Antineoplastic agents s

• S1p receptor agonist krp203 - The hydrochloride salt form of 2-amino-2 propanediol (KRP-203), a sphingosine 1-phosphate (S1P) receptor agonist, with potential immunosuppressive activity. Upon administration of S1P receptor agonist KRP203, this agent binds to S1P receptors on lymphocytes, which prevents binding of serum S1P to S1P receptors and leads to S1P receptor internalization. This reduces the number of circulating blood leukocytes and accelerates lymphocyte homing into peripheral lymph nodes, thereby preventing their infiltration into peripheral inflammatory sites. This agent also decreases the production of inflammatory cytokines by lymphocytes, such as interferon gamma (IFN-g), interleukin-12 (IL-12), and tumor necrosis factor (TNF).

• Sabarubicin - A disaccharide analogue of the anthracycline antineoplastic antibiotic doxorubicin. Sabarubicin intercalates into DNA and interacts with topoisomerase II, thereby inhibiting DNA replication and repair and RNA and protein synthesis. This agent also induces apoptosis through a p53-independent mechanism. Sabarubicin is less cardiotoxic than doxorubicin.

• Sabatolimab - An inhibitor of the inhibitory T-cell receptor T-cell immunoglobulin and mucin domain-containing protein 3 (TIM-3; hepatitis A virus cellular receptor 2; HAVCR2), with potential immune checkpoint inhibitory and antineoplastic activities. Upon administration, sabatolimab binds to TIM-3 expressed on certain immune cells, including tumor infiltrating lymphocytes (TILs). This abrogates T-cell inhibition, activates antigen-specific T-lymphocytes and enhances cytotoxic T-cell-mediated tumor cell lysis resulting in a reduction in tumor growth. TIM-3, a transmembrane protein expressed on certain T-cells, is associated with tumor-mediated immune suppression.

• Sacituzumab govitecan - An antibody drug conjugate containing the humanized monoclonal antibody, hRS7, against tumor-associated calcium signal transducer 2 (TACSTD2 or TROP2) and linked to the active metabolite of irinotecan, 7-ethyl-10-hydroxycamptothecin (SN-38), with potential antineoplastic activity. The antibody moiety of sacituzumab govitecan selectively binds to TROP2. After internalization and proteolytic cleavage, SN-38 selectively stabilizes topoisomerase I-DNA covalent complexes, resulting in DNA breaks that inhibit DNA replication and trigger apoptosis. TROP2, also known as epithelial glycoprotein-1 (EGP-1), is a transmembrane calcium signal transducer that is overexpressed by a variety of human epithelial carcinomas; this antigen is involved in the regulation of cell-cell adhesion and its expression is associated with increased cancer growth, aggressiveness and metastasis.

• S-adenosylmethionine - A nutritional supplement that is synthesized from adenosine triphosphate (ATP) and the amino acid methionine by the endogenous essential enzyme methionine adenosyltransferase (MAT), with potential antineoplastic activity. Upon administration, S-adenosylmethionine acts as a methyl donor for various transmethylation reactions. In cancer cells, this agent induces the methylation of tumor promoting genes, reverses DNA hypomethylation, and leads to the suppression of oncogene transcription. This induces apoptosis in and inhibits proliferation of susceptible tumor cells.

• Safingol - A saturated derivative of sphingosine. As an inhibitor of protein kinase C (PKC), safingol competitively binds to the regulatory phorbol-binding domain of PKC, a kinase involved in tumorigenesis. This agent has been shown to act synergistically with other chemotherapeutic agents and may potentiate chemotherapy drug-induced apoptosis in vitro and in vivo.

• Sagopilone - A fully synthetic low-molecular-weight epothilone with potential antineoplastic activity. Sagopilone binds to tubulin and induces microtubule polymerization while stabilizing microtubules against depolymerization, which may result in the inhibition of cell division, the induction of G2/M arrest, and apoptosis. The agent is not a substrate for the P-glycoprotein (P-gp) efflux pump and so may exhibit activity in multidrug-resistant (MDR) tumors. The epothilone class of metabolites was originally isolated from the myxobacterium Solangium cellulosum.

• Salirasib - A salicylic acid derivative with potential antineoplastic activity. Salirasib dislodges all Ras isoforms from their membrane-anchoring sites, thereby preventing activation of RAS signaling cascades that mediated cell proliferation, differentiation, and senescence. RAS signaling is believed to be abnormally activated in one-third of human cancers, including cancers of the pancreas, colon, lung and breast.

• Salmonella vnp20009 - A genetically stable Salmonella typhimurium strain, attenuated by chromosomal deletion of the purI and msbB genes, with tumor-targeting activity. In rodent models, salmonella VNP20009 has been shown to selectively accumulate and grow in a variety of tumor types, inhibiting the growth of primary and metastatic tumors. This agent may be genetically engineered to contain transgenes that express therapeutic agents or cell surface tumor-associated antigen-specific antibodies, such as CEA-specific antibodies, which may improve its tumor targeting and therapeutic potential.

• Sam68 modulator cwp232291 - A small molecule and prodrug of CWP232204 targeting Src associated in mitosis, of 68 kDa (Sam68 or KHDRBS1), with potential antineoplastic activity. CWP232291 is converted in serum into its active form CWP232204 which binds to Sam68, thereby resulting in the induction of apoptosis in selective cancer cells. Due to the multimodular structure of Sam68, the apoptosis mediated by CWP232204-Sam68 interaction can attribute from 1) activation of transcription factor NF-kB induced by tumor necrosis factor alpha signaling, 2) alternative splicing of BCL-2 apoptosis gene, driving the balance towards pro-apoptotic as opposed to anti-apoptotic isoforms, 3) down-regulation of the anti-apoptotic protein survivin via Wnt signaling. Sam68, a KH domain RNA-binding protein belonging to the signal transduction and activation of RNA (STAR) family, plays a key role in various cellular processes including cell cycle progression and apoptosis; it is upregulated in many types of cancer cells and its expression is associated with increased cell proliferation and survival.

• Samalizumab - A humanized monoclonal antibody directed against the human immunosuppressive molecule CD200 (OX-2) with potential immunomodulating and antineoplastic activities. Samalizumab binds to CD200, blocking the binding of CD200 to its receptor, CD200R, present on cells of the macrophage lineage; inhibition of CD200 may augment the cytotoxic T-lymphocyte (CTL) mediated immune response against CD200-expressing tumor cells. CD200 is a type 1a transmembrane protein, related to the B7 family of co-stimulatory receptors, and is upregulated on the surface of multiple hematologic malignant cells; this transmembrane protein appears to be involved in the downregulation of a Th1 (helper T cell) immune response.

• Samarium sm 153-dotmp - A radioconjugate composed of the phosphonic acid chelator DOTMP (1,4,7,10-tetraazacyclododecane-1,4,7,10-tetramethylenephosphonic acid) conjugated to the beta- and gamma-emitting radioisotope samarium Sm 153, with potential antineoplastic activity. Upon administration of samarium Sm 153-DOTMP, the DOTMP moiety targets and binds to growing bone, thereby selectively delivering samarium Sm 153-mediated cytotoxic radiation to bone tumor and metastases, which may help destroy bone metastases and mitigate pain from bone metastases.

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

• Samrotamab vedotin - An antibody-drug conjugate (ADC) composed of a proprietary monoclonal antibody against a tumor-associated antigen (TAA) linked to an as of yet undisclosed cytotoxic agent, with potential antineoplastic activity. Upon intravenous administration, the monoclonal antibody moiety of ABBV-085 targets and binds to the TAA expressed on tumor cells. Upon binding and internalization, the cytotoxic agent is released and kills the TAA-expressing cancer cells, through an as of yet unknown mechanism of action.

• Samuraciclib - An orally available, selective inhibitor of cyclin-dependent kinase 7 (CDK7) with potential antineoplastic activity. Upon oral administration, samuraciclib selectively and competitively binds to the CDK7 ATP binding site, thereby inhibiting CDK7-mediated signaling. CDK7, a serine/threonine kinase, plays a role in controlling cell cycle progression, transcriptional regulation, and promotes the expression of key oncogenes such as c-Myc through the phosphorylation of RNA polymerase II. Inhibition of CDK7 may inhibit tumor cell proliferation in certain cancers that are dependent on CDK7-mediated transcriptional regulation and signaling.

• Sapacitabine - An orally bioavailable pyrimidine analogue prodrug with potential antineoplastic activity. Sapacitabine is hydrolyzed by amidases to the deoxycytosine analogue CNDAC (2'-Cyano-2'-deoxyarabinofuranosylcytosine), which is then phosphorylated into the active triphosphate form. As an analogue of deoxycytidine triphosphate, CNDAC triphosphate incorporates into DNA strands during replication, resulting in single-stranded DNA breaks during polymerization due to beta-elimination during the fidelity checkpoint process; cell cycle arrest in the G2 phase and apoptosis ensue. The unmetabolized prodrug may exhibit antineoplastic activity as well.

• Sapanisertib - An orally bioavailable inhibitor of raptor-mTOR (TOR complex 1 or TORC1) and rictor-mTOR (TOR complex 2 or TORC2) with potential antineoplastic activity. Sapanisertib binds to and inhibits both TORC1 and TORC2 complexes of mTOR, which may result in tumor cell apoptosis and a decrease in tumor cell proliferation. TORC1 and 2 are upregulated in some tumors and play an important role in the PI3K/Akt/mTOR signaling pathway, which is frequently dysregulated in human cancers.

• Sapitinib - An erbB receptor tyrosine kinase inhibitor with potential antineoplastic activity. erbB kinase inhibitor AZD8931 binds to and inhibits erbB tyrosine receptor kinases, which may result in the inhibition of cellular proliferation and angiogenesis in tumors expressing erbB. The erbB protein family, also called the epidermal growth factor receptor (EGFR) family, plays major roles in tumor cell proliferation and tumor vascularization.

• Saracatinib - An orally available 5-, 7-substituted anilinoquinazoline with anti-invasive and anti-tumor activities. Saracatinib is a dual-specific inhibitor of Src and Abl, protein tyrosine kinases that are overexpressed in chronic myeloid leukemia cells. This agent binds to and inhibits these tyrosine kinases and affects cell motility, cell migration, adhesion, invasion, proliferation, differentiation, and survival. Specifically, Saracatinib inhibits Src kinase-mediated osteoclast bone resorption.

• Saracatinib difumarate - The difumarate salt of saracatinib, an orally available 5-, 7-substituted anilinoquinazoline with anti-invasive and anti-tumor activities. Saracatinib is a dual-specific inhibitor of Src and Abl, protein tyrosine kinases that are overexpressed in chronic myeloid leukemia cells. This agent binds to and inhibits these tyrosine kinases and affects cell motility, cell migration, adhesion, invasion, proliferation, differentiation, and survival. Specifically, Saracatinib inhibits Src kinase-mediated osteoclast bone resorption.

• Sarcnu - An alkylating chloroethylnitrosourea with antineoplastic activity. Selectively accumulating in some tumor cells, SarCNU forms covalent linkages with nucleophilic centers in DNA, causing depurination, base pair miscoding, strand scission, and DNA-DNA cross-linking, which may result in cytotoxicity.

• Sardomozide - A methylglyoxal-bis(guanylhydrazone) (MGBG) derivative with potential antineoplastic and antiviral properties. Sardomozide selectively binds to and inhibits S-adenosylmethionine decarboxylase (SAMDC), an enzyme essential for the biosynthesis of polyamines, such as spermine and spermidine that bind to DNA and play critical roles in cell division, cell differentiation and membrane function. By inhibiting SAMDC, sardomozide reduces the intracellular polyamine concentration, thereby interfering with cell growth and differentiation. In addition, this agent also exhibits anti-HIV effect via suppressing expression of eukaryotic translation initiation factor 5A (eIF-5A), which is essential for retroviral replication.

• Sargramostim - A recombinant therapeutic agent chemically identical to endogenous human GM-CSF except a leucine substitution in position 23. Binding to specific cell surface receptors, sargramostim modulates the proliferation and differentiation of a variety of hematopoietic progenitor cells with some specificity towards stimulation of leukocyte production and may reverse treatment-induced neutropenias. This agent also promotes antigen presentation, up-regulates antibody-dependent cellular cytotoxicity (ADCC), and increases interleukin-2-mediated lymphokine-activated killer cell function; it may also augment host antitumoral immunity.

• Sargramostim plasmid dna pancreatic tumor cell vaccine - A whole cell vaccine comprised of irradiated allogenic pancreatic tumor cells transfected with a plasmid DNA encoding human sargramostim (GM-CSF). Vaccination results in expression of GM-CSF, which induces proliferation and differentiation of hematopoietic lineage cells as well as stimulating macrophage and dendritic cell functions in antigen presentation and antitumor cell-mediated immunity. Furthermore, administration of this pancreatic tumor cell vaccine may elicit a cytotoxic T lymphocyte (CTL) response against similar host tumor cells, resulting in decreased tumor growth.

• Sargramostim plasmid dna sarcoma vaccine - An autologous sarcoma cell vaccine with potential immunostimulatory activity. Tumor cells harvested from a patient with sarcoma are transfected with a plasmid DNA encoding for human sargramostim (GM-CSF) using a particle-mediated gene transfer (PMGT) technique, which avoids the use of infectious components. Vaccination with an autologous sargramostim sarcoma vaccine produces high levels of GM-CSF, a cytokine that enhances antigen presentation by activated macrophages and increases the recognition of weakly immunogenic tumors by cytotoxic T-lymphocytes.

• Sasanlimab - An inhibitor of the human inhibitory receptor programmed cell death 1 (PD-1; PDCD1), with potential immune checkpoint inhibitory and antineoplastic activities. Upon administration, sasanlimab targets and binds to PD-1 and blocks the interaction between PD-1 and its ligands, PD-1 ligand 1 (PD-L1) and PD-1 ligand 2 (PD-L2). This prevents the activation of PD-1 and its downstream signaling pathways. This may restore immune function through the activation of natural killer (NK) cells and cytotoxic T-lymphocytes (CTLs) against tumor cells. PD-1, an inhibitory receptor belonging to the B7-receptor family, is expressed on activated T-lymphocytes, B-cells and NK cells; it functions as an immune checkpoint that negatively regulates T-cell activation and effector function when activated by its ligands, and plays an important role in tumor evasion from host immunity.

• Satraplatin - An orally administered third generation platinum compound with potential antineoplastic activity. Satraplatin forms highly reactive, charged, platinum complexes which bind to nucleophilic groups in DNA, inducing intrastrand and interstrand DNA cross-links, as well as DNA-protein cross-links. These cross-links result in cell growth inhibition and apoptosis.

• Savolitinib - An orally bioavailable inhibitor of the c-Met receptor tyrosine kinase with potential antineoplastic activity. Savolitinib selectively binds to and inhibits the activation of c-Met in an ATP-competitive manner, and disrupts c-Met signal transduction pathways. This may result in cell growth inhibition in tumors that overexpress the c-Met protein. C-Met encodes the hepatocyte growth factor receptor tyrosine kinase and plays an important role in tumor cell proliferation, survival, invasion, and metastasis, and tumor angiogenesis; this protein is overexpressed or mutated in a variety of cancers.

• Sb-as15 adjuvant - A vaccine adjuvant containing CpG 7909, monophosphoryl lipid, and QS-21 with potential antineoplastic and immunostimulatory activities. CpG 7909 is a synthetic 24-mer oligonucleotide containing 3 CpG motifs that selectively targets Toll-like receptor 9 (TLR9), thereby activating dendritic and B cells and stimulating cytotoxic T cell and antibody responses against tumor cells bearing tumor antigens. Monophosphoryl lipid is a detoxified derivative of lipid A, a component of Salmonella minnesota lipopolysaccharide (LPS); this agent may enhance humoral and cellular responses to various antigens. QS-21 is a purified, naturally occurring saponin derived from the South American tree Quillaja saponaria Molina and exhibits various immunostimulatory activities. Combinations of monophosphoryl lipid and QS-21 may be synergistic in inducing humoral and cellular immune responses. (NCI05)

• Sbil-2 - An retroviral vector encoding human IL-2 with potential antineoplastic property. SBIL-2 (Surgery Branch IL-2) can be used to transfect tumor infiltrating lymphocytes, which can then be re-introduced back to cancer patients, thereby stimulate T cell activation and immunopotentiation responses.

• Scopoletin - A coumarin compound found in several plants including those in the genus Scopolia and the genus Brunfelsia, as well as chicory (Cichorium), redstem wormwood (Artemisia scoparia), stinging nettle (Urtica dioica), passion flower (Passiflora), noni (Morinda citrifolia fruit) and European black nightshade (Solanum nigrum) that is comprised of umbelliferone with a methoxy group substituent at position 6. Scopoletin is used to standardize and establish pharmacokinetic properties for products derived from the plants that produce it, such as noni extract. Although the mechanism(s) of action have not yet been established, this agent has potential antineoplastic, antidopaminergic, antioxidant, anti-inflammatory and anticholinesterase effects.

• Sdf-1 receptor antagonist ptx-9908 - A stromal cell-derived factor 1 (SDF-1; CXCL12) analog and inhibitor of C-X-C chemokine receptor type 4 (CXCR4), with potential antineoplastic activity. Upon administration, PTX-9908 selectively targets and binds to CXCR4, thereby preventing the binding of CXCR4 to its ligand SDF-1. This inhibits receptor activation and results in decreased proliferation and migration of CXCR4-overexpressing tumor cells. The G protein-coupled receptor CXCR4, which is overexpressed in several tumor cell types, promotes tumor angiogenesis, tumor cell proliferation, survival, invasion and metastasis. SDF-1, a major chemotactic factor, plays a key role in mediating cell trafficking via selective binding to CXCR4.

• Seclidemstat - An orally available, reversible, noncompetitive inhibitor of lysine-specific demethylase 1 (LSD1, or KDM1A), with potential antineoplastic activity. Upon oral administration, seclidemstat reversibly 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 3 (H3K4) to mono- and unmethylated H3K4, respectively. LSD1 inhibition enhances H3K4 methylation and increases the expression of tumor suppressor genes. This may lead to an inhibition of cell growth in LSD1-overexpressing tumor cells. In addition, LSD1 demethylates mono- or di-methylated H3K9 which increases gene expression of tumor promoting genes; inhibition of LSD1 promotes H3K9 methylation and decreases transcription of these genes.

• Sedoxantrone trihydrochloride - The trihydrochloride salt of the anthrapyrazole antineoplastic antibiotic sedoxantrone with potential antineoplastic activity. Sedoxantrone intercalates into DNA and interacts with topoisomerase II, thereby inhibiting DNA replication and repair and RNA and protein synthesis.

