Antineoplastic agents e

• E1a lipid complex - E1A gene combined with lipids that serve as a means to deliver the E1A gene into the cancer cells. The combination of lipids and the E1A gene is called the E1A Lipid Complex.

• E2f1 pathway activator arq 171 - A second-generation E2F1 pathway activator with potential antineoplastic activity. ARQ 171 induces the expression of E2F transcription factor 1, thereby activating the E2F1-mediated checkpoint process. E2F1, down-regulated in cancer cells, regulates expression of genes involved in the cell cycle progression from G1 into S phase. The G1/S checkpoint process selectively induces cell cycle arrest in cancer cells with irreparable DNA damages and triggers subsequent apoptosis, while allowing cell division to proceed in cells without or with minor reparable DNA damage. As a result, this agent exerts anti-tumor activity through checkpoint activation independent of p53 mediated tumor suppression.

• Ebna-1 inhibitor vk-2019 - An orally available, small molecule inhibitor of Epstein-Barr nuclear antigen 1 (EBNA-1) with potential antineoplastic activity. Upon administration, EBNA-1 inhibitor VK-2019 binds to EBNA-1 and inhibits EBNA-1 DNA binding activity. This disrupts the replication, maintenance and segregation of the Epstein-Barr virus (EBV) genome, which may lead to tumor cell death in EBV-associated malignancies. EBNA1, a sequence-specific DNA binding protein, plays an important role in EBV episomal genome maintenance and gene transactivation.

• Echinomycin - A polypeptide quinoxaline antineoplastic antibiotic isolated from the bacterium Streptomyces echinatus. Echinomycin intercalates into DNA at two locations simultaneously in a sequence-specific fashion, thereby inhibiting DNA replication and RNA synthesis.

• Ecromeximab - A low-fucose, human-mouse chimeric IgG1 monoclonal antibody with potential antineoplastic activity targeting at the ganglioside GD3, a surface antigen expressed on many malignant melanoma cells. Monoclonal antibody KW-2871 binds to GD3-positive cells, thereby initiating antibody-dependent cytotoxicity against GD3-positive cells. This agent is prepared by fusing murine immunoglobulin (Ig) light and heavy variable regions derived from the murine IgG3 antibody KM-641 to a human constant (Fc) region. The low fucose content of the oligosaccharide side chains of this antibody may enhance binding of the antibody Fc region to lymphocyte Fc receptors.

• Edatrexate - A polyglutamatable folate antagonist analogue of methotrexate with antineoplastic activity. Edatrexate inhibits dihydrofolate reductase, thereby increasing cellular levels of polyglutamates, inhibiting thymidylate synthase and glycinamide ribonucleotide formyl transferase, impairing synthesis of purine nucleotides and amino acids, and resulting in tumor cell death. Edatrexate may overcome tumor resistance to methotrexate, which loses its activity after it is polyglutamated.

• Edelfosine - A synthetic analog of lysophosphatidylcholine, an ether lipid, possessing anti-leishmanial and antineoplastic activity. The mechanism of action for edelfosine has not been fully elucidated. Targeting cellular membranes, edelfosine modulates membrane permeability, membrane lipid composition, and phospholipid metabolism. Edelfosine also inhibits the phosphatidylinositol 3 kinase (PI3K)-AKT/PKB survival pathway, possibly activating the pro-apoptotic stress-activated protein kinase (SAPK/JNK) pathways, thereby inducing apoptosis. In addition, this agent inhibits protein kinase C, intracellular activation of the Fas/CD95 receptor, and intracellular acidification. Anti-leishmanial activity may be due to inhibition of a glycosomal alkyl-specific-acylCoA acyltransferase. (NCI)

• Edicotinib - A small molecule and orally available inhibitor of colony-stimulating factor-1 receptor (CSF1R; FMS) with potential antineoplastic activity. Edicotinib blocks the receptor-ligand interaction between FMS and its ligand CSF1, thereby preventing autophosphorylation of FMS. As a result, unphosphorylated FMS can not activate FMS-mediated signaling pathways, thus potentially inhibiting cell proliferation in FMS-overexpressed tumor cells. FMS, a tyrosine kinase receptor, is overexpressed in certain tumor cell types and plays an essential role in macrophage differentiation, recruitment, and activation as well as the regulation of cell proliferation.

