead to an inhibition of cell growth in LSD1-overexpressing tumor cells. LSD1, an enzyme belonging to the flavin adenine dinucleotide (FAD)-dependent amine oxidase family is overexpressed in certain tumor cells and plays a key role in the regulation of gene expression, tumor cell growth and survival.

• Boronophenylalanine-fructose complex - A boronated phenylalanine complexed with fructose to increase its solubility. When exposed to neutron irradiation, boronophenylalanine absorbs neutrons and self-destructs releasing short-range alpha radiation and 'recoil' lithium in tumor cells, resulting in alpha radiation-induced tumor cell death. This highly selective, localized radiotargeting of tumor cells, known as boron neutron capture therapy (BNCT), spares adjacent normal tissues.

• Bortezomib - A dipeptide boronic acid analogue with antineoplastic activity. Bortezomib reversibly inhibits the 26S proteasome, a large protease complex that degrades ubiquinated proteins. By blocking the targeted proteolysis normally performed by the proteasome, bortezomib disrupts various cell signaling pathways, leading to cell cycle arrest, apoptosis, and inhibition of angiogenesis. Specifically, the agent inhibits nuclear factor (NF)-kappaB, a protein that is constitutively activated in some cancers, thereby interfering with NF-kappaB-mediated cell survival, tumor growth, and angiogenesis. In vivo, bortezomib delays tumor growth and enhances the cytotoxic effects of radiation and chemotherapy.

• Bosutinib - A synthetic quinolone derivative and dual kinase inhibitor that targets both Abl and Src kinases with potential antineoplastic activity. Unlike imatinib, bosutinib inhibits the autophosphorylation of both Abl and Src kinases, resulting in inhibition of cell growth and apoptosis. Because of the dual mechanism of action, this agent may have activity in resistant CML disease, other myeloid malignancies and solid tumors. Abl kinase is upregulated in the presence of the abnormal Bcr-abl fusion protein which is commonly associated with chronic myeloid leukemia (CML). Overexpression of specific Src kinases is also associated with the imatinib-resistant CML phenotype.

• Bosutinib monohydrate - The monohydrate form of bosutinib, a synthetic quinolone derivative and dual kinase inhibitor that targets both Abl and Src kinases with potential antineoplastic activity. Unlike imatinib, bosutinib inhibits the autophosphorylation of both Abl and Src kinases, resulting in inhibition of cell growth and apoptosis. Because of the dual mechanism of action, this agent may have activity in resistant CML disease, other myeloid malignancies and solid tumors. Abl kinase is upregulated in the presence of the abnormal Bcr-abl fusion protein which is commonly associated with chronic myeloid leukemia (CML). Overexpression of specific Src kinases is also associated with the imatinib-resistant CML phenotype.

• Botanical agent bel-x-hg - An orally available botanically-based agent with potential antineoplastic activity. Upon oral administration, the components in BEL-X-HG may exert cytotoxic effects against cancer cells.

• Botanical agent leac-102 - A botanical-based formulation derived from the Taiwanese mushroom Antrodia cinnamomea, with potential antineoplastic activity, Upon administration, the components in LEAC-102 may exert cytotoxic effects against cancer cells.

• Bovine cartilage - Cartilage extracted from various parts of a cow and is proposed to stimulate the immune system and inhibit tumor cell growth. It was used in the 1950s and 60s to enhance wound healing. (NCI)

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

• Bp-cx1-platinum complex bp-c1 - A combination agent composed of the benzo-poly-carbonic-acid polymer BP-Cx1 chelated to platinum with potential antineoplastic activity. Upon intramuscular injection, the polymer moiety of BP-Cx1-Platinum Complex BP-C1 (BP-C1) alters the permeability of the cell membranes, which allows for increased penetration of platinum into tumor cells. In turn, platinum binds to nucleophilic groups such as GC-rich sites in DNA and induces intrastrand and interstrand DNA cross-links, as well as DNA-protein cross-links. These cross-links result in apoptosis and cell growth inhibition. In addition, the BP-Cx1 ligand is able to stimulate the innate immune system and upregulates a variety of cytokines including interferon, tumor necrosis factor-alpha (TNF-alpha), granulocyte macrophage-colony stimulating factor (GM-CSF), and various interleukins (ILs) such as IL-6 and IL-25. In comparison to cisplatin and other platinum-based compounds, treatment with BP-C1 allows for less platinum administration, which reduces platinum-associated systemic toxicity and side effects, and enhances the safety profile while maintaining or improving its efficacy.

• Br96-doxorubicin immunoconjugate - An antibody-drug conjugate composed of the chimeric monoclonal antibody BR96 chemically linked to the cytotoxic drug doxorubicin. The antibody moiety of BMS-182248-1 binds to Lewis Y, a cell surface antigen expressed on many solid tumor types. Thus, the doxorubicin conjugate is targeted specifically to Lewis Y-expressing tumor cells, where it intercalates with DNA, thereby inhibiting DNA replication and repair, RNA synthesis and protein synthesis. (NCI)

• Brachyury-expressing modified vaccinia ankara-tricom vaccine - A cancer vaccine composed of a replication-deficient, attenuated derivative of the vaccinia virus strain Ankara expressing both a CD8+ T-cell epitope from the brachyury protein and a triad of T-cell co-stimulatory molecules (MVA Brachyury-TRICOM), with potential immunomodulating and antineoplastic activities. Upon subcutaneous administration of the brachyury-expressing modified vaccinia Ankara (MVA)-TRICOM vaccine, the expressed brachyury protein induces specific CD8+ and CD4+ T-cell responses against brachyury-expressing tumor cells. This causes both tumor cell lysis and a decrease in the growth of brachyury-expressing tumor cells. Brachyury, a member of the T-box family of transcription factors that is overexpressed in numerous cancer cell types, is correlated with increased epithelial-mesenchymal transition (EMT), cancer resistance and cancer progression. TRICOM, a triad of three human T-cell co-stimulatory molecules, B7.1, ICAM-1 and LFA-3, enhances antigen-specific T-cell activation.