• Selatinib ditosilate - An orally bioavailable ditosilate salt form of selatinib, an analog of the quinazoline lapatinib and dual inhibitor of epidermal growth factor receptor (EGFR) and Human Epidermal Growth Factor Receptor 2 (ErbB-2 or HER-2), with potential antineoplastic activity. Upon administration, selatinib reversibly blocks phosphorylation of both EGFR and ErbB2, thereby suppressing tumor growth in EGFR/ErbB-2-overexpressing tumor cells. The tyrosine kinases EGFR and ErbB2 have been implicated in the growth of various tumor types.

• Selective cytokine inhibitory drug cc-1088 - An analog of thalidomide with potential antineoplastic activity that belongs to the functional class of agents called selective cytokine inhibitory drugs (SelCIDs). SelCIDs inhibit phosphodiesterase-4 (PDE 4), an enzyme involved in tumor necrosis factor alpha (TNF alpha) production. CC-1088 inhibits production of the cytokines vascular endothelial growth factor (VEGF) (a pro-angiogenic factor) and interleukin-6 (IL-6).

• Selective estrogen receptor degrader azd9496 - An orally available selective estrogen receptor degrader (SERD), with potential antineoplastic activity. Upon administration, SERD AZD9496 binds to the estrogen receptor (ER) and induces a conformational change that results in the degradation of the receptor. This prevents ER-mediated signaling and inhibits the growth and survival of ER-expressing cancer cells.

• Selective estrogen receptor degrader azd9833 - An orally available selective estrogen receptor degrader (SERD), with potential antineoplastic activity. Upon administration, SERD AZD9833 binds to the estrogen receptor (ER) and induces a conformational change that results in the degradation of the receptor. This prevents ER-mediated signaling and inhibits the growth and survival of ER-expressing cancer cells.

• Selective estrogen receptor degrader lsz102 - An selective estrogen receptor (ER) degrader (SERD), with potential antineoplastic activity. Upon administration of LSZ102, this agent binds to the ER and induces the degradation of the receptor. This prevents ER activation and ER-mediated signaling, and inhibits the growth and survival of ER-expressing cancer cells.

• Selective estrogen receptor degrader lx-039 - An orally available selective estrogen receptor degrader/downregulator (SERD), with potential antineoplastic activity. Upon oral administration, SERD LX-039 specifically targets and binds to the estrogen receptor (ER) and induces a conformational change that results in ER degradation. This prevents ER-mediated signaling and inhibits both the growth and survival of ER-expressing cancer cells.

• Selective estrogen receptor degrader ly3484356 - An orally available selective estrogen receptor degrader (SERD), with potential antineoplastic activity. Upon oral administration, LY3484356 specifically targets and binds to the estrogen receptor (ER) and induces a conformational change that results in ER degradation. This prevents ER-mediated signaling and inhibits both the growth and survival of ER-expressing cancer cells.

• Selective estrogen receptor degrader srn-927 - An orally available, nonsteroidal selective estrogen receptor degrader (SERD), with potential antineoplastic activity. Upon oral administration, SERD SRN-927 specifically binds to the estrogen receptor (ER) and induces a conformational change that results in the degradation of the receptor. This prevents ER-mediated signaling and inhibits the growth and survival of ER-expressing cancer cells.

• Selective estrogen receptor modulator cc-8490 - A benzopyran with potential antineoplastic activity. CC-8490 acts as a selective estrogen receptor modulator (SERM), inhibiting the proliferation of estrogen-sensitive breast cancer cells. This agent also inhibits growth and induces apoptosis of glioblastoma cells via a mechanism independent of estrogen receptor-related mechanisms.

• Selective estrogen receptor modulator tas-108 - A synthetic, antiestrogenic steroidal compound with potential antitumor activity. TAS-108 binds to and inhibits estrogenic receptor alpha (ERa), mainly expressed in the mammary gland and uterus and upregulated in estrogen-dependent tumors. Blockage of ERa by TAS-108 prevents the binding and effects of estrogen and may lead to an inhibition of estrogen-dependent cancer cell proliferation. TAS-108 also is a partial agonist of the estrogenic receptor beta (ERb), expressed in many tissues including the central nervous system, urogenital tract, bone and cardiovascular system, thereby exerting a positive effect on these tissues. In addition, TAS-108 activates the co-repressor Silencing Mediator for Retinoid and Thyroid hormone receptor (SMRT), a protein that inhibits the activities of the estrogen receptors, which may contribute to the antitumor activity of TAS-108.

• Selective human estrogen-receptor alpha partial agonist ttc-352 - A benzothiophene and orally bioavailable selective human estrogen receptor alpha (ERalpha; ESR1; ERa) partial agonist (ShERPA), with potential antineoplastic activity. Upon administration, TTC-352 mimics the naturally-occurring 17beta-estradiol (E2) and targets and binds to ERa located in the nucleus. This causes translocation of ERa to extranuclear sites. Nuclear export of ERa prevents normal ER-mediated signaling and inhibits proliferation of ER-positive tumor cells. TTC-352 causes tumor regression of tamoxifen (TAM)-resistant (TR) tumor cells which often overexpress protein kinase C alpha (PKCalpha; PKCa). PKCa expression is associated with poor patient survival and breast cancer aggressiveness and may predict tumor responses to E2, E2-like compounds and ShERPAs. Unlike E2 and E2-like compounds, TTC-352 does not cause endometrial proliferation.

• Seliciclib - An orally available small molecule and cyclin-dependent kinase (CDK) inhibitor with potential apoptotic and antineoplastic activity. CDKs, serine/threonine kinases that play an important role in cell cycle regulation, are overexpressed in various malignancies. Seliciclib primarily inhibits CDK 2, 7, and 9 by competing for the ATP binding sites on these kinases, leading to a disruption of cell cycle progression. In addition, this agent seems to interfere with CDK-mediated phosphorylation of the carboxy-terminal domain of RNA polymerase II, thereby inhibiting RNA polymerase II-dependent transcription. This may lead to the down-regulation of anti-apoptotic factors, such as myeloid cell leukemia sequence 1 (Mcl-1), a protein crucial for the survival of a range of tumor cell types. The down-regulation of anti-apoptotic factors may lead to an induction of apoptosis, thereby further contributing to seliciclib's antiproliferative effects.

• Selicrelumab - A monoclonal antibody agonist of the cell surface receptor CD40, with potential immunostimulatory and antineoplastic activities. Similar to the endogenous CD40 ligand (CD40L or CD154), CD40 agonist monoclonal antibody RO7009789 binds to CD40 on a variety of immune cell types. This triggers the cellular proliferation and activation of antigen-presenting cells (APCs), and activates B-cells and T-cells, resulting in an enhanced immune response. RO7009789 also binds to and activates CD40 present on the surfaces of some solid tumor cells, leading to apoptosis and decreased tumor growth. CD40, a cell surface receptor and member of the tumor necrosis factor (TNF) receptor superfamily, is expressed on various immune cells and certain cancer cells; it mediates both indirect tumor cell killing through the activation of the immune system and direct tumor cell apoptosis.

• Selinexor - An orally available, small molecule inhibitor of CRM1 (chromosome region maintenance 1 protein, exportin 1 or XPO1), with potential antineoplastic activity. Selinexor modifies the essential CRM1-cargo binding residue cysteine-528, thereby irreversibly inactivates CRM1-mediated nuclear export of cargo proteins such as tumor suppressor proteins (TSPs), including p53, p21, BRCA1/2, pRB, FOXO, and other growth regulatory proteins. As a result, this agent, via the approach of selective inhibition of nuclear export (SINE), restores endogenous tumor suppressing processes to selectively eliminate tumor cells while sparing normal cells. CRM1, the major export factor for proteins from the nucleus to the cytoplasm, is overexpressed in a variety of cancer cell types.

• Selitrectinib - An orally bioavailable, selective tropomyosin-related-kinase (tyrosine receptor kinase; TRK) inhibitor, with potential antineoplastic activity. Upon oral administration, LOXO-195 specifically targets and binds to TRK, including the fusion proteins containing sequences from neurotrophic tyrosine receptor kinase (NTRK) types 1 (NTRK1), 2 (NTRK2), and 3 (NTRK3). This prevents neurotrophin-TRK interaction and TRK activation, which results in both the induction of cellular apoptosis and the inhibition of cell growth in tumors that overexpress TRK and/or express NTRK fusion proteins. LOXO-195 targets specific point mutations that occur after treatment with and result in acquired resistance to another TRK inhibitor; therefore, LOXO-195 is able to overcome acquired resistance to other TRK inhibitors. TRK, a family of receptor tyrosine kinases (RTKs) activated by neurotrophins, is encoded by NTRK family genes. The expression of either mutated forms of or fusion proteins involving NTRK family members results in uncontrolled TRK signaling and plays an important role in tumor cell growth and survival.

• Selonsertib - An orally bioavailable inhibitor of apoptosis signal-regulating kinase 1 (ASK1), with potential anti-inflammatory, antineoplastic and anti-fibrotic activities. Upon oral administration, selonsertib targets and binds to the catalytic kinase domain of ASK1 in an ATP-competitive manner, thereby preventing its phosphorylation and activation. This prevents the phosphorylation of downstream kinases, such as c-Jun N-terminal kinases (JNKs) and p38 mitogen-activated protein kinase (p38 MAPK). By preventing the activation of ASK1-dependent signal transduction pathways, GS-4997 prevents the production of inflammatory cytokines, down-regulates the expression of genes involved in fibrosis, suppresses excessive apoptosis and inhibits cellular proliferation. ASK1, also called mitogen-activated protein kinase kinase kinase 5 (MAP3K5), is activated in response to oxidative and endoplasmic reticulum (ER) stress, calcium influx and infection. It plays a key role in the development of certain cardiovascular and neurodegenerative diseases, diabetes, as well as certain types of cancer.

• Selpercatinib - An orally bioavailable selective inhibitor of wild-type, mutant and fusion products involving the proto-oncogene receptor tyrosine kinase rearranged during transfection (RET), with potential antineoplastic activity. Upon oral administration, selpercatinib selectively binds to and targets wild-type RET as well as various RET mutants and RET-containing fusion products. This results in an inhibition of cell growth of tumors cells that exhibit increased RET activity. In addition, selpercatinib targets, binds to and inhibits vascular endothelial growth factor receptor 1 (VEGFR1) and 3 (VEGFR3), and fibroblast growth factor receptor 1 (FGFR1), 2 (FGFR2), and 3 (FGFR3). RET overexpression, activating mutations, and fusions result in the upregulation and/or overactivation of RET tyrosine kinase activity in various cancer cell types; dysregulation of RET activity plays a key role in the development and progression of these cancers.

• Selumetinib - An orally active, small molecule with potential antineoplastic activity. Selumetinib is an ATP-independent inhibitor of mitogen-activated protein kinase kinase (MEK or MAPK/ERK kinase) 1 and 2. MEK 1 and 2 are dual specificity kinases that are essential mediators in the activation of the RAS/RAF/MEK/ERK pathway, are often upregulated in various cancer cells, and are drivers of diverse cellular responses, including proliferation. Inhibition of both MEK1 and 2 by selumetinib prevents the activation of MEK1/2 dependent effector proteins and transcription factors, thereby leading to an inhibition of cellular proliferation in various cancers.

• Selumetinib sulfate - The sulfate salt of selumetinib, an orally active, small molecule with potential antineoplastic activity. Selumetinib is an ATP-independent inhibitor of mitogen-activated protein kinase kinase (MEK or MAPK/ERK kinase) 1 and 2. MEK 1 and 2 are dual specificity kinases that are essential mediators in the activation of the RAS/RAF/MEK/ERK pathway, are often upregulated in various cancer cells, and are drivers of diverse cellular responses, including proliferation. Inhibition of both MEK1 and 2 by selumetinib prevents the activation of MEK1/2 dependent effector proteins and transcription factors, thereby leading to an inhibition of cellular proliferation in various cancers.

• Semaxanib - A quinolone derivative with potential antineoplastic activity. Semaxanib reversibly inhibits ATP binding to the tyrosine kinase domain of vascular endothelial growth factor receptor 2 (VEGFR2), which may inhibit VEGF-stimulated endothelial cell migration and proliferation and reduce the tumor microvasculature. This agent also inhibits the phosphorylation of the stem cell factor receptor tyrosine kinase c-kit, often expressed in acute myelogenous leukemia cells.

• Semuloparin - An ultralow-molecular-weight heparin (ULMWH) (Mw: 2000-3000 daltons)consisting of a polydisperse mixture of oligomeric heparin fragments with potential anticoagulant activity. Ultralow-molecular-weight heparin AVE5026 binds to and activates antithrombin III (ATIII), which may result in the inhibition of activated factor Xa and, to a much lesser extent, factor IIa (thrombin) and so the inhibition of fibrin formation. Compared to low-molecular-weight heparins (LMWHs), AVE5026 exhibits an even higher ratio of anti-Factor Xa to anti-Factor IIa activity (>30:1). Compared to unfractionated heparins, the use of LMWHs is associated with lower incidences of major bleeding, osteoporosis and heparin-induced thrombocytopenia. Like LMWHs, this agent may inhibit tumor growth by regulating angiogenesis and apoptosis. AVE5026 is prepared by partial depolymerization of unfractionated porcine mucosal heparin.

• Semustine - A methylated derivative of carmustine with antineoplastic activity. As an alkylating agent, semustine forms covalent linkages with nucleophilic centers in DNA, causing depurination, base-pair miscoding, strand scission, and DNA-DNA cross-linking, which may result in cytotoxicity.

• Seneca valley virus-001 - A replication-competent oncolytic picornavirus with potential antineoplastic activity. Administered systemically, Seneca Valley virus-001 specifically targets and infects tumor cells with neuroendocrine characteristics. Upon infection, this agent replicates intracellularly, resulting in tumor cell lysis and reduced tumor cell proliferation. The selective tropism of virus replication may involve receptor-mediated internalization.

• Seocalcitol - A vitamin D3 analogue with potential antineoplastic activity. Seocalcitol binds to and activates the vitamin D receptor, a cytoplasmic polypeptide expressed in normal vitamin D responsive tissues, but also overexpressed in certain cancers including hepatocellular carcinoma and pancreatic cancer. Mediated through vitamin D receptor, this agent induces cancer cell differentiation, inhibits cancer cell growth and induces apoptosis. In addition, seocalcitol may also induce growth arrest and apoptosis independent of vitamin D receptor activation through mechanisms that are not fully elucidated.

• Sepantronium bromide - A small-molecule proapoptotic agent with potential antineoplastic activity. Sepantronium bromide selectively inhibits survivin expression in tumor cells, resulting in inhibition of survivin antiapoptotic activity (via the extrinsic or intrinsic apoptotic pathways) and tumor cell apoptosis. Survivin, a member of the inhibitor of apoptosis (IAP) gene family, is expressed during embryonal development and is absent in most normal, terminally differentiated tissues; upregulated in a variety of human cancers, its expression in tumors is associated with a more aggressive phenotype, shorter survival times, and a decreased response to chemotherapy.

• S-equol - An orally bioavailable, non-steroidal estrogen naturally produced by the metabolism of the isoflavonoid daidzein by human intestinal microflora, with potential chemoprotective and estrogen receptor (ER) modulating activities. S-equol preferentially binds to and activates the beta isoform of ER in certain target tissues, while having an antagonistic effect in other tissues. This modulates the expression of ER-responsive genes in a tissue-specific manner. This agent may increase bone mineral density, affect vasomotor symptoms, and may decrease the proliferation rate of susceptible cancer cells. In addition, this agent interferes with the activity of enzymes involved in steroid biosynthesis. S-equol inhibits dihydrotestosterone (DHT) production and may inhibit the proliferation of androgen-driven prostate cancer. S-equol is the biologically active enantiomer while R-equol is essentially inactive and has a weak affinity for alpha-ER.

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

• Serclutamab talirine - A antibody drug conjugate (ADC) consisting of serclutamab, an affinity-matured humanized monoclonal antibody directed against the epidermal growth factor receptor (EGFR) conjugated to a talirine, a cytotoxic, DNA minor groove crosslinking agent and pyrrolobenzodiazepine (PBD) dimer, with potential antineoplastic activity. Upon intravenous administration of serclutamab talirine, the serclutamab moiety targets and binds to EGFR on tumor cell surfaces. Following receptor internalization and lysosome-mediated cleavage, talirine is released. In turn, the imine groups of the PBD moiety bind to the N2 positions of guanines on opposite strands of DNA. This induces DNA strand breaks, inhibits DNA replication, leads to G2/M cell cycle arrest, induces cell death, and inhibits the proliferation of EGFR-overexpressing tumor cells. EGFR, a receptor tyrosine kinase (RTK) that is overexpressed by a variety of cancers, plays a key role in tumor cell proliferation and survival.

• Serd d-0502 - An orally available, nonsteroidal selective estrogen receptor degrader/downregulator (SERD), with potential antineoplastic activity. Upon oral administration, SERD D-0502 specifically targets and binds to the estrogen receptor (ER) and induces a conformational change that promotes ER degradation. This prevents ER-mediated signaling and inhibits both the growth and survival of ER-expressing cancer cells.

• Serd g1t48 - An orally available selective estrogen receptor degrader/downregulator (SERD), with potential antineoplastic activity. Upon oral administration, SERD G1T48 specifically targets and binds to the estrogen receptor alpha (ERalpha; ERa; ESR1) and induces a conformational change that promotes ERalpha degradation and downregulation. This prevents ERalpha-mediated signaling and inhibits both the growth and survival of ERalpha-expressing cancer cells.

• Serd sar439859 - An orally available, nonsteroidal selective estrogen receptor degrader/downregulator (SERD), with potential antineoplastic activity. Upon oral administration, SERD SAR439859 specifically targets and binds to the estrogen receptor (ER) and induces a conformational change that promotes ER degradation. This prevents ER-mediated signaling and inhibits both the growth and survival of ER-expressing cancer cells.

• Serd shr9549 - An orally available selective estrogen receptor degrader/downregulator (SERD), with potential antineoplastic activity. Upon oral administration, SERD SHR9549 specifically targets and binds to the estrogen receptor (ER) and induces a conformational change that promotes ER degradation. This prevents ER-mediated signaling and inhibits both the growth and survival of ER-expressing cancer cells.

• Serd zn-c5 - An orally available selective estrogen receptor degrader/downregulator (SERD), with potential antineoplastic activity. Upon oral administration, SERD ZN-c5 specifically targets and binds to the estrogen receptor (ER) and induces a conformational change that results in ER degradation. This prevents ER-mediated signaling and inhibits both the growth and survival of ER-expressing cancer cells.

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

• Sergiolide - A quassinoid phytochemical isolated from Cedronia granatensis and other plant species with potential antineoplastic activity.