• Edodekin alfa - A recombinant form of the endogenous heterodimeric cytokine interleukin-12 with potential antineoplastic activity. Edodekin alfa binds to and activates its cell-surface receptor, stimulating the production of interferon-gamma (IFN) which, in turn, induces IFN-gamma-inducible protein-10 (IP-10) and so inhibits tumor angiogenesis.

• Edotecarin - A synthetic indolocarbazole with antineoplastic activity. Edotecarin inhibits the enzyme topoisomerase I through stabilization of the DNA-enzyme complex and enhanced single-strand DNA cleavage, resulting in inhibition of DNA replication and decreased tumor cell proliferation.

• Edrecolomab - A murine monoclonal IgG2a antibody to tumor-associated epithelial cell adhesion molecule (EpCAM, or 17-1A) antigen. Edrecolomab attaches to EpCAM, a human cell surface glycoprotein that is found on normal epithelial cells and some tumor cells, such as those of colon and breast carcinomas. Upon binding, this agent recruits the body's immune effector cells, which may exhibit antitumor cytotoxicity.

• Eed inhibitor mak683 - An inhibitor of embryonic ectoderm development protein (EED) and allosteric inhibitor of polycomb repressive complex 2 (PRC2), with potential antineoplastic activity. Upon administration, MAK683 selectively binds to the domain of EED that interacts with trimethylated lysine 27 on histone 3 (H3K27me3), which leads to a conformational change in the EED H3K27me3-binding pocket and prevents the interaction of EED with the histone methyltransferase enhancer zeste homolog 2 (EZH2). Disruption of the EED-EZH2 protein-protein interaction (PPI) results in a loss of H3K27me3-stimulated PRC2 activity and prevents H3K27 trimethylation. This decrease in histone methylation alters gene expression patterns associated with cancer pathways and results in decreased tumor cell proliferation in EZH2-mutated and PRC2-dependent cancer cells. PRC2, a histone H3 lysine 27 methyltransferase and multi-protein complex comprised of EZH2, EED and suppressor of zeste 12 (SUZ12), plays a key role in gene regulation, especially during embryonic development. EZH2, the catalytic subunit of PRC2, is overexpressed or mutated in a variety of cancer cells. EED is essential for the histone methyltransferase activity of PRC2 because EED directly binds to H3K27me3.

• Efatutazone - An orally bioavailable thiazolidinedione and an agonist of peroxisome proliferator-activated receptor gamma (PPAR-gamma) with potential antineoplastic activity. Efatutazone binds to and activates PPAR-gamma thus inducing cell differentiation and apoptosis, leading to a reduction in cellular proliferation. PPAR-gamma is a nuclear hormone receptor and a ligand-activated transcription factor that controls the expression of genes involved in macromolecule metabolism and cell differentiation, specifically adipocyte differentiation.

• Efatutazone dihydrochloride - The dihydrochloride salt of efatutazone, an orally bioavailable agonist of peroxisome proliferator-activated receptor gamma (PPAR-gamma) with potential antineoplastic activity. Efatutazone binds to and activates PPAR-gamma, a nuclear hormone receptor and a ligand-activated transcription factor controling gene expression involved in macromolecule metabolism and cell differentiation, specifically adipocyte differentiation. Mediated through activation of PPAR-gamma, this agent is capable of inducing cell differentiation and apoptosis, thereby leading to a reduction in cellular proliferation.

• Efizonerimod - An agonistic monoclonal antibody against receptor OX40 (CD134), with potential immunostimulatory activity. Upon administration, efizonerimod selectively binds to and activates the OX40 receptor, by mimicking the action of endogenous OX40 ligand (OX40L). OX40 receptor activation induces proliferation of memory and effector T lymphocytes. In the presence of tumor-associated antigens (TAAs), this may promote an immune response against the TAA-expressing tumor cells. OX40, a cell surface glycoprotein and member of the tumor necrosis factor (TNF) receptor family, is expressed on T-lymphocytes and provides a co-stimulatory signal for the proliferation and survival of activated T cells.

• Eflornithine - A difluoromethylated ornithine compound with antineoplastic activity. Eflornithine irreversibly inhibits ornithine decarboxylase, an enzyme required for polyamine biosynthesis, thereby inhibiting the formation and proliferation of tumor cells. Polyamines are involved in nucleosome oligomerization and DNA conformation, creating a chromatin environment that stimulates neoplastic transformation of cells. This agent has been shown to induce apoptosis in leiomyoma cells.