• Brachyury-expressing yeast vaccine gi-6301 - A cancer vaccine composed of a heat-killed, recombinant form of the yeast Saccharomyces cerevisiae that is genetically modified to express the transcription factor brachyury protein, with potential antineoplastic activity. Upon subcutaneous administration, the brachyury-expressing yeast vaccine GI-6301 is recognized by dendritic cells, processed, and presented by Class I and II MHC molecules on the dendritic cell surface. This elicits a targeted CD4+ and CD8+ T-lymphocyte-mediated immune response. This process kills brachyury-expressing tumor cells. Brachyury is overexpressed in a variety of tumor types and plays an important role in cancer progression and metastasis.

• Braf inhibitor arq 736 - An orally bioavailable, highly soluble phosphate prodrug of B-raf (BRAF) protein kinase with potential antineoplastic activity. BRAF inhibitor ARQ 736 is converted into its active form ARQ 680 in the presence of phosphatases. In turn, ARQ 680 selectively binds to and inhibits the activity of oncogenic B-raf, which may inhibit the proliferation of tumor cells expressing mutated B-raf gene. B-raf belongs to the raf/mil family of serine/threonine protein kinases and plays a role in regulating the MAP kinase/ERKs signaling pathway, which may be constitutively activated due to BRAF gene mutations. The valine to glutamic acid substitution at residue 600 (V600E) accounts for about 90% of BRAF gene mutations.

• Braf inhibitor bgb-3245 - An orally available inhibitor of both monomer and dimer forms of activating mutations of the serine/threonine-protein kinase BRAF (B-raf) protein, including V600 BRAF mutations, non-V600 BRAF mutations, and RAF fusions, with potential antineoplastic activity. Upon administration, BRAF inhibitor BGB-3245 targets and binds to both monomeric and dimeric forms of activating BRAF mutations and fusions. This may result in the inhibition of BRAF-mediated signaling and inhibit proliferation in tumor cells expressing BRAF mutations and fusions. BRAF belongs to the RAF family of serine/threonine protein kinases and plays a role in regulating the mitogen-activated protein kinase (MAPK)/ extracellular signal-regulated kinase (ERK) signaling pathway, which is often dysregulated in human cancers and plays a key role in tumor cell proliferation and survival. BRAF mutations and fusions have been identified in a number of solid tumors and are drivers of cancer growth.

• Braf inhibitor lut014 - A topically bioavailable small molecule inhibitor of serine/threonine-protein kinase B-raf (BRAF) protein with potential chemoprotective activity. Upon topical administration, BRAF inhibitor LUT014 targets and binds BRAF and, through the paradoxical effect of BRAF inhibition, induces mitogen-activated protein kinase (MAPK) signaling, which leads to the proliferation and migration of healthy human keratinocytes. This decreases dermal toxicities associated with epidermal growth factor (EGFR) inhibitor therapy. BRAF, a member of the raf family of serine/threonine protein kinases, plays a role in the regulation of MAPK/extracellular signal-regulated kinase (ERK) signaling pathways.

• Braf inhibitor plx8394 - An orally bioavailable inhibitor of serine/threonine-protein kinase B-raf (BRAF) protein with potential antineoplastic activity. BRAF inhibitor PLX8394 appears to selectively bind to and inhibit the activity of both wild-type and mutated forms of BRAF, which may subsequently inhibit the proliferation of tumor cells which express mutated forms of BRAF. This inhibitor appears to be effective against tumors that express multiple mutated forms of the kinase and may be an effective therapeutic agent for tumors that are resistant to other BRAF inhibitor therapies that are specific for the BRAF V600E mutant. BRAF, a member of the raf family of serine/threonine protein kinases, plays a role in the regulation of MAP kinase/ERK signaling pathways, which may be constitutively activated due to BRAF gene mutations. Mutated forms of BRAF are associated with a number of neoplastic diseases.

• Braf(v600e) kinase inhibitor abm-1310 - An orally bioavailable, small molecule inhibitor of mutant (V600E) v-raf murine sarcoma viral oncogene homolog B1 (BRAF) with potential antineoplastic activity. Upon oral administration, BRAF(V600E) kinase inhibitor ABM-1310 selectively binds to and inhibits the activity of BRAF(V600E) kinase, which may result in the inhibition of an over-activated MAPK signaling pathway downstream in BRAF(V600E) kinase-expressing tumor cells and a reduction in tumor cell proliferation. BRAF belongs to the raf/mil family of serine/threonine protein kinases and plays a role in regulating the MAP kinase/ERKs signaling pathway. The valine to glutamic acid substitution at residue 600 accounts for about 90% of BRAF gene mutations. The oncogenic product, BRAF(V600E) kinase, exhibits a markedly elevated activity that over-activates the MAPK signaling pathway. The BRAF(V600E) mutation has been found to occur in about 8% of all tumors.