• Seribantumab - A fully human monoclonal antibody directed against the human epidermal growth factor receptor ErbB3 (Her3) with potential antineoplastic activity. Seribantumab binds to and inhibits ErbB3 activation, which may result in inhibition of ErbB3-dependent PI3K/Akt signaling and so inhibition of cellular proliferation and differentiation. ErbB3, a member of the epidermal growth factor receptor (EGFR) family of receptor tyrosine kinases, is frequently overexpressed in solid tumors, including breast, lung, and colorectal tumors of epithelial origin; it has no active kinase domain itself but is activated through heterodimerization with other members of the EGFR receptor family that do.

• Serine/threonine kinase inhibitor cbp501 - A peptide with G2 checkpoint-abrogating activity. G2 checkpoint inhibitor CBP501 inhibits multiple serine/threonine kinases, including MAPKAP-K2, C-Tak1, and CHK1, that phosphorylate serine 216 of the dual-specific phosphatase Cdc25C (cell division checkpoint 25 C); disruption of Cdc25C activity results in the inhibition of Cdc25C dephosphorylation of the mitotic cyclin-dependent kinase complex Cdc2/cyclin B, preventing entry into the mitotic phase of the cell cycle.

• Serine/threonine kinase inhibitor xl418 - A selective, orally active small molecule, targeting protein kinase B (PKB or AKT) and ribosomal protein S6 Kinase (p70S6K), with potential antineoplastic activity. XL418 inhibits the activities of PKB and p70S6K, both acting downstream of phosphoinosotide-3 kinase (PI3K). These kinases are often upregulated in a variety of cancers. Inhibition of PKB by this agent will induce apoptosis, while inhibition of p70S6K will result in the inhibition of translation within tumor cells.

• Serplulimab - A humanized monoclonal antibody directed against the negative immunoregulatory human cell receptor programmed cell death protein 1 (PD-1; PDCD1; CD279), with potential immune checkpoint inhibitory and antineoplastic activities. Upon administration, serplulimab targets, binds to and inhibits PD-1 and its downstream signaling pathways. This may restore immune function through the activation of T-cells and T-cell-mediated immune responses against tumor cells. PD-1, a transmembrane protein in the immunoglobulin superfamily (IgSF) expressed on T-cells, functions as an immune checkpoint that negatively regulates T-cell activation and effector function when activated by its ligands programmed cell death-1 ligand 1 (PD-L1) and 2 (PD-L2); it plays an important role in tumor evasion from host immunity.

• Sevacizumab - A monoclonal antibody directed against the human vascular endothelial growth factor (VEGF), with potential antiangiogenic activity. Upon administration, sevacizumab specifically binds to and inhibits VEGF, thereby preventing its binding to VEGF receptors (VEGFRs). This prevents VEGF/VEGFR-mediated signaling and inhibits the proliferation of vascular endothelial cells and tumor cells. VEGF, overexpressed in a variety of cancer cells, is associated with increased invasiveness and decreased survival.

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

• Shared anti-idiotype-ab-s006 - A murine monoclonal anti-idiotype antibody that targets human B-cell lymphomas with potential antineoplastic activity. Shared Anti-Id-Ab-S006 binds to antigens on neoplastic B cells, resulting in tumor cell destruction by the reticuloendothelial system or cytotoxic T lymphocytes (CTL).

• Shared anti-idiotype-ab-s024a - A murine monoclonal anti-idiotype antibody with potential antineoplastic activity. Shared anti-id-Ab-S024A binds to tumor-associated antigens (TAAs) on the surface of neoplastic cells resulting in tumor cell destruction by the reticuloendothelial system or cytotoxic T lymphocytes (CTL).

• Shark cartilage - A nutritional supplement gleaned from the exoskeleton of the shark. Shark cartilage inhibits metalloproteinases (MMPs) and possesses antiangiogenic and antimetastatic properties.

• Shark cartilage extract ae-941 - A multifunctional antiangiogenic agent derived from shark cartilage with potential antineoplastic activity. Shark cartilage extract AE-941 competitively inhibits the binding of pro-angiogenic vascular endothelial growth factor (VEGF) to its cellular receptor, thereby inhibiting endothelial cell proliferation. This agent also inhibits matrix metalloproteinases (MMPs), stimulates tissue plasminogen activator (tPA), and activates caspase-mediated apoptotic pathways in endothelial cells.

• Shenqi fuzheng injection sq001 - An injectable formulation composed of the two Chinese medicinal herbs Radix astragali, the root of astragalus membranaceus (huangqi) and Radix codonopsis, the root of Codonopsis pilosula (dangshen), with potential antineoplastic adjuvant and chemoprotective activities that may prevent cancer-related fatigue. Although the exact mechanisms by which shenqi fuzheng injection (SFI) have yet to be fully elucidated, the herbs may improve tumor response and/or reduce the toxicity of certain chemotherapeutics when administered together. It may also alleviate chemotherapy-associated immunosuppression.

• Short chain fatty acid hqk-1004 - A short chain fatty acid (SCFA) with potential herpes simplex virus thymidine kinase gene (HSV-TK)-inducing activity. Upon administration, short chain fatty acid HQK-1004 may induce the expression of thymidine kinase (TK) by a silenced HSV-TK, which may activate a co-administered antiviral prodrug such as ganciclovir, resulting in the destruction of virally-infected cancer cells.

• Sho-saiko-to - A botanical formulation with potential chemopreventive activities. Sho-Saiko-to, an herbal mixture, contains seven herbal extracts whose mechanism of action if not fully understood. There is evidence of antiproliferative effects against hepatocellular carcinoma in vitro. Other effects of this agent described in animal models include the prevention of liver injury and hepatocyte-regenerating activity. Antitumor effects associated with this herbal product may include induction of apoptosis, cell cycle arrest at the G0/G1 phase, and activation of an immune response, characterized by the release of cytokines as well as activation of effector cells, such as macrophages and natural killer cells.

• Shp-1 agonist sc-43 - An orally available, small molecule agonist of Src homology region 2 domain-containing phosphatase-1 (SHP-1; tyrosine-protein phosphatase non-receptor type 6; PTPN6) with potential antineoplastic activity. Upon administration, SHP-1 agonist SC-43 enhances SHP-1 activity by impairing the association between the N-terminal Src homology 2 (N-SH2) domain and the protein tyrosine phosphatase (PTP) domain of SHP-1, triggering a conformational change of SHP-1 and relieving its autoinhibition. Activation of SHP-1 represses signal transducer and activator of transcription 3 (STAT3) signaling by inhibiting constitutive and interleukin-6 (IL-6)-induced STAT3 phosphorylation. The STAT3 pathway is overly active in many cancer types and is implicated in cancer stem cell-mediated growth, recurrence, stemness, and resistance to conventional chemotherapies.

• Shp2 inhibitor jab-3068 - An orally bioavailable inhibitor of protein tyrosine phosphatase (PTP) non-receptor type 11 (SHP2; Src homology region 2 domain phosphatase; PTPN11), with potential antineoplastic activity. Upon oral administration, SHP2 inhibitor JAB-3068 targets, binds to and inhibits the activity of SHP2. This prevents SHP2-mediated signaling, inhibits MAPK signaling and prevents growth of SHP2-expressing tumor cells. SHP2, an oncoprotein overexpressed in a variety of cancer cell types, regulates cell survival, differentiation and proliferation through activation of the Ras-Raf-MEK-ERK signaling pathway. The Ras-MAPK pathway is often hyperactivated in cancer cells due to specific mutations and rearrangements and are dependent on SHP2 for their oncogenic signaling. SHP2 also regulates programmed cell death 1 (PD-1)-mediated signal transduction and is involved in immune checkpoint modulation.

• Shp2 inhibitor rly-1971 - An orally bioavailable inhibitor of protein tyrosine phosphatase (PTP) non-receptor type 11 (SHP2; Src homology region 2 domain phosphatase; PTPN11), with potential antineoplastic activity. Upon oral administration, SHP2 inhibitor RLY-1971 targets, binds to and inhibits the activity of SHP2. This prevents SHP2-mediated signaling, inhibits MAPK signaling and prevents growth of SHP2-expressing tumor cells. SHP2, an oncoprotein overexpressed in a variety of cancer cell types, regulates cell survival, differentiation and proliferation through activation of the Ras-Raf-MEK-ERK signaling pathway. The Ras-MAPK pathway is often hyperactivated in cancer cells due to specific mutations and rearrangements and are dependent on SHP2 for their oncogenic signaling. SHP2 also regulates programmed cell death 1 (PD-1)-mediated signal transduction and is involved in immune checkpoint modulation.

• Shp2 inhibitor rmc-4630 - An orally bioavailable inhibitor of protein tyrosine phosphatase (PTP) non-receptor type 11 (SHP2; Src homology region 2 domain phosphatase; PTPN11), with potential antineoplastic activity. Upon oral administration, SHP2 inhibitor RMC-4630 targets, binds to and inhibits the activity of SHP2. This prevents SHP2-mediated signaling, inhibits MAPK signaling and prevents growth of SHP2-expressing tumor cells. SHP2, an oncoprotein overexpressed in a variety of cancer cell types, regulates cell survival, differentiation and proliferation through activation of the RAS-RAF-MEK-ERK signaling pathway. The RAS-MAPK pathway is often hyperactivated in cancer cells due to specific mutations and rearrangements and are dependent on SHP2 for their oncogenic signaling. SHP2 also regulates programmed cell death 1 (PD-1)-mediated signal transduction and is involved in immune checkpoint modulation.

• Shp2 inhibitor tno155 - An inhibitor of protein tyrosine phosphatase (PTP) non-receptor type 11 (SHP2; src homology region 2 domain phosphatase; PTPN11), with potential antineoplastic activity. Upon oral administration, SHP2 inhibitor TNO155 binds to and inhibits SHP2. This prevents SHP2-mediated signaling, inhibits MAPK signaling and prevents growth of SHP2-expressing tumor cells. SHP2, an oncoprotein overexpressed in a variety of cancer cell types, regulates cell survival, differentiation and proliferation through activation of the RAS-RAF-ERK signaling pathway. SHP2 also regulates programmed cell death 1 (PD-1)-mediated signal transduction and is involved in immune checkpoint modulation.

• Shu yu wan formula - A traditional Chinese medicine comprising different herbs that may be used for a variety of medical purposes. Shu Yu Wan contains the following herbs: Da Zao (Fructus Jujubae), Shu Yu (Radix Dioscoreae Quinquelobae), Gan Cao (Radix Glycyrrhizae Uralensis), Shu Di Huang (Radix Rehmanniae Glutinosae Praeparata), Dang Gui (Radix Angelicae Sinensis), Shen Qu (Massa Medica Fermentata), Gui Zhi (Ramulus Cinnamomi Cassiae), Da Dou Juan (Semen Glycines Germinatum), E Jiao (Gelatinum Corii Asini), Ren Shen (Radix Ginseng), Bai Zhu (Rhizoma Atractylodis Macrocephalae), Fu Ling (Sclerotium Poriae Cocos), Chuan Xiong (Radix Ligustici Wallichii), Bai Shao Yao (Radix Paeoniae Lactiflorae), Mai Men Dong (Tuber Ophiopogonis Japonici), Chai Hu (Radix Bupleuri), Fang Feng (Radix Ledebouriellae Divaricatae), Jie Geng (Radix Platycodi Grandiflori), Xing Ren (Semen Pruni Armeniacae), Bai Lian (Radix Ampelopsis Japonicae) and Sheng Jiang (Rhizoma Zingiberis Officinalis Recens). This formula may be used to relieve chemotherapeutic side effects or cancer-related symptoms.

• Sialyl lewis-keyhole limpet hemocyanin conjugate vaccine - A vaccine consisting of the oligosaccharide antigen sialyl Lewis (CA19-9) conjugated to the nonspecific immunomodulator keyhole limpet hemocyanin (KLH), with potential antineoplastic activity. Upon administration, sialyl Lewis-keyhole limpet hemocyanin conjugate vaccine may induce production of IgG and IgM antibodies as well as trigger an antibody-dependent cell-mediated cytotoxicity (ADCC) against tumor cells expressing the sialyl Lewis antigen. Sialyl Lewis is a blood group antigen and a tumor-associated antigen associated with epithelial cancers such as breast cancer and various digestive cancers. Sialyl Lewis serves as a ligand for the cytokine-inducible cell adhesion molecule (CAM) E-selectin, an endothelial cell-specific type I transmembrane surface protein, thus facilitating hematogenous metastasis by mediating the adhesion of circulating cancer cells to vascular endothelium.

• Sialyl tn antigen - A tumor-associated core-region carbohydrate antigen of epithelial mucin, expressed in most colon carcinoma, mucinous carcinoma, pancreatic cancer, gastric, lung, breast, and ovarian carcinoma. Sialosyl-Tn (STn) antigen has been shown to be highly sensitive and a specific marker of colorectal cancer, associated with more aggressive diseases and poor prognosis. STn antigen and its immediate precursor, Tn antigen, are mucin type glycoprotein structures associated with the earliest steps of mucin O-linked glycosylation. When combined with a carrier molecule, keyhole limpet hemocyanin (KLH), this antigen may be co-administered with oral cyclophosphamide as an immune modulator.

• Sialyl tn-klh vaccine - A vaccine containing a pancarcinoma carbohydrate antigen conjugated with keyhole limpet hemocyanin (KLH), with potential antineoplastic activity. Sialylated Tn antigen (sTn) is a monosaccharide glycan usually O-linked to serine or threonine residues of mucins found on most epithelial cancers. Conjugation with KLH, a hapten carrier and an immunostimulant, improves host immune responses. Vaccination with sTn-KLH vaccine may produce antibodies and elicit a cytotoxic T lymphocyte (CTL) response against those tumor cells expressing sTn, resulting in decreased tumor growth.

• Sibrotuzumab - A humanized monoclonal antibody (MoAb) against human fibroblast activation protein (FAP). FAP is a 95 kDa cell surface glycoprotein and an inducible tumor stromal antigen of epithelial cancers and of a subset of soft tissue sarcomas. FAP shows a very limited distribution pattern in normal tissues, thereby sibrotuzumab has possible diagnostic and therapeutic applications in epithelial cancers.

• Sig12d loder - A proprietary, miniature biodegradable polymeric matrix containing small-interfering RNAs for the mutated KRAS oncogene, KRASG12D, (siG12D), with potential antitumor activity. Upon intratumoral injection, this siG12D is released locally, thereby preventing translation of KRAS proteins and potentially inhibiting growth of tumor cells overexpressing KRAS. KRAS, a member of the small GTPase superfamily, is mutated in over 90% of human pancreatic ductal adenocarcinomas (PDAC) and is associated with tumor cell proliferation and reduced survival.

• Silatecan ar-67 - A synthetic, highly lipophilic derivative of camptothecin, with potential antineoplastic and radiosensitizing activities. 7-tert-butyldimethylsilyl-10-hydroxycamptothecin binds to and stabilizes the topoisomerase I-DNA covalent complex. This inhibits the religation of topoisomerase I-mediated single-stranded DNA breaks and produces lethal double-stranded DNA breaks when encountered by the DNA replication machinery, thereby inhibiting DNA replication and inducing apoptosis. Camptothecin readily undergoes hydrolysis at physiological pH, changing its conformation from the active lactone structure to an inactive carboxylate form. Modifications on the E ring of camptothecin prevent binding of human serum albumin, which prefers the inactive carboxylate form, thereby enhancing the stability of the active lactone structure and resulting in prolonged agent activity. In addition, this agent sensitizes tumor cells toward radiation treatment.

• Silibinin -

• Silicon phthalocyanine 4 - A synthetic photosensitizer agent containing a large macrocyclic ring chelated with silicon. Silicon phthalocyanine 4 localizes primarily in mitochondrial cytosolic membranes and, after photoexcitation, forms reactive oxygen species that induce apoptosis.

• Silmitasertib sodium - The sodium salt of silmitasertib, an orally bioavailable small-molecule inhibitor of CK2 with potential antineoplastic activity. Silmitasertib selectively binds to and inhibits the enzyme casein kinase II (CK2), which may lead to an inhibition of cellular proliferation. CK2, a protein kinase often overexpressed in a variety of cancer cell types, appears to be correlated with malignant transformation, tumor growth and survival. CK2 regulates a diverse array of pro-survival cellular processes including epidermal growth factor receptor (EGFR) signaling, PI3K/AKT/mTOR signaling, hedgehog (Hh) signaling, Hsp90 machinery, hypoxia, and interleukin (IL)-6 expression. CK2 also regulates the activity of XRCC1 and MDC1, two mediator/adaptor proteins that are essential for DNA repair.

• Siltuximab - A chimeric, human-murine, monoclonal antibody targeting the pro-inflammatory cytokine interleukin 6 (IL-6), with antitumor and anti-inflammatory activities. Upon intravenous administration of siltuximab, this agent targets and binds to IL-6. This inhibits the binding of IL-6 to the IL-6 receptor (IL-6R), which results in the blockade of the IL-6/IL-6R-mediated signal transduction pathway. This inhibits cancer cell growth in tumors overexpressing IL-6.

• Simalikalactone d - A quassinoid phytochemical isolated from Simaba multiflora, Quassia africana and other plant species with potential antineoplastic activity. This agent also has antimalarial and antiviral properties.

• Simeprevir - An orally bioavailable inhibitor of the hepatitis C virus (HCV) protease complex comprised of non-structural protein 3 and 4A (NS3/NS4A), with activity against HCV genotype 1. Upon administration, simeprevir reversibly binds to the active center and binding site of the HCV NS3/NS4A protease and prevents NS3/NS4A protease-mediated polyprotein maturation. This disrupts both the processing of viral proteins and the formation of the viral replication complex, which inhibits viral replication in HCV genotype 1-infected host cells. NS3, a serine protease, is essential for the proteolytic cleavage of multiple sites within the HCV polyprotein and plays a key role during HCV ribonucleic acid (RNA) replication. NS4A is an activating factor for NS3. HCV is a small, enveloped, single-stranded RNA virus belonging to the Flaviviridae family; HCV infection is associated with the development of hepatocellular carcinoma (HCC).

• Simlukafusp alfa - A recombinant fusion protein comprised of a human monoclonal antibody directed against fibroblast activation protein-alpha (FAP) linked to an engineered, variant form of interleukin-2 (IL-2v), with potential immunostimulating and antineoplastic activities. Upon administration of simlukafusp alfa, the monoclonal antibody moiety recognizes and binds to FAP, thereby concentrating IL-2 in FAP-expressing tumor tissue. Subsequently, the IL-2 moiety of this fusion protein may stimulate a local immune response and activate natural killer (NK) cells and cytotoxic T-cells. FAP is a cell surface protein that is expressed on a wide variety of cancer cells. IL-2v cannot bind to IL-2 receptor-alpha (CD25, IL2Ra) and does not activate regulatory T-cells (Tregs).