• Eflornithine hydrochloride - The hydrochloride form of eflornithine, a difluoromethylated ornithine compound with antineoplastic activity. Eflornithine irreversibly inhibits ornithine decarboxylase, an enzyme required for polyamine biosynthesis, thereby inhibiting the formation and proliferation of tumor cells. Polyamines are involved in nucleosome oligomerization and DNA conformation, creating a chromatin environment that stimulates neoplastic transformation of cells.

• Eftilagimod alpha - A T-cell immunostimulatory factor, derived from the soluble form of the lymphocyte-activation gene 3 (LAG-3) protein, with potential antineoplastic activity. Upon administration, alone or in combination with tumor antigens, eftilagimod alpha binds with high affinity to MHC class II molecules expressed by dendritic cells (DC), potentially resulting in DC maturation, DC migration to lymph nodes, enhanced DC cross-presentation of antigens to T cells, and antitumor cytotoxic T cell responses.

• Eftozanermin alfa - A fusion protein composed of a tumor necrosis factor (TNF)-related apoptosis-inducing ligand (TRAIL) receptor agonist consisting of six receptor binding domains (RBDs) of TRAIL fused to the Fc-domain of a human immunoglobulin G1 (IgG1) antibody, with potential pro-apoptotic and antineoplastic activities. Upon administration of eftozanermin alfa, this fusion protein binds to TRAIL-receptors, pro-apoptotic death receptors (DRs) TRAIL-R1 (death receptor 4; DR4) and TRAIL-R2 (death receptor 5; DR5), expressed on tumor cells, thereby inducing tumor cell apoptosis. ABBV-621 is designed to maximize receptor clustering for optimal efficacy. TRAIL, a member of the TNF superfamily of cytokines, plays a key role in the induction of apoptosis through TRAIL-mediated death receptor pathways.

• Eg5 kinesin-related motor protein inhibitor 4sc-205 - A small-molecule inhibitor of the human kinesin-related motor protein Eg5 with potential antineoplastic activity. Eg5 kinesin-related motor protein inhibitor 4SC-205 selectively inhibits the activity of Eg5, which may result in mitotic disruption, apoptosis and cell death. The ATP-dependent Eg5 kinesin-related motor protein (also known as KIF11 or kinesin spindle protein-5) is a plus-end directed kinesin motor protein essential for the regulation of spindle dynamics, including assembly and maintenance, during mitosis.

• Eg5 kinesin-related motor protein inhibitor arq 621 - A small-molecule inhibitor of the kinesin-related motor protein Eg5 with potential antineoplastic activity. Eg5 kinesin-related motor protein inhibitor ARQ 621 selectively inhibits the activity of Eg5, which may result in mitotic disruption, apoptosis and cell death. The ATP-dependent Eg5 kinesin-related motor protein (also known as KIF11 or kinesin spindle protein-5) is a plus-end directed kinesin motor protein involved in the regulation of spindle dynamics, including assembly and maintenance, during mitosis.

• Egb761 - A standardized ginkgo biloba extract with antioxidant and neuroprotective activities. EGb761 has been shown to inhibit the proliferation of certain tumor cells in vitro.

• Egf vaccine egf-pti - A cancer vaccine containing epidermal growth factor (EGF), with immunomodulating and antineoplastic activities. Upon administration of the EGF vaccine EGF-PTI, EGF induces an immune response against EGFR, which results in the formation of anti-EGF-specific neutralizing antibodies. This causes binding of the anti-EGF antibodies to endogenous EGF, reduces levels of circulating EGF and prevents the binding of EGF to its receptor EGFR. This prevents EGF/EGFR pathway activation and may result in an inhibition of proliferation in EGFR-overexpressing tumor cells. EGF/EGFR-mediated signaling is overactivated in certain cancer types and drives tumor cell proliferation and progression.

• Egfr antagonist hemay022 - An orally available, irreversible inhibitor of epidermal growth factor receptor (EGFR), with potential antineoplastic activity. Upon oral administration, Hemay022 covalently binds to and inhibits the activity of EGFR, thereby preventing EGFR-mediated signaling. This may both induce cell death and inhibit tumor growth in EGFR-overexpressing tumor cells. EGFR, a receptor tyrosine kinase mutated in many tumor cell types, plays a key role in tumor cell proliferation and tumor vascularization.