• Braf(v600e) kinase inhibitor ro5212054 - An orally available small-molecule inhibitor of mutant (V600E) v-raf murine sarcoma viral oncogene homolog B1 (BRAF) with potential antineoplastic activity. BRAF(V600E) kinase inhibitor RO5212054 selectively binds to the ATP-binding site of BRAF(V600E) kinase and inhibits its activity, which may result in an inhibition of an over-activated MAPK signaling pathway downstream in BRAF(V600E) kinase-expressing tumor cells and a reduction in tumor cell proliferation. The valine to glutamic acid substitution at residue 600 accounts for about 90% of BRAF gene mutations; the oncogenic product, BRAF(V600E) kinase, exhibits a markedly elevated activity that over-activates the MAPK signaling pathway. The BRAF(V600E) mutation has been found to occur in approximately 60% of melanomas, and in about 8% of all solid tumors.

• B-raf/vegfr-2 inhibitor raf265 - An orally bioavailable small molecule with potential antineoplastic activity. CHIR-265 binds and inhibits Raf kinases, which may result in a reduction of tumor cell growth and proliferation, and tumor cell death. In addition, this agent inhibits vascular endothelial growth factor receptor type 2 (VEGFR-2), thereby disrupting tumor angiogenesis. Raf kinases are critical enzymes in the Ras/Raf/MEK/ERK signaling pathway and are frequently upregulated in neoplasms.

• Brafv600/pi3k inhibitor asn003 - A selective inhibitor of mutated forms of B-RAF kinase at amino acid position 600 (BRAFV600), including BRAFV600E, the alpha, delta and, to a lesser extent, beta isoforms of phosphatidylinositide 3-kinase (PI3K), including mutated forms of PI3KCA, which encodes the p110-alpha catalytic subunit of the class I PI3K, and the phosphatase and tensin homologs (PTEN) with loss-of-function mutation, with potential antineoplastic activity. Upon administration of ASN003, this agent selectively targets, binds to and inhibits the activity of BRAFV600 mutants as well as mutated isoforms of PI3K. This inhibits signaling through B-RAF- and PI3K/mechanistic target of rapamycin (mTOR)-mediated pathways and inhibits cellular proliferation in tumor cells with BRAFV600 mutations, those expressing PI3K and/or those driven by PTEN. Dysregulation of the B-RAF- and PI3K-mediated pathways is frequently seen in a variety of tumors and results in increased tumor cell growth and survival. Dual targeting of both pathways may increase efficacy and anti-tumor potential compared to the targeting of just one pathway by a selective B-RAF inhibitor or selective PI3K pathway inhibitor alone.

• Brain tumor initiating cell vaccine - A cell-based cancer vaccine comprised of brain tumor initiating cells (BTICs), with potential immunostimulating and antineoplastic activity. BITCs are from the glioblastoma multiforme (GBM) cell line GBM-6 and contain glioma stem-like cell-associated antigens. Upon administration, the BITC vaccine may stimulate a specific anti-tumoral cytotoxic T-lymphocyte (CTL) response against brain tumor cancer cells and brain tumor stem like cells, resulting in tumor cell lysis. BITC have unique antigenicity and have the ability to self-renew; vaccination against BITC antigens may kill these cells and may prevent tumor recurrences.

• Branched-chain amino acid supplement - A nutritional supplement containing essential branched-chain amino acids (BCAAs), including leucine, isoleucine and valine, with potential anti-cachectic, antiangiogenic, hepatocellular carcinoma (HCC) inhibiting and hepatoprotective activities. Upon oral administration, BCAAs inhibit the expression of both hypoxia-inducible factor 1-alpha subunit (HIF-1a) and vascular endothelial growth factor (VEGF), which prevents VEGF-mediated angiogenesis in HCC cells. In addition, BCAAs inhibit proliferation and induce apoptosis of HCC cells by both suppressing the expression of insulin-like growth factor (IGF), and inhibiting the phosphatidylinositol 3-kinase (PI3K)/Akt/mammalian target of rapamycin (mTOR) pathway. BCAAs also correct the plasma amino acid imbalance and promote protein metabolism, including the synthesis of albumin and glycogen. They reduce oxidative stress by inducing the activation of genes involved in antioxidant defenses, which prevent the production of reactive oxygen species (ROS). BCAAs also strengthen the immune system by increasing hepatic lymphocytes and stimulating natural killer (NK) cell activity. This supplement is able to improve insulin resistance and promote ammonia detoxification through increased glutamine (Gln) production.

• Brd4 inhibitor plx2853 - An orally bioavailable inhibitor of the bromodomain-containing protein 4 (BRD4), with potential antineoplastic activity. Upon oral administration, the BRD4 inhibitor PLX2853 binds to the acetylated lysine recognition motifs in the bromodomains of the BRD4 protein, thereby preventing the binding of BRD4 to acetylated lysines on histones. This disrupts chromatin remodeling and dyregulates gene expression. This may lead to the downregulation of the expression of certain growth-promoting genes, which may induce apoptosis and inhibit the proliferation of BRD4-overexpressing tumor cells. BRD4, a member of the human bromodomain and extra-terminal (BET) family of proteins, is a transcriptional regulator that is overexpressed in certain tumor cells and plays an important role in cellular proliferation.

• Brd4 inhibitor plx51107 - An inhibitor of the bromodomain-containing protein 4 (BRD4), with potential antineoplastic activity. Upon administration, the BRD4 inhibitor PLX51107 binds to the acetylated lysine recognition motifs in the bromodomains of the BRD4 protein, thereby preventing the binding of BRD4 to acetylated lysines on histones. This disrupts chromatin remodeling and gene expression. Prevention of the expression of certain growth-promoting genes may lead to an induction of apoptosis and an inhibition of proliferation in BRD4-overexpressing tumor cells. BRD4, a member of the human bromodomain and extra-terminal (BET) family of proteins, is a transcriptional regulator that is overexpressed in certain tumor cells and plays an important role in cellular proliferation.