• Simmitinib - An orally bioavailable inhibitor of numerous tyrosine kinases (TKs) including fibroblast growth factor receptor (FGFR), vascular endothelial growth factor receptor type 2 (VEGFR2; KDR), and colony stimulating factor 1 receptor (CSF1R; CSF-1R), with potential antiangiogenic and antineoplastic activities. Upon oral administration, simmitinib binds to and inhibits the activities of these TKs, thereby preventing both the activation of downstream signaling pathways and the proliferation of tumor cells overexpressing these TKs. FGFR, VEGFR2, and CSF1R are upregulated in a variety of cancer cell types and play key roles in tumor cell proliferation, angiogenesis, and metastasis.

• Simotaxel - A semi-synthetic, orally bioavailable, third-generation taxane derivative and microtubule-stabilizing agent, with potential antineoplastic activity. Upon administration, simotaxel binds to tubulin, promotes microtubule assembly and stabilization, and prevents microtubule depolymerization. This results in G2/M arrest, apoptosis and the inhibition of cell proliferation in susceptible tumor cells. This agent is a poor substrate for P-glycoprotein-related drug resistance mechanisms; therefore, it may be useful for treating multi-drug resistant tumors. MST-997 is more potent than paclitaxel and docetaxel and overcomes paclitaxel and docetaxel resistance in certain tumor cell types.

• Simtuzumab - A humanized monoclonal antibody against lysyl oxidase-like 2 (LOXL2), with potential antineoplastic activity. Anti-LOXL2 monoclonal antibody GS 6624 targets and specifically binds to the scavenger receptor cysteine rich domain 4 (SRCR-4) on LOXL2, thereby preventing the crosslinking of collagen and inhibiting the recruitment and activation of fibroblasts. Inhibiting fibroblast activation and the subsequent production of growth factors and chemokines may lead to an inhibition of tumor cell proliferation. LOXL2, a member of the lysyl oxidase (LO) gene family, is an extracellular, copper-dependent enzyme overexpressed in a variety of tumor cell types, and contributes to tumor cell invasion and metastasis.

• Simurosertib - An orally bioavailable inhibitor of cell division cycle 7 (cell division cycle 7-related protein kinase; CDC7), with potential antineoplastic activity. Upon administration, simurosertib binds to and inhibits CDC7; this prevents the initiation of DNA replication during mitosis, which causes cell cycle arrest and induces apoptosis. This inhibits cell growth in CDC7-overexpressing tumor cells. CDC7, a serine/threonine kinase and cell division cycle protein, is overexpressed in a variety of cancers and plays a key role in the activation of DNA replication and the regulation of cell cycle progression.

• Sintilimab - A recombinant human monoclonal antibody directed against the negative immunoregulatory human cell surface receptor programmed cell death 1 (PD-1; PDCD1; PD1), with potential immune checkpoint inhibitory and antineoplastic activities. Upon administration, sintilimab binds to PD-1 and inhibits the binding of PD-1 to the PD-1 ligands programmed cell death-1 ligand 1 (PD-L1), and PD-1 ligand 2 (PD-L2). This prevents the activation of PD-1 and its downstream signaling pathways. This may restore immune function through the activation of both T-cells and T-cell-mediated immune responses against tumor cells. PD-1, a transmembrane protein in the immunoglobulin (Ig) superfamily expressed on activated T-cells, negatively regulates T-cell activation and effector function when activated by its ligands; it plays an important role in tumor evasion from host immunity.

• Siplizumab - A humanized monoclonal immunoglobulin G1 antibody with potential antineoplastic activity. Siplizumab binds to CD2, a specific receptor found in T cells and NK cells, thereby triggering a host immune response that results in lysis of CD2+ cells, selective suppression of the immune system, and control of activated T cell growth.

• Sipuleucel-t - A cell-based vaccine composed of autologous antigen-presenting peripheral blood mononuclear cells (enriched for a dendritic cell fraction) that have been exposed to a recombinant protein consisting of granulocyte-macrophage colony-stimulating factor (GM-CSF) fused to prostatic-acid phosphatase (PAP), a protein expressed by prostate cancer cells. Upon administration, the vaccine may stimulate an antitumor T-cell response against tumor cells expressing PAP. (NCI05)

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

• Sirna-expressing sv40 - A simian virus 40 (SV40)-based shuttle vector, encoding small interfering RNA (siRNA), with potential antineoplastic activity. The expression of siRNA in target tumor cells transfected with an siRNA-expressing SV40 vector may result in siRNA-mediated silencing of target oncogenes and, so, the inhibition of tumor cell growth and the induction of tumor cell death.

• Sirna-transfected peripheral blood mononuclear cells apn401 - Autologous peripheral blood mononuclear cells (PBMCs) transfected ex vivo with small-interfering ribonucleic acid (siRNA) directed against the E3 ubiquitin ligase casitas B-lineage lymphoma-b gene (Cbl-b), with potential immunoactivating and antineoplastic activities. The Cbl-b gene is silenced ex vivo through the binding of Cbl-b siRNA to Cbl-b mRNA, which prevents the translation of the Cbl-b protein in T-lymphocytes. Upon infusion, the activated, Cbl-b-silenced T-lymphocytes are able to increase the production of cytokines, proliferate and activate the immune system, which leads to cancer cell eradication. Cbl-b, a negative regulator of the immune system, is mutated in a variety of cancer cell types. Its expression is inversely correlated with activation of T-lymphocytes and tumor cell eradication.

• Sirpa-4-1bbl fusion protein dsp107 - A bi-functional, trimeric, fusion protein consisting of the extracellular domains (ECDs) of human signal-regulatory protein alpha (SIRPalpha; SIRPa; CD172a) fused to a 4-1BB ligand (4-1BBL), with potential immune checkpoint inhibitory, immunostimulating and antineoplastic activities. Upon administration, the SIRPa-4-1BBL fusion protein DSP107 selectively targets and binds to both CD47 expressed on tumor cells and 4-1BB (CD137; tumor necrosis factor receptor superfamily member 9; TNFRSF9) expressed on T-cells and natural killer (NK) cells. Binding to CD47 blocks the interaction of CD47 with endogenous SIRPa, a cell surface protein expressed on macrophages. This prevents CD47/SIRPa-mediated signaling and abrogates the CD47/SIRPa-mediated inhibition of macrophage activation and phagocytosis of cancer cells. This induces pro-phagocytic signaling mediated by the binding of calreticulin (CRT), which is specifically expressed on the surface of tumor cells, to low-density lipoprotein (LDL) receptor-related protein-1 (LRP-1), which is expressed on macrophages, and results in macrophage activation and the specific phagocytosis of tumor cells. The binding of 4-1BBL to 4-1BB activates 4-1BB-mediated signaling, induces cytotoxic T-lymphocyte (CTL) proliferation, cytokine production and promotes a CTL-mediated anti-tumor immune response as well as NK-mediated tumor cell killing. The crosslinking specifically enables the activation of 4-1BB-mediated signaling in T-cells and NK cells in the tumor microenvironment (TME), allowing targeted immune responses in the TME. CD47, also called integrin-associated protein (IAP), is a tumor-associated antigen (TAA) expressed on normal, healthy hematopoietic stem cells (HSC) and overexpressed on the surface of a variety of cancer cells. Expression of CD47, and its interaction with SIRPa, leads to the inhibition of macrophage activation and protects cancer cells from phagocytosis, thereby allowing cancer cells to proliferate. 4-1BB, a surface glycoprotein of the tumor necrosis factor receptor superfamily, is an inducible costimulatory receptor that plays a key role in T-cell proliferation, survival and cytolytic activity.

• Sirpa-fc-cd40l fusion protein sl-172154 - A bi-functional fusion protein consisting of the extracellular domains (ECDs) of human signal-regulatory protein alpha (SIRPalpha; SIRPa; CD172a) and CD40 ligand (CD40L; CD154; TRAP; TNFSF5) linked via a human Fc domain, with potential immune checkpoint inhibitory and antineoplastic activities. Upon administration, the SIRPa-Fc-CD40L fusion protein SL-172154 selectively targets and binds to both CD47 expressed on tumor cells and CD40, a cell surface receptor that belongs to the tumor necrosis factor (TNF) receptor family, expressed on antigen-presenting cells (APCs). Binding to CD47 blocks the interaction of CD47 with endogenous SIRPa, a cell surface protein expressed on macrophages. This prevents CD47/SIRPa-mediated signaling and abrogates the CD47/SIRPa-mediated inhibition of macrophage activation and phagocytosis of cancer cells. This induces pro-phagocytic signaling mediated by the binding of calreticulin (CRT), which is specifically expressed on the surface of tumor cells, to low-density lipoprotein (LDL) receptor-related protein-1 (LRP-1), which is expressed on macrophages, and results in macrophage activation and the specific phagocytosis of tumor cells. The binding of CD40L to CD40 activates CD40, increases CD40-mediated signaling and induces proliferation and activation of B-lymphocytes, shifts the induction of suppressive macrophages towards immunostimulatory macrophages, activates monocyte-derived dendritic cells (moDCs), and leads to the secretion of inflammatory cytokines. This activates the immune system to induce the proliferation and activation of cytotoxic T-lymphocytes (CTLs) against tumor cells. The crosslinking specifically enhances antigen presentation to CD8+ and CD4+ T lymphocytes and tumor cell phagocytosis by the APC. CD47, also called integrin-associated protein (IAP), is a tumor-associated antigen (TAA) expressed on normal, healthy hematopoietic stem cells (HSC) and overexpressed on the surface of a variety of cancer cells. Expression of CD47, and its interaction with SIRPa, leads to the inhibition of macrophage activation and protects cancer cells from phagocytosis, thereby allowing cancer cells to proliferate.

• Sirpa-igg4-fc fusion protein tti-622 - A soluble recombinant antibody-like fusion protein composed of the N-terminal CD47 binding domain of human signal-regulatory protein alpha (SIRPa; CD172a) linked to an Fc domain derived from human immunoglobulin G subtype 4 (IgG4), with potential immune checkpoint inhibitory, phagocytosis-inducing and antineoplastic activities. Upon administration, the SIRPa-IgG4-Fc fusion protein TTI-622 selectively targets and binds to CD47 expressed on tumor cells and blocks the interaction of CD47 with endogenous SIRPa, a cell surface protein expressed on macrophages. This prevents CD47/SIRPa-mediated signaling and abrogates the CD47/SIRPa-mediated inhibition of macrophage activation. This induces pro-phagocytic signaling resulting from the binding of calreticulin (CRT), which is specifically expressed on the surface of tumor cells, to low-density lipoprotein (LDL) receptor-related protein-1 (LRP-1) expressed on macrophages, and results in macrophage activation and the specific phagocytosis of tumor cells. CD47, also called integrin-associated protein (IAP), is a tumor-associated antigen (TAA) expressed on normal, healthy hematopoietic stem cells (HSC) and overexpressed on the surface of a variety of cancer cells. Expression of CD47, and its interaction with SIRPa, leads to the inhibition of macrophage activation and protects tumor cells from phagocytosis, thereby allowing these cells to proliferate and survive.

• Sitimagene ceradenovec - A replication-deficient adenovirus type 5 (Ad5) with E1 and partial E3 deletions containing cDNA for the herpes simplex virus thymidine kinase (HSV-Tk), which, when administered in combination with ganciclovir (GCV), possesses potential antineoplastic activity. Following administration, transgene-expressing cells produce thymidine kinase, which phosphorylates GCV to ganciclovir triphosphate, a cytotoxic nucleotide analog that is incorporated into DNA resulting in chain termination and induction of apoptosis in rapidly dividing cells. This process spares normal neurons as they do not proliferate and are therefore not susceptible to the toxic effects of GCV metabolites.

• Sitravatinib - An orally bioavailable, receptor tyrosine kinase (RTK) inhibitor with potential antineoplastic activity. Upon administration, sitravatinib binds to and inhibits the activity of several RTKs including hepatocyte growth factor receptor (HGFR; c-Met; MET), tyrosine-protein kinase receptor UFO (AXL receptor tyrosine kinase; AXL), mast/stem cell growth factor receptor (SCFR; c-kit; KIT), the receptor tyrosine kinase MER, discoidin domain receptor 2 (DDR2), vascular endothelial growth factor receptor (VEGFR) types 1 (VEGFR-1; FLT1), 2 (VEGFR-2; KDR; Flk-1) and 3 (VEGFR-3), members of the platelet-derived growth factor receptor (PDGFR) family, RET (rearranged during transfection), tropomyosin-related kinases (TRK) and members of the ephrin (Eph) family of receptor tyrosine kinases. This may result in both the inhibition of signal transduction pathways mediated by these RTKs and the reduction of tumor cell proliferation in cancer cell types that overexpress these RTKs.

• Sivifene - The phenylhydrazone 4,4'-dihydroxybenzophenone-2,4-dinitrophenylhydrazone formulated as a topical agent with immunomodulating and potential antineoplastic activities. Applied topically as a gel, sivifene may stimulate a local immune response against human papillomavirus (HPV)-induced cervical intraepithelial neoplasia (CIN).

• Sizofiran - A soluble beta-D-glucan produced by the Basidiomycetes fungus, Schizophyllum commune Fries, with potential immunomodulating and antitumor activities. Although sizofiran's exact mechanism of action has yet to be fully elucidated, this agent appears to stimulate the immune system by increasing cytokine production, activating macrophages and enhancing the activity of polymorphonuclear leukocytes (PML) and natural killer (NK) cells.

• Slc6a8 inhibitor rgx-202 - An orally available, small molecule inhibitor of the creatine transporter, solute carrier family 6, member 8 (SLC6a8), with potential antineoplastic activity. Upon oral administration, RGX-202 inhibits phosphocreatine uptake by SLC6a8, thereby reducing intracellular levels of phosphocreatine available for ATP synthesis in tumor cells. SLC6a8 is overexpressed in some cancer types and inhibition of its activity may potentially limit tumor cell growth and metastasis.

• Slct inhibitor gns561 - An orally available, quinolone-derived, small molecule inhibitor of an as of yet not disclosed solute carrier transporter (SLCT), with potential antineoplastic activity. Upon oral administration, GNS561 demonstrates multiple cellular effects including inhibition of SLCT activity, induction of apoptosis via caspase 3/7 activation, and inhibition of autophagy through lysosomal disruption. Several SLCTs are upregulated in cancer and serve as tumor promoters. Over-expression of SLCT in some tumors is associated with stemness features and may be associated with poor outcomes. Inhibition of autophagy and induction of apoptosis may potentially inhibit tumor cell growth.

• Smac mimetic bi 891065 - A mimetic of second mitochondrial-derived activator of caspases (Smac/DIABLO) and inhibitor of IAPs (Inhibitor of Apoptosis Proteins), with potential antineoplastic activity. Upon administration, Smac mimetic BI 891065 targets and binds to the Smac binding groove on IAPs, including the caspase inhibitor X chromosome-linked IAP (XIAP) and the cellular IAPs 1 and 2. This inhibits the activities of these IAPs and promotes the induction of apoptosis through apoptotic signaling pathways. IAPs are overexpressed by many cancer cell types and suppress apoptosis by binding to and inhibiting certain caspases.

• Smac mimetic gdc-0152 - A second mitochondrial activator of caspases (Smac) mimetic inhibitor of IAPs (Inhibitor of Apoptosis Proteins) with potential antineoplastic activity. Smac mimetic GDC-0152 binds to the Smac binding groove on IAPs, including the direct caspase inhibitor X chromosome-linked IAP (XIAP) and the cellular IAPs 1 and 2, which may inhibit their activities and promote the induction of apoptosis through apoptotic signaling pathways. IAPs are overexpressed by many cancer cell types and suppress apoptosis by binding to and inhibiting active caspases-3, -7 and -9 via their baculoviral lAP repeat (BIR) domains. Smac, the endogenous IAP antagonist, relies on its N-terminal four amino-acid motif for binding to IAPs.

• Smac mimetic gdc-0917 - An orally available, monovalent mimetic of second mitochondrial-derived activator of caspases (Smac/DIABLO) and inhibitor of IAPs (Inhibitor of Apoptosis Proteins) with potential antineoplastic activity. Smac mimetic GDC-0917 binds to the Smac binding groove on IAPs, including the direct caspase inhibitor X chromosome-linked IAP (XIAP) and the cellular IAPs 1 and 2. This inhibits the activities of these IAPs and promotes the induction of apoptosis through apoptotic signaling pathways. IAPs are overexpressed by many cancer cell types and suppress apoptosis by binding to and inhibiting active caspases-3, -7 and -9 via their baculoviral lAP repeat (BIR) domains.

• Smac mimetic lcl161 - An orally bioavailable second mitochondrial-derived activator of caspases (SMAC) mimetic and inhibitor of IAP (Inhibitor of Apoptosis Protein) family of proteins, with potential antineoplastic activity. SMAC mimetic LCL161 binds to IAPs, such as X chromosome-linked IAP (XIAP) and cellular IAPs 1 and 2. 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. IAPs are overexpressed by many cancer cell types and suppress apoptosis by binding and inhibiting active caspases-3, -7 and -9, which play essential roles in apoptosis (programmed cell death), necrosis and inflammation.

• Smo protein inhibitor zsp1602 - An orally bioavailable small molecule SMO (Smoothened) inhibitor with potential antineoplastic activity. SMO inhibitor BMS-833923 inhibits the sonic hedgehog (SHH) pathway protein SMO, which may result in a suppression of the SHH signaling pathway. SMO is a G-protein coupled receptor that lies just downstream of the SHH ligand cell surface receptor Patched-1 in the SHH pathway; in the absence of ligand Patched-1 inhibits SMO and ligand binding to Patched-1 results in increased levels of SMO. The SHH signaling pathway plays an important role in cellular growth, differentiation and repair; constitutive activation of this pathway is associated with uncontrolled cellular proliferation and has been observed in a variety of cancers.

• Smoothened antagonist bms-833923 - An orally bioavailable small molecule SMO (Smoothened) inhibitor with potential antineoplastic activity. SMO inhibitor BMS-833923 inhibits the sonic hedgehog (SHH) pathway protein SMO, which may result in a suppression of the SHH signaling pathway. SMO is a G-protein coupled receptor that lies just downstream of the SHH ligand cell surface receptor Patched-1 in the SHH pathway; in the absence of ligand Patched-1 inhibits SMO and ligand binding to Patched-1 results in increased levels of SMO. The SHH signaling pathway plays an important role in cellular growth, differentiation and repair; constitutive activation of this pathway is associated with uncontrolled cellular proliferation and has been observed in a variety of cancers.