• Egfr antisense dna - A synthetic sequence of DNA constructed in the antisense orientation to a sequence of DNA in epidermal growth factor receptor (EGFR), a member of the erbB gene family. EGFR antisense DNA suppresses the expression of EGFR by tumor cells, thereby inhibiting tumor cell proliferation and decreasing tumor growth. This agent also appears to reduce the invasiveness of certain breast cancer cells. Members of the erbB gene family are overexpressed in many cancers and play roles in carcinogenesis and the regulation of cell proliferation.

• Egfr antisense dna bb-401 - A recombinant, plasmid DNA expression vector encoding a 39 nucleotide (nt) short hairpin RNA (shRNA) specific for the epidermal growth factor receptor (EGFR), with potential antineoplastic activity. Upon intratumoral administration, the EGFR antisense DNA BB-401 is taken up by tumor cells and shRNA is transcribed. The shRNA is converted into small interfering RNA (siRNA) via the RNA interference (RNAi) pathway. The siRNA targets and binds to EGFR RNA expressed by tumor cells. This blocks EGFR mRNA translation and prevents EGFR protein expression.

• Egfr car-cd3zeta-4-1bb-expressing autologous t-lymphocytes - Autologous human T-lymphocytes transduced with a retroviral vector encoding an anti-epidermal growth factor receptor (EGFR) chimeric T cell receptor (chimeric antigen receptor or CAR) gene coupled to the signaling domains from both CD3 zeta and CD137 (4-1BB), with potential immunostimulatory and antineoplastic activities. Upon administration, the chimeric EGFR antigen receptor-modified autologous T lymphocytes bind to the EGFR antigen on tumor cell surfaces; subsequently, EGFR-expressing tumor cells may be lysed. Following binding to EGFR, the 4-1BB co-stimulatory molecule signaling domain enhances both activation and signaling. Inclusion of the 4-1BB signaling domain may also increase the antitumor activity when compared to the inclusion of the CD3-zeta chain alone. EGFR, a receptor tyrosine kinase (RTK) overexpressed by a variety of cancer cell types, plays key roles in tumor cell proliferation and tumor angiogenesis.

• Egfr inhibitor bibx 1382 - A pyrimido-pyrimidine with antitumor activity. BIBX 1382 inhibits the intracellular tyrosine kinase domain of the Epidermal Growth Factor Receptor (EGFR) thus specifically reversing the aberrant enzymatic activity from overexpressed and constitutively activated EGFR, and subsequently inhibiting cell proliferation and inducing cell differentiation.

• Egfr inhibitor dbpr112 - An orally available inhibitor of the epidermal growth factor receptor (EGFR), with potential antineoplastic activity. Upon oral administration, DBPR112 binds to and inhibits the activity of EGFR as well certain mutant forms of EGFR, including EGFR L858R and EGFR T790M. This prevents EGFR-mediated signaling, and may lead to both induction of cell death and inhibition of tumor growth in EGFR-overexpressing cells. EGFR, a receptor tyrosine kinase mutated in many tumor cell types, plays a key role in tumor cell proliferation and tumor vascularization.

• Egfr inhibitor pd-168393 - A quinazolone compound with anti-tumor activity. PD-168393 is a cell-permeable, irreversible, and selective inhibitor of ligand-dependent epidermal growth factor (EGF) receptor (EGFR). This agent binds to the catalytic domain of EGFR with a 1:1 stoichiometry and inactivates the EGFR tyrosine kinase activity through alkylation of a cystine residue (Cys-773) within the ATP-binding pocket, thereby inhibiting proliferation of EGFR-expressing tumor cells.

• Egfr inhibitor ty-9591 - An orally available inhibitor of epidermal growth factor receptor (EGFR), including activating mutations, with potential antineoplastic activity. Upon administration, the EGFR inhibitor TY-9591 binds to and inhibits EGFR activating mutations, including the resistance mutation T790M, which prevents EGFR mutant-mediated signaling and leads to cell death in EGFR mutant-expressing tumor cells. EGFR, a receptor tyrosine kinase mutated in many tumor cell types, plays a key role in tumor cell proliferation and tumor vascularization.

• Egfr mutant-selective inhibitor tqb3804 - A fourth-generation, orally bioavailable, mutant-selective, epidermal growth factor receptor (EGFR) inhibitor, with potential antineoplastic activity. Upon oral administration, EGFR mutant-selective inhibitor TQB3804 binds to and inhibits the activity of mutant forms of EGFR, including the C797S EGFR mutant, thereby preventing EGFR-mediated signaling. This may both induce cell death and inhibit tumor growth in EGFR-overexpressing tumor cells. EGFR, a receptor tyrosine kinase mutated in many tumor cell types, plays a key role in tumor cell proliferation and tumor vascularization. TQB3804 inhibits mutated forms of EGFR including C797S, which prevents covalent bond formation with third-generation EGFR inhibitor osimertinib leading to drug resistance. TQB3804 may have enhanced anti-tumor effects in tumors with C797S-mediated resistance when compared to other EGFR tyrosine kinase inhibitors.