• Breflate - A water soluble analogue of the antineoplastic agent brefeldin A (BFA).

• Brentuximab - A genetically-engineered, chimeric mouse-human, anti-CD30 monoclonal antibody with potential antineoplastic activity. Brentuximab specifically binds to the receptor CD-30, a member of the tumor necrosis factor receptor super-family, which may be overexpressed on the surfaces of Hodgkin lymphoma cells and anaplastic-large cell lymphoma cells. After binding to CD30, this agent interferes with the G1 phase of the cell cycle, thereby inducing growth arrest and apoptosis in susceptible tumor cell populations.

• Brentuximab vedotin - An antibody-drug conjugate (ADC) directed against the tumor necrosis factor (TNF) receptor CD30 with potential antineoplastic activity. Brentuximab vedotin is generated by conjugating the chimeric anti-CD30 monoclonal antibody SGN-30 to the cytotoxic agent monomethyl auristatin E (MMAE) via a valine-citrulline peptide linker. Upon administration and internalization by CD30-positive tumor cells, brentuximab vedotin undergoes enzymatic cleavage, releasing MMAE into the cytosol; MMAE binds to tubulin and inhibits tubulin polymerization, which may result in G2/M phase arrest and tumor cell apoptosis. Transiently activated during lymphocyte activation, CD30 (tumor necrosis factor receptor superfamily, member 8;TNFRSF8) may be constitutively expressed in hematologic malignancies including Hodgkin lymphoma and some T-cell non-Hodgkin lymphomas. The linkage system in brentuximab vedotin is highly stable in plasma, resulting in cytotoxic specificity for CD30-positive cells.

• Brequinar - A synthetic quinolinecarboxylic acid analogue with antineoplastic properties. Brequinar inhibits the enzyme dihydroorotate dehydrogenase, thereby blocking de novo pyrimidine biosynthesis. This agent may also enhance the in vivo antitumor effect of antineoplastic agents such as 5-FU.

• Brequinar sodium - The sodium salt form of Brequinar. Brequinar inhibits the enzyme dihydroorotate dehydrogenase, thereby blocking de novo pyrimidine biosynthesis. This agent may also enhance the in vivo antitumor effect of antineoplastic agents such as 5-FU.

• Brexucabtagene autoleucel - A preparation of autologous peripheral blood T-lymphocytes (PBTL) that have been transduced with a retroviral vector expressing a chimeric antigen receptor (CAR) consisting of an anti-CD19 single chain variable fragment (scFv) coupled to the costimulatory signaling domain CD28 and the zeta chain of the T-cell receptor (TCR)/CD3 complex (CD3 zeta), with potential immunostimulating and antineoplastic activities. Upon intravenous infusion and re-introduction of abrexucabtagene autoleucel into the patient, these cells bind to and induce selective toxicity in CD19-expressing tumor cells. CD19 antigen is a B-cell specific cell surface antigen that is expressed in all B-cell lineage malignancies. CD3 zeta is one of several membrane-bound polypeptides found in the TCR/CD3 complex; it regulates both the assembly and cell surface expression of TCR complexes. CD28 is essential for CD4+ T-cell proliferation, interleukin-2 production, and T-helper type-2 (Th2) development. KTE-X19 has the same construct as axicabtagene ciloleucel, but differs in the manufacturing process in that KTE-X19 includes specific T-cell selection and lymphocyte enrichment necessary for activity against certain B-cell malignancies.

• Briciclib sodium - A benzyl styryl sulfone analog, and a disodium phosphate ester prodrug of ON 013100, with potential antineoplastic activity. Upon hydrolysis, briciclib is converted to ON 013100, which blocks cyclin D mRNA translation and decreases protein expression of cyclin D. This may induce cell cycle arrest and apoptosis in cancer cells overexpressing cyclin D and eventually decrease tumor cell proliferation. This agent may exhibit synergistic antitumor activity in combination with other chemotherapeutic agents. Cyclin D, a member of the cyclin family of cell cycle regulators, plays a key role in cell cycle division and is often overexpressed in a variety of hematologic and solid tumors and is correlated with poor prognosis.

• Brigatinib - An orally available inhibitor of receptor tyrosine kinases anaplastic lymphoma kinase (ALK) and the epidermal growth factor receptor (EGFR) with potential antineoplastic activity. Brigatinib binds to and inhibits ALK kinase and ALK fusion proteins as well as EGFR and mutant forms. This leads to the inhibition of ALK kinase and EGFR kinase, disrupts their signaling pathways and eventually inhibits tumor cell growth in susceptible tumor cells. In addition, AP26113 appears to overcome mutation-based resistance. 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. EGFR is overexpressed in a variety of cancer cell types.

• Brilanestrant - An orally available, nonsteroidal selective estrogen receptor degrader (SERD), with potential antineoplastic activity. Upon oral administration, brilanestrant binds to the estrogen receptor and induces a conformational change that results in the degradation of the receptor. This may inhibit the growth and survival of ER-expressing cancer cells.