• Smoothened antagonist lde225 topical - A topical formulation of the small-molecule Smoothened (Smo) antagonist LDE225 with potential antineoplastic activity. Upon topical application, smoothened antagonist LDE225 selectively binds to the Hedgehog (Hh)-ligand cell surface receptor Smo, which may result in the suppression of the Hh signaling pathway and, so, the inhibition of tumor cells in which this pathway is abnormally activated. The Hh signaling pathway plays an important role in cellular growth, differentiation and repair. Inappropriate activation of Hh pathway signaling and uncontrolled cellular proliferation, as is observed in a variety of cancers, may be associated with mutations in the Hh-ligand cell surface receptor Smo.

• Smoothened antagonist leq506 - An orally bioavailable small-molecule Smoothened (Smo) antagonist with potential antineoplastic activity. Smoothened antagonist LEQ506 selectively binds to the Hedgehog (Hh)-ligand cell surface receptor Smo, which may result in the suppression of the Hh signaling pathway, thereby inhibiting tumor cell growth. The Hh signaling pathway plays an important role in cellular growth, differentiation and repair. Dysregulated activation of Hh pathway signaling and uncontrolled cellular proliferation, as is observed in a variety of cancers, may be associated with mutations in the Hh-ligand cell surface receptor Smo.

• Smoothened antagonist tak-441 - An orally bioavailable pyrrolopyridine derivative and Smoothened (Smo) antagonist with potential antineoplastic activity. Smo antagonist TAK-441 selectively binds to and inhibits the activity Smo, which is a cell surface co-receptor for ligands in the Hedgehog (Hh) family. This may result in a suppression of Hh-mediated signaling pathways, thereby inhibiting the growth of tumor cells in which this pathway is aberrantly activated. Smo is a G-protein coupled receptor that lies just downstream of the Hh cell surface receptor Patched-1 in the Hh pathway; in the absence of ligand, Patched-1 (Ptch1) inhibits Smo, and ligand binding to Ptch1 results in increased levels of Smo. The Hh-mediated signaling pathways play an important role in cellular growth and differentiation, and tissue repair; constitutive activation of this pathway is associated with uncontrolled cellular proliferation in a variety of cancers.

• Sn-38-loaded polymeric micelles nk012 - A formulation consisting of polymeric micelles loaded with the irinotecan metabolite SN-38 with potential antineoplastic activity. SN-38-loaded polymeric micelles NK012 is an SN-38-releasing nanodevice constructed by covalently attaching SN-38 to the block copolymer PEG-PGlu, followed by self-assembly of amphiphilic block copolymers in an aqueous milieu. SN-38 (7-ethyl-10-hydroxy-camptothecin), a biological active metabolite of the prodrug irinotecan (CPT-11), binds to and inhibits topoisomerase I by stabilizing the cleavable complex between topoisomerase I and DNA, resulting in DNA breaks, inhibition of DNA replication, and apoptosis. SN-38 has been reported to exhibit up to 1,000-fold more cytotoxic activity against various cancer cells in vitro than irinotecan. This formulation increases the water-solubility of SN-38 and allows the delivery of higher doses of SN-38 than those achievable with SN-38 alone.

• Sns01-t nanoparticles - A colloidal mixture of nanoparticles consisting of small interfering RNA (siRNA) targeting the native eukaryotic translation initiation factor 5A (eIF5A), plasmids expressing a pro-apoptotic mutant of elF5A under the control of a B-cell specific promoter (B29), and a synthetic cationic polymer polyethylenimine (PEI) as a delivery vehicle, with potential antineoplastic activity. Upon administration, the siRNA component of SNS01-T suppresses elF5A expression, thereby interfering with translation of eIF5A and reducing levels of hypusinated elF5A in cancer cells. In turn, this inhibits activation of the transcription factor NF-kB and induces apoptosis. In addition, the B-cell specific plasmid component expresses an arginine substituted form of eIF5A, eIF5AK50R, which can not be hypusinated, thus leads to a selective induction of apoptosis in B-cells. The native unhypusinated form of eIF5A is pro-apoptotic and can be modified at the lysine residue, by deoxyhypusine synthase (DHS) and subsequently deoxyhypusine hydroxylase (DHH), to the anti-apoptotic hypusinated form which is associated with tumor cell growth and survival. The delivery vehicle protects the siRNA and plasmid from degradation.

• Sobuzoxane - The orally available active prodrug of ICRF-154, a bisdioxopiperazine derivative, with cardioprotective and antineoplastic activities. Like other ICRF compounds, sobuzoxane and its active metabolite ICRF-154 interfere with topoisomerase II activity prior to the formation of intermediate cleavable DNA-enzyme complexes during the catalytic cycle resulting in tumor cell growth inhibition. Furthermore, sobuzoxane chelates metal cations thereby limiting the formation of free radical-generating anthracycline-metal complexes and may prevent anthracycline-induced oxidative damage to cardiac and soft tissues.

• Sodium borocaptate - A boron-carrying compound. After parenteral administration, sodium borocaptate accumulates preferentially in tumor cells. When exposed to neutron irradiation, borocaptate 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.

• Sodium butyrate - The sodium salt of butyrate with potential antineoplastic activity. Butyrate, a short chain fatty acid, competitively binds to the zinc sites of class I and II histone deacetylases (HDACs). This binding affects hyperacetylation of histones, resulting in a modified DNA conformation, which subsequently leads to the uncoiling or relaxing of chromatin. Enhanced accessibility of chromatin to transcription-regulatory complexes leads to increased transcriptional activation of various epigenetically suppressed genes. Butyrate, a HDAC inhibitor, induces cell cycle arrest in G1 or G2/M and also increases the expression of other genes and proteins involved in cellular differentiation and apoptotic signaling.

• Sodium dichloroacetate - The sodium salt of dichloroacetic acid with potential antineoplastic activity. Dichloroacetate ion inhibits pyruvate dehydrogenase kinase, resulting in the inhibition of glycolysis and a decrease in lactate production. This agent may stimulate apoptosis in cancer cells by restoring normal mitochondrial-induced apoptotic signaling.

• Sodium iodide i-131 - A radiopharmaceutical containing the beta- and gamma-emitting radioisotope I-131. After absorption, the iodide is distributed through the extracellular fluid of the body and accumulates in the thyroid gland, thereby allowing the imaging of the thyroid.

• Sodium metaarsenite - A highly soluble, orally available trivalent arsenic-containing telomerase inhibitor with potential antitumor activity. Although the exact mechanism through which sodium metaarsenite exerts its effect has yet to be fully elucidated, this agent appears to target and bind to telomeric sequences, specifically TTAGGG repeats, leading to a shortening of telomeres, and subsequent induction of apoptosis and inhibition of tumor cell growth. In addition, sodium metaarsenite also leads to the translocation of the catalytic subunit of telomerase into the cytoplasm and inhibition of the activity of telomerase. Telomerase is active in most tumors cells and is responsible for the maintenance of telomere length and plays a key role in cellular proliferation, but is quiescent in normal, healthy cells. The susceptibility to sodium metaarsenite seems to be inversely correlated with initial length of telomeres.

• Sodium phenylbutyrate - The sodium salt of phenylbutyrate, a derivative of the short-chain fatty acid butyrate, with potential antineoplastic activity. Phenylbutyrate reversibly inhibits class I and II histone deacetylases (HDACs), which may result in a global increase in gene expression, decreased cellular proliferation, increased cell differentiation, and the induction of apoptosis in susceptible tumor cell populations.

• Sodium salicylate - The sodium salt of salicylic acid. As a nonsteroidal anti-inflammatory drug (NSAID), sodium salicylate irreversibly acetylates cyclooxygenases I and II, thereby inhibiting prostaglandin synthesis and associated inflammation and pain. This agent may also activate mitogen-activated protein kinase (p38MAPK), thereby inducing apoptosis in cancer cells.

• Sodium selenite - An inorganic form of the trace element selenium with potential antineoplastic activity. Selenium, administered in the form of sodium selenite, is reduced to hydrogen selenide (H2Se) in the presence of glutathione (GSH) and subsequently generates superoxide radicals upon reaction with oxygen. This may inhibit the expression and activity of the transcription factor Sp1; in turn Sp1 down-regulates androgen receptor (AR) expression and blocks AR signaling. Eventually, selenium may induce apoptosis in prostate cancer cells and inhibit tumor cell proliferation.

• Sodium stibogluconate - Pentavalent antimony (Sb) in differential complex formation with gluconic acid with leishmanicidal and potential antineoplastic activities. The Sb moiety of sodium stibogluconate (SSG) may inhibit protein tyrosine phosphorylases (PTPases) by covalently modifying sulfhydryl groups in PTPase cysteine residues, resulting in specific inactivation of SH2 domain-containing tyrosine phosphatases-1 and -2 (SHP-1 and SHP-2), PTPases which negatively regulate interferon (IFN) signaling; enhancement of IFN-induced Stat1 tyrosine phosphorylation; and induction of cellular protein tyrosine phosphorylation. SSG in combination with IFN-alpha may synergize to overcome tumor cell resistance to IFN-alpha-mediated apoptosis.

• Sodium-potassium adenosine triphosphatase inhibitor rx108 - A small-molecule, inhibitor of sodium-potassium adenosine triphosphatase (Na+/K+-ATPase) with potential antineoplastic activity. Upon administration, RX108 inhibits the activity of the Na+/K+-ATPase, which prevents the activation of various signal transduction pathways that play a key role in tumor proliferation. This may lead to cell-cycle arrest, apoptosis, and autophagic cell death. Na+/K+-ATPase is overexpressed in certain tumor types and may serve as a scaffold for the assembly of multiple-protein signaling complexes that regulate cell proliferation and motility. In normal, healthy cells, the Na+/K+-ATPase controls transportation of Na+ and K+ across the cell membrane and is essential for electrochemical gradient maintenance, osmotic balance, and cellular pH.

• Sofituzumab vedotin - An antibody drug conjugate (ADC) consisting of a humanized IgG1 monoclonal antibody targeting the MUC16 protein (CA-125) conjugated to, via a cleavable linker, the antimicrotubulin agent monomethyl auristatin E (MMAE), with potential antineoplastic activity. The monoclonal antibody moiety of sofituzumab vedotin selectively binds to MUC16. After internalization of the drug conjugate and proteolytic cleavage of the linker, MMAE binds to tubulin and inhibits its polymerization, which results in G2/M-phase growth arrest and tumor cell apoptosis. MUC16, a transmembrane protein, is overexpressed on the cell surface of more than 80 percent of ovarian cancer cells but not on healthy cells.

• Solitomab - A recombinant bispecific monoclonal antibody directed against both CD3 and epithelial cell adhesion molecule (EpCAM) with potential immunomodulating and antineoplastic activities. Solitomab attaches to both CD3-expressing T lymphocytes and EpCAM-expressing tumor cells, thereby selectively cross-linking tumor and T lymphocytes; this may result in the recruitment of cytotoxic T lymphocytes (CTL) to T lymphocyte/tumor cell aggregates and the CTL-mediated death of EpCAM-expressing tumor cells. CD3 is an antigen expressed on mature T cells; EpCAM, a cell surface protein, is expressed by a variety of tumor cells and is frequently found in head and neck cancers.

• Sonepcizumab - A humanized monoclonal antibody directed against sphingosine 1-phosphate (S1P) with potential antiangiogenic and antineoplastic activities. Upon administration, sonepcizumab binds S1P, which may result in the inhibition of tumor angiogenesis. S1P is the extracellular ligand for the G protein-coupled lysophospholipid receptor EDG-1 (endothelial differentiation gene-1).

• Sonidegib - An orally bioavailable small-molecule smoothened (Smo) antagonist with potential antineoplastic activity. Sonidegib selectively binds to the hedgehog (Hh)-ligand cell surface receptor Smo, which may result in the suppression of the Hh signaling pathway and, so, the inhibition of tumor cells in which this pathway is abnormally activated. The Hh signaling pathway plays an important role in cellular growth, differentiation and repair. Inappropriate activation of Hh pathway signaling and uncontrolled cellular proliferation, as is observed in a variety of cancers, may be associated with mutations in the Hh-ligand cell surface receptor Smo.

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

• Sorafenib - A synthetic compound targeting growth signaling and angiogenesis. Sorafenib blocks the enzyme RAF kinase, a critical component of the RAF/MEK/ERK signaling pathway that controls cell division and proliferation; in addition, sorafenib inhibits the VEGFR-2/PDGFR-beta signaling cascade, thereby blocking tumor angiogenesis.

• Sorafenib tosylate - The tosylate salt of sorafenib, a synthetic compound targeting growth signaling and angiogenesis. Sorafenib blocks the enzyme RAF kinase, a critical component of the RAF/MEK/ERK signaling pathway that controls cell division and proliferation; in addition, sorafenib inhibits the VEGFR-2/PDGFR-beta signaling cascade, thereby blocking tumor angiogenesis.

• Sorghum bicolor supplement - An herbal-based nutritional supplement containing the leaf sheaths of the plant Sorghum bicolor, with potential antioxidant, anti-inflammatory, chemopreventive and immunomodulating activities. Sorghum bicolor supplement contains various phytochemicals, including phenolic acids and polyphenols such as proanthocyanidins. Sorghum bicolor supplement is particularly rich in 3-deoxyanthocyanins, such as luteolinidin and apigeninidin, and appears to induce apoptosis and inhibit cell proliferation in cancer cells through the stimulation of various apoptosis promoter genes and the downregulation of certain apoptosis inhibitor genes. In addition, due to the strong antioxidant nature of the phytochemicals, these compounds are able to scavenge free radicals and prevent tissue damage. Also, intake of this supplement modulates the immune system by both increasing the activity of natural killer (NK) cells and initiating the activation of macrophages.

• Sotigalimab - A humanized monoclonal antibody agonist of the cell surface receptor CD40, with potential immunostimulatory and antineoplastic activities. Similar to the endogenous CD40 ligand (CD40L or CD154), sotigalimab binds to CD40 on a variety of immune cell types. This triggers the cellular proliferation and activation of antigen-presenting cells (APCs), and activates B-cells, and effector and memory T-cells. This results in an enhanced immune response against tumor cells. Sotigalimab also binds to and activates CD40 present on the surfaces of some solid tumor cells, leading to apoptosis and decreased tumor growth. CD40, a cell surface receptor and member of the tumor necrosis factor (TNF) receptor superfamily, is expressed on various immune cells and certain cancer cells; it mediates both indirect tumor cell killing through the activation of the immune system and direct tumor cell apoptosis.

• Sotorasib - An orally available agent that targets the specific KRAS mutation, p.G12C, with potential antineoplastic activity. Upon oral administration, sotorasib selectively targets the KRAS p.G12C mutant, at either the DNA, RNA or protein level, and prevents, through an as of yet not elucidated manner, expression of and/or tumor cell signaling through the KRAS p.G12C mutant. This may inhibit growth in KRAS p.G12C-expressing tumor cells. The KRAS p.G12C mutation is seen in some tumor cell types and plays a key role in tumor cell proliferation.

• Sotrastaurin - An orally available pan-protein kinase C (PKC) inhibitor with potential immunosuppressive and antineoplastic activities. Sotrastaurin inhibits both T- and B-cell activations via PKC theta and beta isozymes, respectively. Both PKCs are important in the activation of nuclear factor-kappaB (NF-kB). Inhibition of PKC beta in B-cells results in prevention of NF-kB-mediated signaling and down regulation of NF-kB target genes. This may eventually lead to an induction of G1 cell cycle arrest and tumor cell apoptosis in susceptible tumor cells. This agent may act synergistically with other chemotherapeutic agents. PKC, a family of serine/threonine protein kinases overexpressed in certain types of cancer cells, is involved in cell differentiation, mitogenesis, inflammation, and the activation and survival of lymphocytes.

• Sotrastaurin acetate - The acetate salt form of sotrastaurin, an orally available pan-protein kinase C (PKC) inhibitor with potential immunosuppressive and antineoplastic activities. Sotrastaurin inhibits both T- and B-cell activations via PKC theta and beta isozymes, respectively. Both PKCs are important in the activation of nuclear factor-kappaB (NF-kB). Inhibition of PKC beta in B-cells results in prevention of NF-kB-mediated signaling and down regulation of NF-kB target genes. This may eventually lead to an induction of G1 cell cycle arrest and tumor cell apoptosis in susceptible tumor cells. This agent may act synergistically with other chemotherapeutic agents. PKC, a family of serine/threonine protein kinases overexpressed in certain types of cancer cells, is involved in cell differentiation, mitogenesis, inflammation, and the activation and survival of lymphocytes.

• Soy isoflavones - A dietary supplement isolated from soybeans containing phytoestrogen isoflavones. Although the mechanism of action is unclear, soy isoflavones mimic estrogen action mediated through estrogen receptors. In addition, this agent also modulates estrogen metabolism. As a result, soy isoflavones have been shown to reduce tumor cell proliferation and induce tumor cell apoptosis, as well as to be able to regulate hormone balance and reduce the risks of breast cancer, heart disease, and osteoporosis.

• Soy protein isolate - A dietary protein isolated from soybeans that contains isoflavone phytoestrogens. Soy protein isolate has been shown to reduce tumor incidence and growth in some animal studies, possibly by modulating estrogen metabolism, reducing tumor cell proliferation, and inducing tumor cell apoptosis. Soy protein isolate may also inhibit endothelial cell proliferation. Isoflavone phytoestrogens display mild estrogen-like activities which may regulate hormone balance and reduce the risks of breast cancer, heart disease, and osteoporosis.

• Sparfosate sodium - The disodium salt form of N-phosphonacetyl-L-aspartate (PALA), a pyrimidine antimetabolite with antineoplastic activity. PALA inhibits pyrimidine biosynthesis and increases the extent to which fluorouracil is incorporated into RNA.

• Sparfosic acid - A stable transition state analogue for an aspartate transcarbamylase-catalyzed reaction with antineoplastic activity. Sparfosic acid is a stable transition analogue of the activated complex for the reaction catalyzed by aspartate transcarbamylase, the first step in the pyrimidine biosynthetic pathway. This agent inhibits de novo pyrimidine biosynthesis and increases the extent to which fluorouracil metabolites are incorporated into RNA.

• Spartalizumab - A humanized monoclonal antibody directed against the negative immunoregulatory human cell surface receptor programmed death-1 (PD-1, PCD-1), with immune checkpoint inhibitory and antineoplastic activities. Upon administration, spartalizumab binds to PD-1 expressed on activated T-cells and blocks the interaction with its ligands, programmed cell death 1 ligand 1 (PD-L1, PD-1L1) and PD-1 ligand 2 (PD-L2, PD-1L2). The inhibition of ligand binding prevents PD-1-mediated signaling and results in both T-cell activation and the induction of T-cell-mediated immune responses against tumor cells. PD-1, an immunoglobulin (Ig) superfamily transmembrane protein and inhibitory receptor, negatively regulates T-cell activation.