• Egfr mutant-specific inhibitor ck-101 - An orally available third-generation and selective inhibitor of certain epidermal growth factor receptor (EGFR) activating mutations, including the resistance mutation T790M, and the L858R and del 19 mutations, with potential antineoplastic activity. Upon administration, the EGFR mutant-specific inhibitor CK-101 specifically and covalently binds to and inhibits selective EGFR mutations, with particularly high selectivity against the T790M mutation, which prevents EGFR mutant-mediated signaling and leads to cell death in EGFR mutant-expressing tumor cells. Compared to some other EGFR inhibitors, CK-101 may have therapeutic benefits in tumors with T790M-mediated drug resistance. This agent shows minimal activity against wild-type EGFR (WT EGFR), and does not cause dose-limiting toxicities that occur during the use of non-selective EGFR inhibitors, which also inhibit WT EGFR. EGFR, a receptor tyrosine kinase mutated in many tumor cell types, plays a key role in tumor cell proliferation and tumor vascularization.

• Egfr mutant-specific inhibitor d-0316 - An orally available inhibitor of the epidermal growth factor receptor (EGFR) mutant form T790M, with potential antineoplastic activity. Upon administration, the EGFR mutant-specific inhibitor D-0316 specifically binds to and inhibits EGFR T790M, a secondarily acquired resistance mutation, which prevents EGFR-mediated signaling and leads to cell death in EGFR T790M-expressing tumor cells. Compared to some other EGFR inhibitors, D-0316 may have therapeutic benefits in tumors with T790M-mediated drug resistance. EGFR, a receptor tyrosine kinase that is mutated in many tumor cell types, plays a key role in tumor cell proliferation and tumor vascularization.

• Egfr mutant-specific inhibitor zn-e4 - An orally available selective inhibitor of certain epidermal growth factor receptor (EGFR) activating mutations, including the resistance mutation T790M, with potential antineoplastic activity. Upon administration, the EGFR mutant-specific inhibitor ZN-e4 specifically binds to and inhibits selective EGFR mutations, which prevents EGFR mutant-mediated signaling and leads to cell death in EGFR mutant-expressing tumor cells. Compared to other EGFR inhibitors, ZN-e4 may offer therapeutic benefits in tumors with T790M-mediated drug resistance and may limit toxicities associated with non-selective EGFR inhibitors. EGFR, a receptor tyrosine kinase mutated in many tumor cell types, plays a key role in tumor cell proliferation and tumor vascularization.

• Egfr t790m antagonist bpi-15086 - An orally available inhibitor of the epidermal growth factor receptor (EGFR) mutant form T790M, with potential antineoplastic activity. EGFR T790M antagonist BPI-15086 specifically binds to and inhibits EGFR T790M, a secondarily acquired resistance mutation, which prevents EGFR-mediated signaling and leads to cell death in EGFR T790M-expressing tumor cells. EGFR, a receptor tyrosine kinase that is mutated in many tumor cell types, plays a key role in tumor cell proliferation and tumor vascularization.

• Egfr t790m inhibitor hs-10296 - An orally available inhibitor of the epidermal growth factor receptor (EGFR) mutant form T790M, with potential antineoplastic activity. Upon administration, HS-10296 binds to and inhibits EGFR T790M, a secondarily acquired resistance mutation, inhibits the tyrosine kinase activity of EGFR T790M, prevents EGFR T790M-mediated signaling and leads to cell death in EGFR T790M-expressing tumor cells. EGFR, a receptor tyrosine kinase that is mutated in many tumor cell types, plays a key role in tumor cell proliferation and tumor vascularization.