• Brivanib - A pyrrolotriazine-based compound and an inhibitor of vascular endothelial growth factor receptor-2 (VEGFR-2) with potential antineoplastic activity. BMS-540215 specifically targets and binds strongly to human VEGFR-2, a tyrosine kinase receptor and pro-angiogenic growth factor expressed almost exclusively on vascular endothelial cells. Blockade of VEGFR-2 by this agent may lead to an inhibition of VEGF-stimulated endothelial cell migration and proliferation, thereby inhibiting tumor angiogenesis.

• Brivanib alaninate - The alaninate salt of a vascular endothelial growth factor receptor 2 (VEGFR2) inhibitor with potential antineoplastic activity. Brivanib strongly binds to and inhibits VEGFR2, a tyrosine kinase receptor expressed almost exclusively on vascular endothelial cells; inhibition of VEGFR2 may result in inhibition of tumor angiogenesis, inhibition of tumor cell growth, and tumor regression.

• Brivudine - A uridine derivative and nucleoside analog with pro-apoptotic and chemosensitizing properties. In vitro, bromovinyl-deoxyuridine (BVDU) has been shown to downregulate the multifunctional DNA repair enzyme APEX nuclease 1, resulting in the inhibition of DNA repair and the induction of apoptosis. In addition, this agent may inhibit the expression of STAT3 (signal transducer and activator of transcription 3), which may result in the downregulation of vascular endothelial growth factor (VEGF). BVDU has also been found to inhibit the upregulation of chemoresistance genes (Mdr1 and DHFR) during chemotherapy. Overall, the gene expression changes associated with BVDU treatment result in the decrease or prevention of chemoresistance. In addition, this agent has been shown to enhance the cytolytic activity of NK-92 natural killer cells towards a pancreatic cancer cell line in vitro.

• Brivudine phosphoramidate - A small molecule phosphoramidate derivative of (E)-5-(2-bromovinyl)-2'-deoxyuridine (BVdU) with potential antineoplastic activity. Selectively active against tumor cells expressing high levels of thymidylate synthase (TS), brivudine is converted intracellularly by TS to bromovinyldeoxyuridine monophosphate (BVdUMP) which competes with the natural substrate, deoxyuridine monophosphate, for binding to TS. Unlike TS inhibitors, this agent is a reversible substrate for TS catalysis. Thus, TS retains activity and converts BVdUMP into cytotoxic metabolites. As key enzyme in the de novo synthesis of dTMP, TS is an enzyme critical to DNA biosynthesis and is overexpressed in many solid tumors.

• Broad-spectrum human papillomavirus vaccine v505 - A non-infectious recombinant cancer vaccine prepared from the human papillomavirus (HPV) with potential immunoprophylactic activity. Vaccination with broad-spectrum human papillomavirus vaccine V505 may stimulate the host immune system to mount humoral and cytotoxic T lymphocyte (CTL) responses against HPV-infected cells. HPV infection, the cause of genital warts, is a risk factor for the development of cancers of the cervix, vagina, vulva, anus, and penis.

• Broccoli sprout/broccoli seed extract supplement - A tablet-based nutritional supplement composed of a mixture of sprout and seed extracts of the cruciferous vegetable broccoli, with potential chemopreventive and antioxidant activities. Broccoli sprout/broccoli seed extract contains a high amount of both the glycosinolate glucoraphanin and the enzyme myrosinase, which catalyzes the production of glucoraphanin to sulforaphane. Upon administration of the broccoli sprout/broccoli seed extract, sulforaphane activates the transcription factor NF-E2-related factor 2 (Nrf2), a member of the basic leucine zipper family, which binds to and activates antioxidant-response elements (AREs). Subsequently, activated AREs promote the transcription of antioxidant and detoxifying enzymes, particularly glutathione-S-transferase and NAD(P)H dehydrogenase [quinone] 1 (NAD(P)H:quinone oxidoreductase; NQO1), resulting in the detoxification of highly reactive carcinogens. This accelerates the elimination of carcinogens, may protect against cellular damage, and prevents cancer formation. AREs are cis-acting regulatory enhancer elements found in the 5' flanking region of many phase II detoxification enzymes.

• Bromacrylide - A propenamide-based agent with antineoplastic activity. Bromacrylide has been shown to decrease tumor growth in animal models, but is accompanied with severe toxicity, including severe bone marrow suppression and weight loss.

• Bromebric acid - A derivative of bromoacrylic acid with cytostatic and antineoplastic activity. Bromebric acid appears to inhibit purine synthesis, oxidative phosphorylation and DNA synthesis. This agent inhibits tumor cell growth and causes cell cycle arrest. This agent may also have some use in the phrophylaxis of migraine.

• Bromocriptine mesylate - The mesylate salt of bromocriptine, a semisynthetic ergot alkaloid with dopaminergic, antidyskinetic, and antiprolactinemic activities. Bromocriptine selectively binds to and activates postsynaptic dopamine D2 receptors in the corpus striatum of the central nervous system (CNS). Activation of these D2 receptors activate inhibitory G-proteins, which inhibit adenylyl cyclase, preventing signal transduction mediated via cAMP and resulting in the inhibition of neurotransmission and an antidyskinetic effect. This agent also stimulates dopamine D2 receptors in the anterior pituitary gland, which results in the inhibition of prolactin secretion and lactation and may inhibit the proliferation of prolactin-dependent breast cancer cells.

• Brontictuzumab - A humanized monoclonal antibody directed against the Notch-1 receptor with potential antineoplastic activity. Upon administration, brontictuzumab binds to Notch-1 on the cell surface, thereby inhibiting Notch-mediated signaling and tumor cell proliferation. Notch 1, a type 1 transmembrane protein belonging to the Notch family, functions as a receptor for membrane bound ligands and has various roles during development; dysregulated Notch signaling is associated with increased cell growth and chemoresistance in cancers.