• Spebrutinib - An orally bioavailable, selective inhibitor of Bruton's agammaglobulinemia tyrosine kinase (BTK), with potential antineoplastic activity. Upon administration, spebrutinib targets and covalently binds to BTK, thereby preventing its activity. By irreversibly inhibiting BTK, administration of this agent may lead to an inhibition of B cell receptor (BCR) signaling and may inhibit 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.

• Spherical nucleic acid nanoparticle nu-0129 - A spherical nucleic acid (SNA) gold nanoparticle formulation composed of small interfering RNAs (siRNAs) targeting the Bcl-2-like protein 12 (BCL2L12) sequence and conjugated to gold nanoparticles, with potential antineoplastic activity. Upon administration of SNA NU-0129, the siRNA prevents the translation of the BCL2L12 gene. Inhibiting the expression of BCL2L12 by NU-0129 induces tumor cell apoptosis. Bcl2L12, a protein belonging to the Bcl-2 protein family, is overexpressed in glioblastoma multiforme (GBM) and plays a role in tumor cell progression and tumor cell resistance to apoptosis. NU-0129 is able to cross the blood brain barrier (BBB).

• Spirogermanium - A synthetic organometallic compound containing the element germanium with possible antineoplastic activity. Spirogermanium exhibits significant toxicity, particularly neurotoxicity.

• Spiromustine - A bifunctional nitrogen alkylating agent with antineoplastic activity and lipophilic properties. Containing a lipophilic hydantoin group that serves as a carrier to cross the blood brain barrier, spiromustine forms covalent linkages with nucleophilic centers in DNA, causing depurination, base-pair miscoding, strand scission, and DNA-DNA cross-linking, which may result in cytotoxicity.

• Spiroplatin - A synthetic derivative of cyclohexane sulfatoplatinum with antineoplastic properties. Spiroplatin induces DNA cross-links, thereby inhibiting DNA replication and RNA and protein synthesis. Similar to other platinum compounds, this agent has been shown to be mutagenic and carcinogenic.

• Splicing inhibitor h3b-8800 - An orally bioavailable inhibitor of the splicing factor 3B subunit 1 (SF3B1), with potential antineoplastic activity. Upon administration, H3B-8800 binds to and blocks the activity of SF3B1, a core spliceosome protein that is mutated in various cancer cells. This modulates RNA splicing by preventing aberrant mRNA splicing by the spliceosome, blocks RNA mis-splicing, enhances proper RNA splicing and prevents the expression of certain tumor-associated genes. This leads to an induction of apoptosis and prevents tumor cell proliferation. In many cancer cells, core spliceosome proteins, including SF3B1, U2 small nuclear ribonucleoprotein auxiliary factor 1 (U2AF1), serine/arginine-rich splicing factor 2 (SRSF2) and U2 small nuclear ribonucleoprotein auxiliary factor subunit-related protein 2 (ZRSR2), are mutated and aberrantly activated leading to a dysregulation of mRNA splicing.

• Spongistatin - A highly cytotoxic macrocyclic lactone polyether with antitumor activity. Spongistatin, originally isolated from marine Spongia species, binds to the vinca domain of tubulin, thereby interferes with microtubule assembly and results in inhibition of mitosis. This agent does not affect the binding of colchicine to tubulin, but it was a potent inhibitor of the binding of vinblastine and GTP to tubulin.

• Squalamine lactate - The lactate salt form of squalamine, an aminosterol isolated from tissues of the dogfish shark Squalus acanthias. Possessing anti-angiogenic properties, squalamine inhibits the sodium-hydrogen exchanger NHE3, resulting in suppression of endothelial cell proliferation and migration. This agent also has broad-spectrum antimicrobial properties.

• Sr-bp1/hsi inhibitor sr31747a - A synthetic peripheral sigma receptor ligand with immunomodulatory and potential antitumor activities. Although the exact mechanism by which SR31747A exerts its antitumor effects has not been fully established, SR31747A binds to and inhibits the sigma1 receptor (SR31747A-binding protein-1 or SR-BP1), human sterol isomerase (HSI), also known as emopamil-binding protein (EBP), and the sigma2 receptor, which may result in a reduction in tumor cell proliferation and tumor cell apoptosis. In addition, this agent inhibits the production of pro-inflammatory cytokines while increasing anti-inflammatory cytokines. Upregulated in various cancers, the sigma1 and sigma2 receptors and human sterol isomerase are proteins that are involved in the regulation of cell proliferation and survival.

• Src kinase inhibitor ap 23846 - A novel small molecule Src family kinase inhibitor with potential antiangiogenic activity. Upon administration, Src kinase inhibitor AP23846 selectively binds to and stabilizes an inactive ATP-binding site conformation leading to reduced Src kinase activity. This may reduce the production of pro-angiogenic factors, vascular endothelial growth factor (VEGF) and interleukin (IL)-8. Src tyrosine kinases are upregulated in many tumor cells and play important roles in tumor cell proliferation, survival, migration, invasion and angiogenesis.

• Src kinase inhibitor kx2-391 ointment - An ointment containing an inhibitor for both Src tyrosine kinase and tubulin polymerization, with potential antineoplastic activity. Unlike other Src kinase inhibitors which bind to the ATP-binding site, Src kinase inhibitor KX2-391 binds to the peptide substrate binding site of Src kinase, upon topical application. This inhibits both downstream signaling and the proliferation of tumor cells overexpressing Src. Src tyrosine kinase, a non-receptor tyrosine kinase upregulated in many tumor cell types, plays an important role in tumor cell proliferation, motility, invasiveness and survival. KX2-391 also binds to tubulin heterodimers and inhibits microtubule polymerization, which disrupts microtubule formation and mitosis, leading to further inhibition of cell proliferation. In addition, KX2-391 inhibits T-cell migration.

• Src kinase inhibitor m475271 - An inhibitor of Src tyrosine kinase, with potential antineoplastic activity. Upon administration, Src kinase inhibitor M-475271 targets and binds to Src kinase. This inhibits Src-mediated signaling and the proliferation of tumor cells overexpressing Src. Src tyrosine kinase, a non-receptor tyrosine kinase upregulated in many tumor cell types, plays an important role in tumor cell proliferation, motility, invasiveness and survival.

• Src/abl kinase inhibitor azd0424 - An orally bioavailable small molecule tyrosine kinase inhibitor that targets both Abl and Src kinases with potential antineoplastic activity. Upon oral administration, AZD0424 selectively inhibits both Src and Abl kinase activity which may result in the inhibition of tumor growth in susceptible tumor cells. Src and Abl kinases are upregulated in certain tumor cells and play important roles in tumor cell proliferation and metastasis.

• Src/tubulin inhibitor kx02 - A lipophilic, orally available inhibitor of both Src kinase activity and tubulin polymerization, with potential antineoplastic activity. Upon oral administration, src/tubulin inhibitor KX02 binds to and inhibits the activity of Src kinase. This inhibits both downstream signaling and the proliferation of Src kinase-expressing tumor cells. KX02 also binds to tubulin heterodimers and inhibits microtubule polymerization, thereby disrupting microtubule formation, mitosis, and further proliferation. Src, a non-receptor tyrosine kinase, is overexpressed in a variety of tumor cell types and plays a key role in tumor cell proliferation, angiogenesis, migration, and metastasis.

• Srpk1/abcg2 inhibitor sco-101 - An orally bioavailable inhibitor of the serine/arginine-rich splicing factor protein kinase 1 (SRPK1) and the ATP-binding cassette sub-family G member 2 (ABCG2), with potential chemosensitizing and antineoplastic activities. Upon oral administration, SRPK1/ABCG2 inhibitor SCO-101 targets, binds to and inhibits the activity of SRPK1 and ABCG2. Inhibition of the cellular efflux pump ABCG2 by SCO-101 prevents the efflux of co-administered chemotherapeutic agents from cancer cells. This may abrogate cancer cell drug resistance and may re-sensitize cancer cells to the chemotherapeutic agents. Inhibition of SRPK1 kinase by SCO-101 inhibits the SRPK1-mediated phosphorylation of splicing factors rich in serine/arginine domains, thereby inhibiting the activation of proteins that are involved in the regulation of alternative splicing. This may inhibit cancer cell proliferation. SRPK1 is upregulated in various cancer cell types. Its upregulation is correlated with higher tumor staging, grading, and shorter survival.

• Sr-t100 gel - A cutaneous gel preparation containing an extract from Solanum incanum with potential antineoplastic activity. SR-T100 gel contains high amounts of the steroidal alkaloid glycoside solamargine. Solamargine is able to upregulate expression of tumor necrosis factor receptors 1 (TNFR1) and 6 (TNFRSF6 or Fas), and their signaling adaptors TNFR1-associated death domain, and Fas-associated death domain. In addition, this agent is able to upregulate expression of apoptosis promoter Bax, and suppress the expression of the anti-apoptotic proteins Bcl-xL and Bcl-2. Altogether, this induces apoptosis in tumor cells and may lead to an inhibition of tumor cell proliferation.

• Ss1(dsfv)-pe38 immunotoxin - A recombinant immunotoxin consisting of the single chain anti-mesothelin monoclonal antibody SS1(dsFv) linked to Pseudomonas exotoxin PE-38. The monoclonal antibody moiety of the agent binds to cells that express mesothelin, a cell surface glycoprotein which may be overexpressed in ovarian cancer, mesotheliomas, and some squamous cell carcinomas; after internalization, the exotoxin moiety inactivates eukaryotic translation elongation factor 2, thereby disrupting tumor cell protein synthesis.

• Ssrna-based immunomodulator cv8102 - A 547 nucleotide (nt), noncoding, uncapped single-stranded RNA (ssRNA) containing several polyU-repeats complexed with a polymeric carrier formed by disulfide-crosslinked cationic peptides, with potential immunostimulating activity. Upon intratumoral injection, the ssRNA in CV8102 activates toll-like receptors (TLRs) and retinoic acid-inducible gene I (RIG I; RIG-I; DDX58). This stimulates a T-helper type 1 cell (Th1) response, the production of a variety of pro-inflammatory cytokines and chemokines, and activates a systemic cytotoxic-T-lymphocyte (CTL)-mediated immune response against the tumor cells when simultaneously exposed to tumor-associated antigens (TAAs). The cationic carrier peptides protect the ssRNA from RNase degradation.

• Sstr2-targeting protein/dm1 conjugate pen-221 - A miniaturized drug conjugate composed of a peptide analog of somatostatin that targets the somatostatin receptor 2 (SSTR2) and is conjugated, through a cleavable linker, to the microtubule-binding cytotoxic maytansinoid DM1 (mertansine), with potential anti-tumor activity. Upon administration, the peptide ligand moiety of PEN-221 targets and binds to SSTR2, which is overexpressed on certain tumor cell types. Binding stimulates SSTR2-mediated endocytosis of the agent; upon internalization, the DM1 moiety is released and binds to tubulin, thereby disrupting microtubule assembly/disassembly dynamics. This inhibits both cell division and the proliferation of SSTR2-expressing cancer cells. Compared to antibody-drug conjugates (ADCs), miniaturized drug conjugates are much smaller and can more easily penetrate and distribute in dense tumor tissue.

• St. John's wort - An herbal extract prepared from the plant Hypericum perforatum (St. John's wort) with photodynamic, antineoplastic, and antidepressant activities. Hypericin, one of the active compounds found in Hypericum perforatum, is a photosensitizer that, when exposed to a particular wavelength and intensity of light, may induce tumor cell apoptosis. Another compound, hyperforin, induces caspase-dependent apoptosis in certain tumor cell lines. Hypericum perforatum preparations may also stimulate the activity of cytochrome P450 enzymes and P-glycoprotein drug transporters, resulting in increased metabolism and decreased efficacy of various chemotherapeutic agents and other drugs.

• Stallimycin - An oligopeptide antineoplastic antibiotic isolated from the bacterium Streptomyces distallicus. Distamycin preferentially binds to adenine-thymine (A-T) rich sequences in the minor groove of DNA, thereby inhibiting DNA replication and RNA transcription. In addition to antitumor effects, distamycin also possesses antiviral and antiprotozoal activities and is used as a chromosome dye.

• Staphylococcal enterotoxin a - A bacterial enterotoxin with potential immunostimulatory activity. Staphylococcal enterotoxin A (SEA), a gram positive bacterial superantigen (SAg), is a potent stimulator of T-cell activation. SEA superantigen binds directly to class II major histocompatibility complex (MHC) molecules and to the V beta region of the T-cell receptor (TCR), leading to an amplified T-cell response. In response to SEA, both CD4+ and CD8+ cells proliferate, secrete cytokines, and demonstrate enhanced cytotoxic activity against a broad range of antigens. Vaccination with the SEA protein, administered by direct transfection into tumor cells, may elicit a non-specific cytotoxic T-cell (CTL) response and result in decreased tumor cell growth.

• Staphylococcal enterotoxin b - A bacterial enterotoxin with potential immunostimulatory activity. Staphylococcal enterotoxin B (SEB), a gram positive superantigen produced by Staphylococcus aureus, is a potent stimulator of T-cell activation. SEB binds directly to class II major histocompatibility complex (MHC) molecules and the V beta region of the T-cell receptor (TCR), leading to an amplified T-cell response. In response to SEB, both CD4+ and CD8+ cells proliferate, secrete cytokines and demonstrate enhanced cytotoxic activity against a broad range of antigens. Co-administration of SEB with interleukin-2 (IL-2) by direct injection into tumor cells, may induce clonal T-cell expansion and potentiate apoptosis of tumor cells, resulting in decreased tumor growth.

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

• Stat inhibitor opb-111077 - An orally bioavailable inhibitor of one or more signal transducer and activator of transcription (STAT) protein(s), with potential antineoplastic activity. Upon oral administration, OPB-111077 binds to and inhibits the phosphorylation of STATs. This prevents binding of STATs to DNA sequences on a variety of STAT-responsive gene promoters, which may result in the inhibition of both STAT-mediated transcription and tumor cell proliferation. STATs are constitutively activated in a variety of cancers and play a key role in tumor cell proliferation.

• Stat3 decoy oligonucleotide - A double-stranded 15-mer oligonucleotide, corresponding closely to the signal transducer and activator of transcription 3 (STAT3) response element within the c-fos promoter, with potential antineoplastic activity. STAT3 decoy oligonucleotide binds specifically to activated STAT3 and blocks binding of STAT3 to DNA sequences on a variety of STAT3-responsive promoters, which results in the inhibition of STAT3-mediated transcription and, potentially, the inhibition of tumor cell proliferation. STAT3 is constitutively activated in a variety of cancers including squamous cell carcinoma of the head and neck, contributing to the loss of cell growth control and neoplastic transformation.

• Stat3 inhibitor dsp-0337 - An orally administered prodrug of napabucasin, a small molecule cancer stemness inhibitor with potential antineoplastic activity. Upon administration, DSP-0337 is converted to its active form, napabucasin. Napabucasin targets and inhibits signal transducer and activator of transcription 3 (STAT3), thereby preventing STAT-3-mediated signaling. The STAT3 pathway is overly active in many cancer types and is implicated in cancer stem cell-mediated growth, recurrence and resistance to conventional chemotherapies.

• Stat3 inhibitor opb-31121 - An orally bioavailable inhibitor of signal transducer and activator of transcription 3 (STAT3), with potential antineoplastic activity. OPB-31121 inhibits the phosphorylation of STAT3, which prevents binding of STAT3 to DNA sequences on a variety of STAT3-responsive promoters and may result in the inhibition of STAT3-mediated transcription and, potentially, the inhibition of tumor cell proliferation. STAT3 is constitutively activated in a variety of cancers, contributing to the loss of cell growth control and neoplastic transformation.

• Stat3 inhibitor opb-51602 - An orally bioavailable inhibitor of signal transducer and activator of transcription 3 (STAT3), with potential antineoplastic activity. STAT3 inhibitor OPB-51602 inhibits the phosphorylation and thus the activation of STAT3 protein, impeding STAT3 protein from translocating from the cytoplasm to the nucleus and thereby blocking STAT3's regulation of gene expression through direct binding to the promoters of responsive genes. STAT3 regulates the cellular functions that lead to the cancer phenotype, and constitutive activation of STAT3 is observed in a wide range of human cancers, inducing uncontrolled proliferation and neoplastic transformation.

• Stat3 inhibitor tti-101 - An orally bioavailable, binaphthol-sulfonamide-based inhibitor of signal transducer and activator of transcription 3 (STAT3), with potential antineoplastic activity. Upon oral administration, the STAT3 inhibitor TTI-101 specifically targets and binds to the phosphotyrosyl peptide binding site within the Src homology 2 (SH2) domain of STAT3. This inhibits the Janus kinase (JAK)-mediated tyrosine phosphorylation and activation of STAT3. This impedes nuclear translocation of STAT3, prevents STAT3 binding to responsive gene promoters and blocks STAT3-mediated regulation of gene expression. STAT3 regulates the transcription of genes involved in several cellular functions. STAT3 is constitutively activated in a variety of human cancers and plays a key role in neoplastic transformation, uncontrolled tumor cell proliferation, resistance to apoptosis, metastasis, immune evasion, tumor angiogenesis, epithelial-mesenchymal transition (EMT) and the Warburg effect.

• Stat3 inhibitor wp1066 - An orally bioavailable, small molecule inhibitor of signaling transducer and activator 3 (STAT3), with potential antineoplastic and immunomodulatory activities. Upon administration, STAT3 inhibitor WP1066 blocks the intranuclear translocation of p-STAT, thereby suppressing STAT3 signaling and decreasing the levels of downstream products including c-Myc. Additionally, WP1066 may upregulate costimulatory molecules including CD80 and CD86 on human microglia, and reverse glioma cancer stem cell (gCSC)-mediated innate and adaptive immune suppression allowing for the restoration of antitumor effector immune responses. The STAT3 pathway is overly active in many cancer types and is implicated in CSC-mediated growth, recurrence and resistance to conventional chemotherapies.

• Staurosporine - A cell permeable alkaloid isolated from Streptomyces staurosporeus exhibiting anti-cancer activity. Staurosporine is a potent, non-selective inhibitor of protein kinases, including protein kinase C. This agent induces apoptosis by an undetermined mechanism. (NCI)

• Sting agonist bms-986301 - An agonist of stimulator of interferon genes (STING) protein, with potential immunoactivating and antineoplastic activities. Upon administration, STING agonist BMS-986301 targets and binds to STING and activates the STING pathway, which promotes IKK-related kinase TANK-binding kinase 1 (TBK1) signaling and activates nuclear factor-kappa B (NF-kB) and interferon regulatory factor 3 (IRF3) in immune cells in the tumor microenvironment (TME). This leads to the production of pro-inflammatory cytokines, including interferons (IFNs). Specifically, expression of IFN-beta (IFNb) enhances the cross-presentation of tumor-associated antigens (TAAs) by dendritic cells (DCs) to cytotoxic T-lymphocytes (CTLs). This results in a CTL-mediated immune response against tumor cells and causes tumor cell lysis. STING, a transmembrane protein that activates immune cells in the TME, plays a key role in the activation of the innate immune system.