• Egfr/egfrviii inhibitor wsd0922-fu - A blood-brain-barrier (BBB) penetrable selective inhibitor of epidermal growth factor receptor (EGFR) and various EGFR mutations, including but not limited to the EGFR variant III (EGFRvIII) mutant form, with potential antineoplastic activity. Upon administration of EGFR/EGFRvIII inhibitor WSD0922-FU, this agent is able to penetrate the BBB and specifically targets, binds to and inhibits EGFR and specific EGFR mutations, which prevents EGFR/EGFR mutant-mediated signaling and leads to cell death in EGFR/EGFR mutant-expressing tumor cells. Compared to other EGFR inhibitors that are not able to penetrate the BBB, WSD0922-FU may have therapeutic benefits in brain tumors, such as glioblastoma (GBM) and metastatic CNS tumors. EGFR, a receptor tyrosine kinase (RTK) that is mutated in many tumor cell types, plays a key role in tumor cell proliferation and survival.

• Egfr/flt3/abl inhibitor sklb1028 - An orally available inhibitor of epidermal growth factor receptor (EGFR), FMS-related tyrosine kinase 3 (FLT3, STK1, CD135 or FLK2), and the non-receptor tyrosine kinase ABL (Abl), with potential antineoplastic activity. Upon administration, the EGFR/FLT3/Abl inhibitor SKLB1028 specifically binds to and inhibits EGFR, FLT3 and Abl, which interferes with the activation of EGFR-, FLT3- and Abl-mediated signal transduction pathways and reduces cell proliferation in cancer cells that overexpress EGFR, FLT3 and/or Abl. EGFR, EGFR and Abl are all overexpressed in a variety of cancers and play key roles in tumor cell proliferation.

• Egfr/her1/her2 inhibitor pki166 - A pyrrolo-pyrimidine epidermal growth factor receptor (EGFR) protein kinase inhibitor with anti-tumor activity. PKI-166 reversibly inhibits HER1 and HER2 tyrosine kinases, belong to the epidermal growth factor receptor family, thereby inhibiting tumor growth and metastasis.

• Egfr/her2 inhibitor av-412 - A second-generation, orally bioavailable dual kinase inhibitor with potential antineoplastic activity. EGFR/HER2 inhibitor AV-412 binds to and inhibits the epidermal growth factor receptor (EGFR) and the human epidermal growth factor receptor 2 (HER2), which may result in the inhibition of tumor growth and angiogenesis, and tumor regression in EGFR/HER2-expressing tumors. This agent may be active against EGFR/HER2-expressing tumor cells that are resistant to first-generation kinase inhibitors. EGFR and HER2 are receptor tyrosine kinases that play major roles in tumor cell proliferation and tumor vascularization.

• Egfr/her2 inhibitor dzd9008 - An orally available, irreversible, dual kinase inhibitor of epidermal growth factor receptor (EGFR) and human epidermal growth factor receptor 2 (HER2) that shows similar activity against certain activating mutations, including exon 20 insertions (exon20ins), with potential antineoplastic activity. Upon oral administration, EGFR/HER2 inhibitor DZD9008 binds to and inhibits EGFR and HER2, which may result in the inhibition of tumor growth and angiogenesis, and tumor regression in EGFR/HER2-expressing tumors. EGFR and HER2 are receptor tyrosine kinases that play major roles in tumor cell proliferation and tumor vascularization. In contrast to other agents active against exon20ins mutations, DZD9008 appears to be more selective against mutated EGFR than wild-type (wt) EGFR. This may lessen wtEGFR-related dose-limiting toxicity and may allow for the administration of the desired therapeutic dose of DZD9008.

• Egfr/her2 kinase inhibitor tak-285 - An orally bioavailable, small molecule and dual kinase inhibitor of human epidermal growth factor receptors 1 (EGFR/ErbB1) and 2 (HER2/ErbB2), with potential antineoplastic activity. EGFR/HER2 kinase inhibitor TAK-285 binds to and inhibits EGFR and HER2, which may result in the inhibition of tumor growth and angiogenesis, and tumor regression in EGFR/HER2-expressing tumors. This agent may be active against EGFR/HER2-expressing tumor cells that are resistant to trastuzumab. EGFR and HER2, receptor tyrosine kinases overexpressed in a variety of tumor cell types, play major roles in tumor cell proliferation and tumor vascularization. In addition, TAK-285 appears to pass the blood brain barrier (BBB) and does not appear to be a substrate for efflux pumps.