• Brostacillin hydrochloride - The hydrochloride salt form of brostacillin, a synthetic, alpha-bromoacrylic, second-generation minor groove binder (MGB), related to distamycin A, with potential antineoplastic activity. Brostallicin binds to DNA minor groove DNA, after having formed a highly reactive glutathione (GSH)-brostallicin complex in the presence of the enzyme glutathione S-transferase (GST), which is overexpressed in cancer cells; DNA replication and cell division are inhibited, resulting in tumor cell death. Compared to typical MGBs, this agent appears to bind covalently to DNA in a different manner and its activity does not depend on a functional DNA mismatch repair (MMR) mechanism. Accordingly, brostallicin may be effective against MMR-defective tumors that are refractory to various anticancer agents.

• Brostallicin - A synthetic, alpha-bromoacrylic, second-generation minor groove binder (MGB), related to distamycin A, with potential antineoplastic activity. Brostallicin binds to DNA minor groove DNA, after having formed a highly reactive glutathione (GSH)-brostallicin complex in the presence of the enzyme glutathione S-transferase (GST), which is overexpressed in cancer cells; DNA replication and cell division are inhibited, resulting in tumor cell death. Compared to typical MGBs, this agent appears to bind covalently to DNA in a different manner and its activity does not depend on a functional DNA mismatch repair (MMR) mechanism. Accordingly, brostallicin may be effective against MMR-defective tumors that are refractory to various anticancer agents.

• Broxuridine - A halogenated thymidine analogue with potential antineoplastic and radiosensitizing activities. Bromodeoxyuridine competes with thymidine for incorporation into DNA, resulting in DNA mutation and the inhibition of cell proliferation. As a radiosensitizer, this agent is associated with the inhibition of repair of radiation-induced DNA double-strand breaks.

• Bruceanol a - A quassinoid phytochemical isolated from the plant Brucea antidysenterica with potential antineoplastic activity.

• Bruceanol b - A quassinoid phytochemical isolated from the plant Brucea antidysenterica with potential antineoplastic activity.

• Bruceanol c - A quassinoid phytochemical isolated from the plant Brucea antidysenterica with potential antineoplastic activity.

• Bruceanol d - A quassinoid phytochemical isolated form the plant Brucea antidysenterica with potential antineoplastic activity.

• Bruceanol e - A quassinoid phytochemical isolated from the plant Brucea antidysenterica with potential antineoplastic activity.

• Bruceanol f - A quassinoid phytochemical isolated from the plant Brucea antidysenterica with potential antineoplastic activity.

• Bruceanol g - A natural quassinoid agent extracted from Brucea antidysenterica with potential antineoplastic activity that is cytotoxic to certain cancer cell lines.

• Bruceanol h - A quassinoid phytochemical isolated from the plant Brucea antidysenterica with potential antineoplastic activity.

• Bruceantin - A triterpene quassinoid antineoplastic antibiotic isolated from the plant Brucea antidysenterica. Bruceantin inhibits the peptidyl transferase elongation reaction, resulting in decreased protein and DNA synthesis. Bruceantin also has antiamoebic and antimalarial activity.

• Bryostatin 1 - A macrocyclic lactone isolated from the bryozoan Bugula neritina with antineoplastic activity. Bryostatin 1 binds to and inhibits the cell-signaling enzyme protein kinase C, resulting in the inhibition of tumor cell proliferation, the promotion of tumor cell differentiation, and the induction of tumor cell apoptosis. This agent may act synergistically with other chemotherapeutic agents.

• Btk inhibitor arq 531 - An orally available reversible inhibitor of Bruton's tyrosine kinase (BTK; Bruton agammaglobulinemia tyrosine kinase), with potential antineoplastic activity. Upon administration, ARQ 531 non-covalently binds to and inhibits the activity of both the wild-type and the C481S mutated form of BTK, a resistance mutation in the BTK active site in which cysteine is substituted for serine at residue 481. This prevents the activation of the B-cell antigen receptor (BCR) signaling pathway and BTK-mediated activation of downstream survival pathways. This leads to an inhibition of the growth of malignant B-cells that overexpress BTK. Compared to other BTK inhibitors, ARQ 531 does not require interaction with the BTK C481 site and inhibits the proliferation of cells harboring the BTK C481S mutation. 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.

• Btk inhibitor ct-1530 - An inhibitor of Bruton's tyrosine kinase (BTK; Bruton agammaglobulinemia tyrosine kinase), with potential antineoplastic activity. Upon administration, CT-1530 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. This leads to an inhibition of 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.

• Btk inhibitor dtrmwxhs-12 - An orally available inhibitor of Bruton's tyrosine kinase (BTK; Bruton agammaglobulinemia tyrosine kinase), with potential antineoplastic activity. Upon administration, DTRMWXHS-12 inhibits the activity of BTK and prevents the activation of the B-cell antigen receptor (BCR) signaling pathway. This prevents both B-cell activation and BTK-mediated activation of downstream survival pathways. This leads to an inhibition of 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 in B-cell malignancies; it plays an important role in the development, activation, signaling, proliferation and survival of B-lymphocytes.

• Btk inhibitor hz-a-018 - An orally bioavailable inhibitor of Bruton's tyrosine kinase (BTK), with potential antineoplastic activity. Upon administration, BTK inhibitor HZ-A-018 targets, binds to and inhibits the activity of BTK and prevents the activation of the B-cell antigen receptor (BCR) signaling pathway. This prevents both B-cell activation and BTK-mediated activation of downstream survival pathways. This leads to an inhibition of 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 in B-cell malignancies; it plays an important role in B lymphocyte development, activation, signaling, proliferation and survival.