• Sting agonist gsk3745417 - An agonist of the stimulator of interferon genes protein (STING; transmembrane protein 173; TMEM173), with potential immunoactivating and antineoplastic activities. Upon intravenous administration, STING agonist GSK3745417 targets and binds to STING and activates the STING pathway in immune cells in the tumor microenvironment (TME). This leads to the production of pro-inflammatory cytokines, including interferons (IFNs), enhances the cross-presentation of tumor-associated antigens (TAAs) by dendritic cells (DCs), and induces a cytotoxic T-lymphocyte (CTL)-mediated immune response against cancer cells. STING, a transmembrane protein that activates immune cells in the TME, plays a key role in the activation of the innate immune system.

• Sting agonist imsa101 - A small molecule analogue of cyclic GMP-AMP (cGAMP) that acts as an agonist of the stimulator of interferon genes protein (STING; transmembrane protein 173; TMEM173) with potential immunoactivating and antineoplastic activities. Upon intratumoral administration, STING agonist IMSA101 binds to STING and activates STING-mediated pathways. This activates the immune response through the activation of certain immune cells which induces the expression of pro-inflammatory cytokines and chemokines, promotes tumor-associated antigen (TAA) processing and presentation by dendritic cells (DCs) and leads to an antigen-specific T-cell mediated immune response against cancer cells. STING, a transmembrane protein that activates immune cells in the tumor microenvironment, plays a key role in the activation of the innate immune system.

• Sting agonist mk-1454 - A synthetic cyclic dinucleotide (CDN) and agonist of stimulator of interferon genes protein (STING), with potential immunoactivating and antineoplastic activities. Upon intratumoral (IT) administration, STING agonist MK-1454 binds to STING and activates the STING pathway, which promotes IKK-related kinase TANK-binding kinase 1 (TBK1) signaling and activates nuclear factor-kappa B (NF-kB) and interferon regulatory factor 3 (IRF3) in immune cells in the tumor microenvironment; this leads to the production of pro-inflammatory cytokines, including interferons (IFNs). Specifically, expression of IFN-beta (IFNb) enhances the cross-presentation of tumor-associated antigens by CD8alpha-positive and CD103-positive dendritic cells (DCs) to cytotoxic T-lymphocytes (CTLs). This results in a CTL-mediated immune response against tumor cells and causes tumor cell lysis.

• Sting agonist sb 11285 - An agonist of stimulator of interferon genes (STING) protein, with potential immunoactivating and antineoplastic activities. Upon intravenous administration, STING agonist SB 11285 targets and binds to STING and activates the STING pathway, which promotes IKK-related kinase TANK-binding kinase 1 (TBK1) signaling and activates nuclear factor-kappa B (NF-kB) and interferon regulatory factor 3 (IRF3) in immune cells in the tumor microenvironment (TME). This leads to the production of pro-inflammatory cytokines, including interferons (IFNs). Specifically, expression of IFN-beta (IFNb) enhances the cross-presentation of tumor-associated antigens (TAAs) by CD8alpha-positive and CD103-positive dendritic cells (DCs) to cytotoxic T-lymphocytes (CTLs). This results in a CTL-mediated immune response against tumor cells and causes tumor cell lysis.

• Sting agonist tak-676 - An agonist of the stimulator of interferon genes protein (STING; transmembrane protein 173; TMEM173), with potential immunoactivating and antineoplastic activities. Upon intravenous administration, STING agonist TAK-676 targets and binds to STING and activates the STING pathway in immune cells in the tumor microenvironment (TME). This leads to the production of pro-inflammatory cytokines, including interferons (IFNs), enhances the cross-presentation of tumor-associated antigens (TAAs) by dendritic cells (DCs), and induces a cytotoxic T-lymphocyte (CTL)-mediated immune response against cancer cells. STING, a transmembrane protein that activates immune cells in the TME, plays a key role in the activation of the innate immune system.

• Sting-activating cyclic dinucleotide agonist miw815 - A synthetic, cyclic dinucleotide (CDN) and agonist of stimulator of interferon genes protein (STING; transmembrane protein 173; TMEM173), with potential immunomodulating and antineoplastic activities. Upon intratumoral administration, the STING agonist MIW815 binds to STING and stimulates STING-mediated pathways. This activates the immune response through the activation of certain immune cells, including dendritic cells (DCs), which induces the expression of cytokines and chemokines, and leads to an antigen-specific T-cell mediated immune response against cancer cells. STING, a transmembrane protein that activates immune cells in the tumor microenvironment, plays a key role in the activation of the innate immune system.

• Sting-expressing e. coli synb1891 - A non-pathogenic strain of Escherichia coli (E. coli) bacteria that has been engineered to express stimulator of interferon genes (STING; transmembrane protein 173; TMEM173) protein, with potential immunoactivating and antineoplastic activities. Upon intratumoral administration, STING-expressing E. coli SYNB1891 are engulfed by antigen presenting cells (APCs) within the tumor. STING-mediated pathways within the APCs are then activated resulting in a type I interferon (IFN) response which promotes initiation and propagation of tumor-specific T-cell responses. In addition, the bacterial component of SYNB1891 may further stimulate the innate immune system via Toll-like receptors (TLRs) which may enhance the magnitude of the overall immune response. STING, a transmembrane protein that activates immune cells in the tumor microenvironment (TME), plays a key role in the activation of the innate immune system.

• Strawberry-blackberry-black raspberry-blueberry mixture - A dietary supplement consisting of a mixture of strawberries, blackberries, black raspberries and blueberries with potential antineoplastic activity. Although the exact mechanism of action through which berries may exert their anti-tumor effect has yet to be elucidated, in vivo studies suggest that the ingestion of a mixture of berries seems to result in a reduction in tumor growth and tumor development. As berries are rich in phytonutrients, such as anthocyanins, flavonols, ellagitannins, galltannins, proanthocyanidins, and phenolic acids, the antineoplastic effects of strawberry-blackberry-black raspberry-blueberry berry mixture on cancer cells may be attributable to phytonutrient antioxidant and apoptotic activities. In addition, phytoestrogens in berries may be protective against estrogen-sensitive tumors.

• Streptonigrin - An aminoquinone antineoplastic antibiotic isolated from the bacterium Streptomyces flocculus. Streptonigrin complexes with DNA and topoisomerase II, resulting in DNA cleavage and inhibition of DNA replication and RNA synthesis. This agent also acts as a reverse transcriptase inhibitor and causes free radical-mediated cellular damage.

• Streptozocin - A methylnitrosourea antineoplastic antibiotic isolated from the bacterium Streptomyces achromogenes. Streptozocin alkylates DNA, forming inter-strand DNA cross-links and inhibiting DNA synthesis. Due to its glucose moiety, this agent is readily taken up by pancreatic beta cells, inducing diabetes mellitus at high concentrations. Unlike other nitrosoureas, streptozocin causes little myelosuppression.

• Strontium chloride sr-89 - The chloride salt of a radioactive isotope of strontium. Strontium chloride Sr 89 is taken up and incorporated preferentially in metastatic lesions in bone where it emits cytotoxic beta radiation, resulting in an inhibition and/or reduction of tumor growth and so tumor-related bone pain.

• Submicron particle paclitaxel sterile suspension - A suspension composed of uncoated, stable, submicron particles of the water-insoluble taxane paclitaxel, with potential antineoplastic activity. Upon intra-tumoral administration of the submicron particle paclitaxel sterile suspension, paclitaxel binds to tubulin and inhibits the disassembly of microtubules, which leads to the inhibition of cell division, thereby halting the proliferation of rapidly-dividing tumor cells. The submicron particle paclitaxel is produced through a specific proprietary method of submicron particle production without the need for coating agents or carriers and allows for prolonged retention and sustained release at the tumor site.

• Sugemalimab - A fully human monoclonal antibody directed against the immunosuppressive ligand, programmed cell death-1 ligand 1 (PD-L1; cluster of differentiation 274; CD274), with potential immune checkpoint inhibitory and antineoplastic activities. Upon administration, sugemalimab specifically targets and binds to PD-L1, blocking its binding to and activation of its receptor, programmed cell death 1 (PD-1). This reverses T-cell inactivation caused by PD-1/PD-L1 signaling and enhances the cytotoxic T-lymphocyte (CTL)-mediated anti-tumor immune response against PD-L1-expressing tumor cells. PD-L1 is overexpressed by many human cancer cell types. PD-L1 binding to PD-1 on T-cells suppresses the immune system and results in immune evasion. PD-1, a transmembrane protein belonging to the immunoglobulin superfamily expressed on activated T-cells, is a negative regulator of the immune system that limits the expansion and survival of CD8-positive T-cells. Anti-PD-L1 monoclonal antibody CS1001 mirrors natural immunoglobulin G4 (IgG4), potentially reducing immunogenicity and other toxicities.

• Sulfatinib - An orally bioavailable, small molecule inhibitor of vascular endothelial growth factor receptors (VEGFR) 1, 2, and 3, and the fibroblast growth factor receptor type 1 (FGFR1), with potential antineoplastic and anti-angiogenic activities. Upon oral administration, sulfatinib binds to and inhibits VEGFRs and FGFR1 thereby inhibiting VEGFR- and FGFR1-mediated signal transduction pathways. This leads to a reduction of angiogenesis and tumor cell proliferation in VEGFR/FGFR1-overexpressing tumor cells. Expression of VEGFRs and FGFR1 may be upregulated in a variety of tumor cell types.

• Sulforaphane - A naturally-occurring phytochemical belonging to the class of isothiocyanates. As the aglycone metabolite of glucosinolate glucoraphanin (sulforaphane glucosinolate), sulforaphane acts as an antioxidant and potent stimulator of endogenous detoxifying enzymes. This agent displays anticarcinogenic properties due to its ability to induce phase II detoxification enzymes, such as glutathione S-transferase and quinone reductase, thereby providing protection against certain carcinogens and toxic, reactive oxygen species. Broccoli sprouts contain large amounts of sulforaphane, which is also found in other cruciferous vegetables including cabbage and kale.

• Sulindac - A sulfinylindene derivative prodrug with potential antineoplastic activity. Converted in vivo to an active metabolite, sulindac, a nonsteroidal anti-inflammatory drug (NSAID), blocks cyclic guanosine monophosphate-phosphodiesterase (cGMP-PDE), an enzyme that inhibits the normal apoptosis signal pathway; this inhibition permits the apoptotic signal pathway to proceed unopposed, resulting in apoptotic cell death.

• Sulofenur - A diarylsulfonylurea with potential antineoplastic activity. Sulofenur's antineoplastic mechanism of action is unknown.

• Sumoylation inhibitor tak-981 - A small molecule inhibitor of sumoylation, with potential immune-activating and antineoplastic activities. Upon intravenous administration, TAK-981 targets and covalently binds to the small ubiquitin-like modifier (SUMO; small ubiquitin-related modifier) protein, forming an adduct with SUMO protein (TAK-981-SUMO adduct). This prevents the transfer of SUMO from the SUMO-activating enzyme (SAE) to SUMO-conjugating enzyme UBC9. This prevents SUMO conjugation to lysine residues on target proteins and abrogates many sumoylated protein-mediated cellular processes that play key roles in tumor cells, including proliferation, DNA repair, metastasis and survival. In addition, by preventing sumoylation, TAK-981 is able to increase the production of type 1 interferon (IFN), thereby increasing type 1 IFN-mediated signaling, activating innate effector cells and enhancing the antitumor innate immune responses. This may further increase tumor cell killing. Sumoylation, a post-translational modification that attaches the SUMO protein to target proteins, plays a key role in regulating their activity, function, subcellular localization and stability. Sumoylation also plays a key role in inhibiting innate immune responses, specifically by inhibiting the pattern recognition receptor (PRR) pathway and preventing type 1 IFN expression. Abnormal sumoylation of target proteins is associated with many cancers.

• Sunitinib - An indolinone derivative and tyrosine kinase inhibitor with potential antineoplastic activity. Sunitinib blocks the tyrosine kinase activities of vascular endothelial growth factor receptor 2 (VEGFR2), platelet-derived growth factor receptor b (PDGFRb), and c-kit, thereby inhibiting angiogenesis and cell proliferation. This agent also inhibits the phosphorylation of Fms-related tyrosine kinase 3 (FLT3), another receptor tyrosine kinase expressed by some leukemic cells.

• Sunitinib malate - The orally bioavailable malate salt of an indolinone-based tyrosine kinase inhibitor with potential antineoplastic activity. Sunitinib blocks the tyrosine kinase activities of vascular endothelial growth factor receptor 2 (VEGFR2), platelet-derived growth factor receptor b (PDGFRb), and c-kit, thereby inhibiting angiogenesis and cell proliferation. This agent also inhibits the phosphorylation of Fms-related tyrosine kinase 3 (FLT3), another receptor tyrosine kinase expressed by some leukemic cells.

• Super enhancer inhibitor gz17-6.02 - A synthetic formulation of the Arum palaestinum plant that has been fortified with the already naturally occurring constituents of isovanillin, linolenic acid, and beta-sitosterol, with potential antineoplastic activity. Upon oral administration, GZ17-6.02 may induce apoptosis through caspase-3 activation and poly(ADP-ribose) polymerase (PARP) cleavage, inhibit tumor cell progression by attenuating macrophage infiltration, and inhibit the phosphorylation of several mediators of tumor cell proliferation including Src kinase, extracellular signal-regulated kinases 1 (ERK1) and 2 (ERK2), epidermal growth factor receptor (EGFR), serine/threonine protein kinase AKT (protein kinase B), signal transducer and activator of transcription 2 (STAT-2), and serine/threonine-protein kinase Chk2 (Chk-2). GZ17-6.02 may also inhibit certain super enhancers (SEs) that play an important role in the regulation of the sonic hedgehog (SHH) pathway and cancer stem cell activity. Super enhancers (SEs) are unique areas of the genome that are densely bound by numerous transcription factors and play a pivotal role in the cell, including tissue specification, identity and maintenance. SEs are known to regulate the expression of associated genes and often drive high-level transcription.

• Superoxide dismutase mimetic gc4711 - A mimetic of the enzyme superoxide dismutase (SOD) that may potentially be used to increase the anti-cancer efficacy of stereotactic body radiation therapy (SBRT). Upon administration, SOD mimetic GC4711 may mimic native SODs and catalyze the formation of molecular oxygen and hydrogen peroxide from the burst of superoxide anion present in the irradiated tissues upon radiation. As hydrogen peroxide is less toxic than superoxide to normal tissues, but more toxic to cancer cells, this may increase the anti-cancer efficacy of SBRT and decrease its damage to normal tissues.

• Suramin - A polysulphonated naphthylurea with potential antineoplastic activity. Suramin blocks the binding of various growth factors, including insulin-like growth factor I (IGF-I), epidermal growth factor (EGF), platelet-derived growth factor (PDGF), and tumor growth factor-beta (TGF-beta), to their receptors, thereby inhibiting endothelial cell proliferation and migration. This agent also inhibits vascular endothelial growth factor (VEGF)- and basic fibroblast growth factor (bFGF)-induced angiogenesis; retroviral reverse transcriptase; uncoupling of G-proteins from receptors; topoisomerases; cellular folate transport; and steroidogenesis.

• Suramin sodium - A sodium salt form of suramin, a polysulphonated naphthylurea with potential antineoplastic activity. Suramin blocks the binding of various growth factors, including insulin-like growth factor I (IGF-I), epidermal growth factor (EGF), platelet-derived growth factor (PDGF), and tumor growth factor-beta (TGF-beta), to their receptors, thereby inhibiting endothelial cell proliferation and migration. This agent also inhibits vascular endothelial growth factor (VEGF)- and basic fibroblast growth factor (bFGF)-induced angiogenesis; retroviral reverse transcriptase; uncoupling of G-proteins from receptors; topoisomerases; cellular folate transport; and steroidogenesis.

• Survivin antigen - A tumor-associated antigen. Vaccination with survivin antigen may result in a cytotoxic T-cell response against survivin antigen-expressing tumor cells, resulting in decreased tumor cell proliferation and tumor cell death. Overexpressed in many tumors, endogenous survivin inhibits tumor cell apoptosis.

• Survivin antigen vaccine dpx-survivac - A lipid depot-based therapeutic cancer vaccine composed of survivin epitopes, a universal T Helper peptide and a polynucleotide adjuvant encapsulated in liposomes and then formulated in the hydrophobic carrier Montanide ISA51 VG, with potential immunopotentiating and antineoplastic activities. Upon injection of the survivin antigen vaccine DPX-Survivac, a depot is created at the injection site from which the antigens and adjuvant are released. This vaccine may elicit a long lasting cellular response against survivin-expressing cancers, resulting in a decrease in tumor cell proliferation and an induction of tumor cell death. Survivin, a member of the inhibitor of apoptosis (IAP) family expressed during embryonic development, is upregulated in a variety of human cancers while absent in most normal adult cells; its expression in tumors is associated with a more aggressive phenotype, decreased survival, and increased resistance to chemotherapy.

• Survivin mrna antagonist ezn-3042 - A locked nucleic acid (LNA) antisense oligonucleotide targeting survivin mRNA, with potential antineoplastic activity. EZN-3042 hybridizes to survivin mRNA, thereby blocking translation of survivin protein and inhibiting survivin-induced anti-apoptotic activity and promoting tumor cell apoptosis in survivin-overexpressing tumor cells. Survivin, a member of the inhibitor of apoptosis (IAP) family expressed during embryonic development, is upregulated in a variety of human cancers while absent in most normal adult cells; its expression in tumors is associated with a more aggressive phenotype, decreased survival, and increased resistance to chemotherapy. LNAs contain a methylene bridge linking 2'-oxygen and 4'-carbon of ribose sugar rings, thereby increasing their stability and decreasing degradation.

• Survivin sur1m2 peptide vaccine - A modified recombinant nonapeptide (LMLGEFLKL) derived from the anti-apoptosis protein survivin with potential immunopotentiating and antineoplastic activities. Upon administration, survivin Sur1M2 peptide vaccine may elicit humoral and cellular immune responses against survivin-expressing cancers, resulting in decreased tumor cell proliferation and tumor cell death. The survivin protein inhibits caspase activation and apoptosis; it is undetectable in normal adult tissues but is expressed by several human cancers including lung, colon, breast, pancreas, and prostate cancer as well as hematopoietic malignancies and skin cancers.