• Btk inhibitor loxo-305 - An orally available, selective, non-covalent Bruton's tyrosine kinase (BTK) inhibitor with potential antineoplastic activity. Upon oral administration, BTK inhibitor LOXO-305 selectively and reversibly binds to BTK. This prevents both the activation of the B-cell antigen receptor (BCR) signaling pathway and BTK-mediated activation of downstream survival pathways, thereby inhibiting the growth of malignant B-cells that overexpress BTK. Reversible binding of LOXO-305 may preserve antitumor activity in the presence of certain acquired resistance mutations, including C481 mutated BTK, and limit toxicity associated with inhibition of other non-BTK kinases. 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.

• Btk inhibitor m7583 - An orally bioavailable, selective inhibitor of Bruton's tyrosine kinase (BTK), with potential antineoplastic activity. Upon administration, M7583 targets and covalently binds to BTK, thereby preventing its activity. This leads to an inhibition of B cell receptor (BCR) signaling and inhibits cell proliferation of B-cell malignancies. BTK, a cytoplasmic tyrosine kinase and member of the Tec family of kinases, plays an important role in B lymphocyte development, activation, signaling, proliferation and survival.

• Btk inhibitor tg-1701 - An orally available irreversible inhibitor of Bruton's tyrosine kinase (BTK; Bruton agammaglobulinemia tyrosine kinase) with potential antineoplastic activity. Upon administration, BTK inhibitor TG-1701 covalently binds to and irreversibly inhibits BTK activity, thereby preventing the activation of the B-cell antigen receptor (BCR) signaling pathway and BTK-mediated activation of downstream survival pathways. This may inhibit 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.

• Budigalimab - A monoclonal antibody directed against the negative immunoregulatory human cell surface receptor programmed cell death 1 (PD-1, PCD-1; PDCD1), with potential immune checkpoint inhibitory and antineoplastic activities. Upon administration, anti-PD-1 monoclonal antibody ABBV-181 targets and binds to PD-1, thereby blocking its binding to the PD-1 ligand, programmed cell death-1 ligand 1 (PD-L1), and preventing the activation of PD-1/PD-L1 downstream signaling pathways. This may restore immune function through the activation of cytotoxic T-lymphocytes (CTLs). PD-1, a transmembrane protein in the immunoglobulin superfamily expressed on activated T-cells, negatively regulates T-cell activation and effector function when activated by its ligand; it plays an important role in tumor evasion from host immunity.

• Budotitane - A titanium metal complex, coordinated with asymmetric beta-diketonate ligands, with antineoplastic activity. Although the exact mechanism of action remains to be elucidated, budotitane potentially binds either to macromolecules via coordinative covalent bonds, or via intercalation between nucleic acids strands by the aromatic ring of the beta-diketonate. In addition, this agent appears to cause cardiac arrhythmias and is toxic to the liver and kidneys at higher doses. The development of budotitane was halted due to the rapid loss of its labile groups under physiological conditions.

• Bufalin - An active ingredient and one of the glycosides in the traditional Chinese medicine ChanSu; it is also a bufadienolide toxin originally isolated from the venom of the Chinese toad Bufo gargarizans, with potential cardiotonic and antineoplastic activity. Although the mechanism of action of bufalin is still under investigation, this agent is a specific Na+/K+-ATPase inhibitor and can induce apoptosis in cancer cell lines through the activation of the transcription factor AP-1 via a mitogen activated protein kinase (MAPK) pathway.

• Buparlisib - An orally bioavailable specific oral inhibitor of the pan-class I phosphatidylinositol 3-kinase (PI3K) family of lipid kinases with potential antineoplastic activity. Buparlisib specifically inhibits class I PI3K in the PI3K/AKT kinase (or protein kinase B) signaling pathway in an ATP-competitive manner, thereby inhibiting the production of the secondary messenger phosphatidylinositol-3,4,5-trisphosphate and 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.

• Burixafor - An orally bioavailable inhibitor of CXC chemokine receptor 4 (CXCR4) with receptor binding and hematopoietic stem cell-mobilization activities. Burixafor binds to the chemokine receptor CXCR4, thereby preventing the binding of stromal derived factor-1 (SDF-1 or CXCL12) to the CXCR4 receptor and subsequent receptor activation; this may induce the mobilization of hematopoietic stem and progenitor cells from the bone marrow into blood. CXCR4, a chemokine receptor belonging to the G protein-coupled receptor (GPCR) gene family, plays an important role in chemotaxis and angiogenesis and is upregulated in several tumor cell types; CXCL12/CXCR4 interaction induces retention of hematopoietic cells in the bone marrow.

• Burixafor hydrobromide - The hydrobromide salt form of burixafor, an orally bioavailable inhibitor of CXC chemokine receptor 4 (CXCR4) with hematopoietic stem cell (HSC)-mobilization and chemosensitizing activities. Upon administration, burixafor binds to the chemokine receptor CXCR4, thereby preventing the binding of stromal cell-derived factor-1 (SDF-1 or CXCL12) to the CXCR4 receptor and subsequent receptor activation. This may induce the mobilization of hematopoietic stem and progenitor cells from the bone marrow into the peripheral circulation. Additionally, burixafor-mediated mobilization of disseminated tumor cells (DTCs) from the bone marrow into the blood may make these metastatic tumor cells more susceptible to the actions of chemotherapeutic agents. CXCR4, a chemokine receptor belonging to the G protein-coupled receptor (GPCR) gene family, plays an important role in chemotaxis and angiogenesis and is upregulated in several tumor cell types. CXCL12/CXCR4 interaction induces retention of hematopoietic cells in the bone marrow.

• Burosumab - An orally bioavailable recombinant human immunoglobulin G1 monoclonal antibody directed against human fibroblast growth factor 23 (FGF23), that can be used to increase serum phosphate levels. Upon subcutaneous administration, burosumab binds to and inhibits FGF23, thereby interfering with FGF23 signaling. This increases tubular phosphate reabsorption, decreases excretion of phosphate, and increases serum phosphate levels, resulting in enhanced bone mineralization. FGF23, a member of the fibroblast growth factor (FGF) family produced by osteocytes, plays a key role in hypophosphatemic rickets/osteomalacia, such as X-linked hypophosphatemia (XLH) and tumor-induced rickets/osteomalacia. Increased FGF23 levels lead to decreased expression of the sodium-phosphate co-transporters in the proximal tubules, reduced renal phosphate reabsorption, increased excretion by the kidneys, and low serum phosphate concentration.

• Buserelin - A synthetic analog of gonadotropin-releasing hormone (GnRH). Buserelin binds to and activates pituitary gonadotropin releasing hormone (GnRH) receptors. Prolonged administration of buserelin results in sustained inhibition of gonadotropin production, suppression of testicular and ovarian steroidogenesis, and reduced levels of circulating gonadotropin and gonadal steroids. Buserelin is more potent that GnRH.

• Bushen culuan decoction - A traditional Chinese medicine (TCM) decoction containing a mixture of ten Chinese herbs including Tusizi, Yinyanghuo, Xianmao, Xuduan, Gouqizi, Nvzhenzi, Zelan, Shengpuhuang, Xiangfu and Chuanshanlong, with potential to induce ovulation. Upon oral administration, Bushen Culuan decoction may, through a not yet fully elucidated mechanism, depress follicle-stimulating hormone (FSH) levels, elevate anti-Mullerian hormone (AMH) levels, and increase the number of antral follicle counts (AFCs), thereby promoting ovulation.

• Bushen-jianpi decoction - A traditional Chinese medicine (TCM) that is used for Yin deficiency of the liver, kidney and spleen, with potential immunomodulating and antineoplastic activities. Bushen-Jianpi decoction (BSJPD; BJD) consists of various herbs, including, but not limited to, Radix Codonopsis (Dang Shen), Fructus Lycii (the fruit of Chinese wolfberry), Rhizoma Atractylodis Macrocephalae (Baishu; Bai Zhu), Fructus Ligustri Lucidi, Cuscuta chinensis (Chinese dodder) seed, and Psoralea corylifolia Linn. As a TCM, Bushen-Jianpi is used as an antineoplastic agent as it is thought to invigorate the spleen and tonify the kidney, which presumably prevents or treats a variety of cancers. Upon administration of Bushen-Jianpi decoction, the ingredients in the decoction may affect signaling pathways involved in carcinogenesis and enhance the immune system by increasing the levels of numerous cytokines and a variety of immune cells, such as cytotoxic T-lymphocytes (CTLs), natural killer cells (NKs) and macrophages. It may also reduce the expression of various proteins involved in tumorigenesis.

• Busulfan - A synthetic derivative of dimethane-sulfonate with antineoplastic and cytotoxic properties. Although its mechanism of action is not fully understood, busulfan appears to act through the alkylation of DNA. Following systemic absorption of busulfan, carbonium ions are formed, resulting in DNA alkylation and DNA breaks and inhibition of DNA replication and RNA transcription.

• Buthionine sulfoximine - A synthetic amino acid. Buthionine sulfoximine irreversibly inhibits gamma-glutamylcysteine synthase, thereby depleting cells of glutathione, a metabolite that plays a critical role in protecting cells against oxidative stress, and resulting in free radical-induced apoptosis. Elevated glutathione levels are associated with tumor cell resistance to alkylating agents and platinum compounds. By depleting cells of glutathione, this agent may enhance the in vitro and in vivo cytotoxicities of various chemotherapeutic agents in drug-resistant tumors. Buthionine sulfoximine may also exhibit antiangiogenesis activity.

• Bxq-350 nanovesicle formulation - A stable, nanovesicle formulation composed of a synthetic form of the human glycoprotein saposin C (SapC) linked to the phospholipid dioleoylphosphatidylserine (DOPS), with potential antineoplastic activity. Upon intravenous administration, the BXQ-350 nanovesicle formulation selectively targets and preferentially accumulates in tumor vessels and cells, due to the leaky nature of tumor vasculature and the presence of phosphatidylserine (PS) lipids in tumor cell membranes. Upon binding to the phospholipids in the tumor cell membrane, SapC fuses with the membrane and is internalized leading to its accumulation within the internal membrane. SapC becomes active in the acidic tumor microenvironment and as a lysosomal sphingolipid activator protein, activates lysosomal enzymes, such as beta-glucosidase, acid sphingomyelinase, and beta-galactosylceramidase. This leads to the degradation of glucosylceramide and sphingomyelin, and the conversion of galactosylceramide to ceramide, respectively. This elevates intracellular ceramide levels, activates caspases and induces ceramide-mediated apoptosis, which together lead to an inhibition of tumor cell growth. SapC plays key roles in lipid transport and organization of biological membranes and has strong lipid membrane binding activity.

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