• Survivin/p53/her2 antigen-loaded autologous dendritic cell vaccine - An autologous dendritic cell (DC) vaccine loaded with tumor-associated antigens (TAAs) derived from survivin, p53 and human epidermal growth factor receptor 2 (HER2 or ERBB2), with immunostimulating and antineoplastic activities. Upon administration, this DC vaccine may elicit a potent cytotoxic T-cell (CTL) response against tumor cells expressing these TAAs, resulting in tumor cell death. Survivin, p53 and HER2 are essential in neoplastic growth, and are considered to be universal tumor antigens.

• Sustained-release lipid inhaled cisplatin - A sustained-release formulation for inhalation in which the inorganic platinum (Pt) agent cisplatin is encapsulated in lipids, with potential antineoplastic activity. Upon inhalation of the sustained-release lipid inhalation targeting (SLIT) cisplatin into the lungs, this agent forms highly reactive, positively charged, Pt complexes, which covalently bind to nucleophilic groups in DNA, preferably at the N7 position of guanine bases. Pt complex binding introduces intrastrand and interstrand DNA cross-links, and DNA-Pt-protein cross-links. These cross-links result in apoptosis and cell growth inhibition of lung cancer cells. Encasement in liposomes prolongs cisplatin's efficacy when compared to intravenously administered cisplatin; inhalation of cisplatin improves its concentration at tumor sites in the lungs while minimizing its systemic toxicity.

• Sustained-release mitomycin c hydrogel formulation ugn-101 - A sustained-release (SR) hydrogel polymer-based formulation containing the antineoplastic antibiotic mitomycin C (MMC), with potential antineoplastic activity. Upon local administration of the SR MMC hydrogel formulation to the upper urinary tract via a ureteral catheter, the gel solidifies and deposits MMC locally to prevent the excretion of this chemotherapeutic agent via urinary flow. In turn, MMC alkylates DNA, and produces interstrand DNA cross-links, thereby inhibiting DNA synthesis. Due to its reverse thermal-gelation properties, this gel is able to stay in a liquid state at cold temperatures and solidifies at body temperature. This allows for increased accumulation of MMC locally in the upper urinary tract which leads to increased efficacy compared to standard intravesical delivery of MMC for upper tract urothelial carcinoma (UTUC).

• Sustained-release mitomycin c hydrogel formulation ugn-102 - A sustained-release (SR) reverse thermal (RT) hydrogel formulation containing the antineoplastic antibiotic mitomycin C (MMC), with potential antineoplastic activity. Upon intravesical instillation of the SR MMC hydrogel formulation UGN-102, the liquid converts into gel form and conforms to the bladder wall, allowing MMC to be deposited locally in the bladder to prevent the excretion of this chemotherapeutic agent via urinary flow. In turn, MMC alkylates DNA, and produces interstrand DNA cross-links, thereby inhibiting DNA synthesis resulting in inhibition of tumor cell proliferation. Due to its reverse thermal-gelation properties, this gel is able to stay in a liquid state at cold temperatures, at 4 degrees Celsius, and transition to a water-soluble gel at body temperature. This allows for increased accumulation of MMC locally in the upper urinary tract which leads to increased efficacy compared to standard intravesical delivery of MMC for bladder cancer. Compared to UGN-101, in UGN-102 the strength of MMC is lower.

• Svn53-67/m57-klh peptide vaccine - A peptide vaccine containing a 15-mer peptide (DLAQMFFCFKELEGW), with C to M alteration at amino acid position 57, derived from the anti-apoptosis protein survivin, and conjugated with keyhole limpet hemocyanin (KLH), with potential immunopotentiating and antineoplastic activities. Upon subcutaneous administration of SVN53-67/M57-KLH peptide vaccine, this peptide is able to bind both HMC class I and II molecules and may activate the immune system to mount a cytotoxic T-lymphocyte (CTL) as well as a T-helper cell response against survivin-expressing cancer cells. This may result in decreased tumor cell proliferation and ultimately tumor cell death. Survivin, a member of the inhibitor of apoptosis (IAP) family, expressed during embryonic development while absent in most normal adult cells, is upregulated in a variety of human cancers; its expression in tumors is associated with a more aggressive phenotype, decreased survival, and increased resistance to chemotherapy. KLH may enhance immune recognition and may promote an enhanced response. As SVN53-67 is weakly immunogenic in humans, the M57 alteration may lead to greater affinity towards HLA-A*0201 and thus an enhanced antitumor immune response.

• Syk inhibitor hmpl-523 - An orally available inhibitor of spleen tyrosine kinase (Syk), with potential immunomodulating and antineoplastic activities. Upon oral administration of Syk inhibitor HMPL-523, this agent binds to and inhibits the activity of Syk. This inhibits B-cell receptor (BCR) signaling, which leads to the inhibition of B-cell activation, and prevents tumor cell activation, migration, adhesion and proliferation. Syk, a non-receptor cytoplasmic, BCR-associated tyrosine kinase, is expressed in hematopoietic tissues and is often overexpressed in hematopoietic malignancies; it plays a key role in B-cell receptor signaling.

• Synchrotope ta2m plasmid dna vaccine - A recombinant plasmid DNA vaccine encoding epitopes of tyrosinase with potential antineoplastic activity. Synchrotope TA2M vaccine contains a plasmid encoding 2 epitopes, amino acid sequences 207-216 and 1-17 of tyrosinase, a protein frequently expressed by melanoma cells. Vaccination with the TA2M plasmid DNA vaccine may induce the production of anti-tyrosinase antibodies as well as elicit a cytotoxic T-lymphocyte (CTL) response against tyrosinase-expressing tumor cells, resulting in decreased tumor growth.

• Synchrovax sem plasmid dna vaccine - A bivalent DNA vaccine encoding epitopes for both Melan-A (MART-1) and tyrosinase with potential antineoplastic activity. Synchrovax SEM plasmid DNA vaccine contains a plasmid pSEM that encodes 4 epitopes: Melan-A (26-35), Melan-A (31-96), tyrosinase (1-9), and tyrosinase (369-377). Both Melan-A and tyrosinase are tumor antigens associated with melanoma. Vaccination with this plasmid DNA vaccine may induce both humoral and cytotoxic lymphocyte (CTL) responses against cells expressing either or both of these antigens, resulting in decreased tumor growth.

• Synthetic alkaloid pm00104 - A synthetic alkaloid compound, related to natural alkaloid compounds, found in molluscs (jorumycin) and sponges (renieramycins), with potential antineoplastic activity. PM00104 reversibly binds to DNA, thereby inducing cytotoxicity due to its interference with DNA replication, transcription, and translation processes. DNA binding by this agent does not trigger DNA damage checkpoint responses, hence PM00104 demonstrates a manageable and reversible cytotoxicity as part of its antitumor activity.

• Synthetic brain tumor peptides-pulsed autologous dendritic cell vaccine - A cell-based cancer vaccine composed of autologous dendritic cells (DCs) pulsed with synthetic brain tumor peptides with potential immunostimulatory and antineoplastic activities. Upon administration, synthetic brain tumor peptides-pulsed autologous dendritic cell vaccine may stimulate anti-tumoral cytotoxic T lymphocyte (CTL)l and antibody responses against glioma tumor cells, resulting in glioma tumor cell lysis.

• Synthetic breast cancer peptides-tetanus toxoid-montanide isa-51 vaccine - A cancer vaccine comprised of multiple synthetic breast cancer peptides and the adjuvant tetanus toxoid helper peptide emulsified in the adjuvant Montanide ISA-51 with immunopotentiation activity. Vaccination with this cancer vaccine may elicit a specific cytotoxic T-lymphocyte response against breast cancer cells. Synthetic breast cancer peptides may stimulate the immune response against cells that produce breast cancer markers such as erbB2 (HER2/neu) while tetanus toxoid helper peptide binds to class II MHC molecules as a nonspecific vaccine helper epitope, resulting in a long-term immunopotentiation by increasing the helper T-cell response. Montanide ISA-51, also known as incomplete Freund's adjuvant or IFA, is a stabilized water-in-oil emulsion adjuvant containing mineral oil with mannide oleate added as a surfactant that non-specifically stimulates cell-mediated immune responses to antigens.

• Synthetic breast cancer peptides-tetanus toxoid-poly iclc vaccine - A cancer vaccine comprised of nine class I major histocompatibility complex (MHC)-restricted breast cancer associated peptides, the tetanus toxoid helper peptide and the Toll-like receptor 3 (TLR3) agonist poly ICLC, with potential immunostimulatory and antineoplastic activities. The nine peptides derived from six cancer associated proteins are epidermal growth factor receptor 2 (HER2/neu), carcinoembryonic antigen (CEA) and four cancer/testis antigens (CTAs: MAGE-A1, -A3, -A10, and NY-ESO-1). Vaccination with this vaccine may elicit a specific cytotoxic T-lymphocyte (CTL) response against cells overexpressing these tumor associated antigens (TAAs). As a nonspecific T-helper epitope, tetanus toxoid helper peptide binds to class II MHC and results in long-term immunopotentiation by increasing the helper T-cell response. Poly ICLC, the double-stranded RNA molecules of polyinosinic-polycytidylic acid stabilized with poly L-lysine in carboxymethylcellulose, binds to TLR3 and induces the release of cytokines which may help boost the immune response against the TAAs.

• Synthetic glioblastoma mutated tumor-specific peptides vaccine therapy apvac2 - A personalized peptide-based cancer vaccine comprised of one or two de novo synthesized patient-specific tumor-mutated peptides associated with glioblastoma (GB), with potential immunomodulating and antineoplastic activities. Vaccination with synthetic GB mutated tumor-specific peptides vaccine therapy APVAC2 stimulates the host immune system to mount a cytotoxic T-lymphocyte (CTL) response against tumor cells expressing the selected mutated tumor-associated peptides, which results in decreased GB growth. These peptides are specifically selected and synthesized based on the expression of the patient's own mutated tumor-associated antigens, which were detected during individual tumor genome sequencing.

• Synthetic glioblastoma tumor-associated peptides vaccine therapy apvac1 - A personalized peptide-based cancer vaccine comprised of five to ten peptides associated with glioblastoma (GB), with potential immunomodulating and antineoplastic activities. Vaccination with synthetic GB tumor-associated peptides vaccine therapy APVAC1 stimulates the host immune system to mount a cytotoxic T-lymphocyte (CTL) response against tumor cells expressing the tumor associated peptides, and results in decreased GB growth. The peptides are derived from a glioma actively personalized vaccine consortium (GAPVAC) warehouse and are specifically selected based on the patient's expression of tumor-associated antigens.

• Synthetic htert dna vaccine ino-1400 - A DNA vaccine consisting of a plasmid encoding the full-length sequence of the tumor-associated antigen (TAA) human telomerase reverse transcriptase (hTERT), which is the catalytic subunit of human telomerase and synthesizes telomeric DNA at the chromosome ends, containing two immunogenic mutations, with potential immunostimulating and antineoplastic activities. Upon intradermal vaccination of the hTERT encoding DNA vaccine INO-1400 in combination with electroporation, hTERT protein is expressed and activates the immune system to mount a cytotoxic T-cell (CTL) response against telomerase-expressing tumor cells, which may result in tumor cell death. Telomerase prolongs the functional lifespan of cells via the restoration and maintenance of telomere length. Abnormally activated in tumorigenesis, telomerase is expressed in the majority of human cancer cells, but its expression is low or non-existent in normal cells.

• Synthetic htert dna vaccine ino-1401 - A DNA vaccine consisting of a plasmid encoding a synthetic, full-length sequence of the tumor-associated antigen (TAA) telomerase reverse transcriptase (TERT), which was derived from the consensus sequence from humans and primates and contains two immunogenic mutations (SynCon TERT), with potential immunostimulating and antineoplastic activities. Upon intramuscular administration of INO-1401 in combination with electroporation, TERT protein is expressed and activates the immune system to mount a cytotoxic T-cell (CTL) response against telomerase-expressing tumor cells, which may result in tumor cell death. TERT is the catalytic subunit of telomerase and synthesizes telomeric DNA at the chromosome ends. Telomerase prolongs the functional lifespan of cells via the restoration and maintenance of telomere length. Abnormally activated in tumorigenesis, TERT is expressed by many types of human cancer cells, but its expression is low or non-existent in normal cells.

• Synthetic human papillomavirus 16 e6 peptide - A synthetic peptide sequence of human papillomavirus (HPV) type 16 oncoprotein E6. The E6 oncoprotein is implicated in the tumorigenesis of cervical carcinoma. Vaccination with HPV 16 E6 peptide may stimulate the host immune system to mount a cytotoxic T lymphocyte (CTL) response against cells expressing the E6 oncoprotein, resulting in tumor cell lysis.

• Synthetic hypericin - A topical ointment formulation containing a synthetic form of hypericin, an anthraquinone derivative that is naturally found in the yellow flower of Hypericum perforatum (St. John's wort), with potential antineoplastic and photosensitizing activities. Upon topical administration of the ointment to the tumor site, hypericin becomes activated through the application of visible fluorescent light. During photoactivation, hypericin generates singlet oxygen, which induces DNA damage, necrosis and apoptosis, thereby inhibiting tumor cell growth. The use of visible light for activation avoids the risk of developing secondary malignancies, which are frequently associated with other photodynamic therapies that are dependent on ultraviolet A exposure.

• Synthetic long e6 peptide-toll-like receptor ligand conjugate vaccine isa201 - A therapeutic peptide vaccine consisting of two highly immunogenic synthetic long peptides (SLPs), which are 25-35 amino acids in size, derived from the human papillomavirus (HPV) type 16 oncoprotein E6, and conjugated to a proprietary toll-like receptor 2 (TLR2) ligand (TLR2-L) immunoadjuvant, with potential immunostimulating and antitumor activities. Upon administration, the TLR2-L moiety of the synthetic long E6 peptides TLR ligand conjugate vaccine targets and binds to TLRs expressed on antigen-presenting cells (APCs), particularly dendritic cells (DCs). This increases the direct targeting of, binding to, uptake by, and processing of the SLPs into small pieces by the DCs. The processed viral epitopes are presented by DCs, which activate and stimulate the host immune system to mount specific cytotoxic T-lymphocyte (CTL) and helper T (Th) cell responses against HPV E6-expressing tumor cells. This results in the destruction of tumor cells and leads to decreased growth of HPV E6-expressing tumor cells. The E6 oncoprotein is implicated in tumorigenesis in a variety of cancers. The TLR2-L improves antigen processing and presentation by, and activation of APCs, thereby improving the immunostimulatory effect of the vaccine. The two peptides cover the most immunodominant regions of the HPV16 E6 oncogenic protein and contain both Th and CTL epitopes.

• Synthetic long e6/e7 peptides vaccine hpv-01 - A therapeutic peptide vaccine consisting of thirteen synthetic long peptides (SLPs), which are 25-35 amino acids in size, derived from the human papillomavirus (HPV) type 16 oncoproteins E6 and E7, with potential immunostimulating and antitumor activities. Upon administration, synthetic long E6/E7 peptides vaccine HPV-01 is taken up and degraded into small pieces by dendritic cells. The processed viral epitopes are presented by dendritic cells, which may stimulate the host immune system to mount both cytotoxic T-cell lymphocyte (CTL) and helper T cell responses against HPV E6/E7-expressing tumor cells. This results in the destruction of tumor cells and leads to decreased tumor growth. The E6 and E7 oncoproteins are implicated in the tumorigenesis in a variety of cancers. The SLPs allow for optimal presentation by antigen-presenting cells.

• Synthetic long hpv16 e6/e7 peptides vaccine isa101b - A therapeutic peptide vaccine consisting of nine overlapping synthetic long peptides (SLPs), 25 to 32 amino acids in size, derived from the human papillomavirus (HPV) type 16 (HPV16) oncoprotein E6 and three SLPs, each 35 amino acids in size, derived from HPV16 E7, with potential immunostimulating and antineoplastic activities. Upon subcutaneous administration, the synthetic long HPV16 E6/E7 peptides vaccine ISA101b is taken up and the long peptides are proteolytically degraded to form shorter peptide epitopes by dendritic cells (DCs). The processed viral epitopes are presented by DCs, which stimulate the host immune system to mount helper T-cell and cytotoxic T-lymphocyte (CTL) responses against HPV16 E6/E7-expressing tumor cells. This results in the destruction of tumor cells and leads to decreased tumor growth. The HPV16 E6 and E7 oncoproteins are implicated in the tumorigenesis of a variety of cancers. The SLPs allow optimal presentation by antigen-presenting cells (APCs). Compared to ISA101, the E6 SLPs in ISA101b are identical, overlap by ten to eighteen residues and cover the complete sequence of HPV16 E6. However, ISA101 has four overlapping SLPs E7 peptides while ISA101b has three E7 SLPs, which leaves seven amino acids of the E7 SLPs uncovered in ISA101b but this modification is not likely to alter the immunogenicity of ISA101b.

• Synthetic melanoma-associated antigens vaccine - A cancer vaccine containing synthetic epitope peptides derived from melanoma tumor-associated antigens (TAAs), including melanoma-melanocyte antigen gp100(280-288), melanoma-associated antigen tyrosinase(1-9), and melanoma-associated antigen melan-A(27-35). Upon administration, synthetic melanoma-associated antigens vaccine may stimulate a cytotoxic T-lymphocyte immune response against melanoma cells that express TAAs which share epitopes with the vaccine epitope peptides, resulting in tumor cell lysis.

• Synthetic peptides e-pra and e-psm vaccine - A cancer vaccine consisting of E-PRA and E-PSM, two synthetic peptide analogs of PRAME (PReferential Antigen MElanoma) and PSMA (Prostate Specific Membrane Antigen), with potential immunostimulating activity. Upon direct administration into lymph nodes, synthetic peptides E-PRA and E-PSM vaccine may stimulate a cytotoxic T-lymphocyte (CTL) response against PRAME- and PSMA-expressing tumor cells. PRAME and PSMA are tumor-associated antigens upregulated and expressed on the cell surfaces of certain tumor cell types.

• Synthetic plumbagin pcur-101 - A synthetic form of the plant-derived medicinal agent, plumbagin, with potential antineoplastic activity. Plumbagin may act by inhibiting the expression of protein kinase C epsilon (PKCe), signal transducers and activators of transcription 3 phosphorylation (Stat3), protein kinase B (AKT), and certain epithelial-to-mesenchymal transition (EMT) markers, including vimentin and slug. This results in possible inhibition of proliferation in susceptible tumor cells. PKCe, Stat3, AKT, and the EMT markers vimentin and slug have been linked to the induction and progression of prostate cancer.

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