• Egfr/tgfb fusion monoclonal antibody bca101 - A bifunctional monoclonal antibody targeting both the receptor tyrosine kinase epidermal growth factor receptor (EGFR) and the pro-inflammatory cytokine human transforming growth factor beta (TGF-beta; TGFb), with potential antineoplastic activity. Upon administration of EGFR/TGFb fusion monoclonal antibody BCA101, the anti-EGFR moiety targets, binds to and prevents activation of EGFR-mediated signaling. This leads to an inhibition of EGFR-dependent downstream pathways and EGFR-dependent tumor cell proliferation and metastasis. The anti-TGFb moiety targets and binds to TGFb, thereby preventing the activation of TGFb-mediated signaling pathways. This may inhibit the proliferation of tumor cells in which TGFb is overactivated. EGFR and TGFb, mutated and/or overexpressed on the surfaces of various tumor cell types, play key roles in tumor cell proliferation and progression.

• Egfr/vegfr/ret inhibitor ha121-28 - An orally available inhibitor of the epidermal growth factor receptor (EGFR), the proto-oncogene receptor tyrosine kinase rearranged during transfection (RET) and vascular endothelial growth factor receptor (VEGFR), with potential anti-angiogenic and antineoplastic activities. Upon oral administration of HA121-28, this agent targets, binds to and inhibits the activity of EGFR, RET and VEGFR. This prevents EGFR-, RET- and VEGFR-mediated signaling, and may lead to the induction of apoptosis and inhibition of tumor growth in EGFR-, RET- and VEGFR-overexpressing cells. EGFR, a receptor tyrosine kinase mutated in many tumor cell types, plays a key role in tumor cell proliferation and tumor vascularization. Dysregulation of RET activity plays a key role in the development and progression of a variety of cancers. Expression of VEGFR is upregulated in a variety of tumor cell types; it plays a key role in the migration, proliferation and survival of endothelial cells, microvessel formation, the inhibition of tumor cell proliferation, and tumor cell death.

• Egfrbi-armed autologous t cells - Autologous activated T cells, loaded with a bispecific antibody produced by heteroconjugation of anti-CD3 and anti-epidermal growth factor receptor (EGFR) monoclonal antibodies, with potential antineoplastic activity. Binding of EGFRBi-armed autologous activated T cells to EGFR-positive tumor cells may result in increased T cell-mediated cytotoxicity towards tumor cells expressing EGFR. Arming activated T cells with this bispecific antibody may significantly increase T cell secretion of anti-tumor associated cytokines such as IL2, RANTES, IFN-gamma, and TNF-alpha.

• Egfrviii-specific car-transduced autologous t lymphocytes - Autologous human T-lymphocytes transduced with a retroviral vector encoding an anti-epidermal growth factor receptor variant III (EGFRvIII) mutant chimeric T-cell receptor (chimeric antigen receptor or CAR) gene, with potential immunostimulatory and antineoplastic activities. Upon administration, the EGFRvIII-specific CAR-transduced autologous T-lymphocytes bind to the EGFRvIII antigen on tumor cell surfaces; subsequently, EGFRvIII-expressing tumor cells may be lysed. EGFRvIII, an in-frame deletion of exons 2-7 in the EGFR gene, is overexpressed by a variety of cancer cell types but absent in normal, healthy cells. It plays a key role in tumor cell proliferation, tumor angiogenesis and resistance to both radio- and chemotherapy.

• Eicosapentaenoic acid - An essential, polyunsaturated, 20-carbon omega-3 fatty acid with anti-inflammatory and potential antineoplastic and chemopreventive activities. Eicosapentaenoic acid (EPA) may activate caspase 3, resulting in apoptosis in susceptible tumor cell populations. In addition, this agent may inhibit cyclooxygenase-2 (COX-2), resulting in inhibition of prostaglandin synthesis and prostaglandin-mediated inflammatory processes.

• Eicosapentaenoic acid monoacylglyceride - An eicosapentaenoic acid derivative with potential antineoplastic activities. Upon oral administration, eicosapentaenoic acid monoacylglyceride (MAG-EPA) may inhibit epidermal growth factor receptor (EGFR), vascular endothelial growth factor receptor (VEGFR) and serine/threonine protein kinase AKT (protein kinase B)-mediated signaling pathways and reduce vascular endothelial growth factor (VEGF) and hypoxia-inducible factor 1-alpha (HIF1-alpha) expression levels in tumor cells. This may promote apoptosis and inhibit tumor cell growth in cells expressing EGFR, AKT, and VEGFR. MAG-EPA may also inhibit androgen-stimulated tumor cell growth and repress androgenic induction of prostate-specific antigen (PSA) expression. PSA, a tumor associated antigen (TAA), is expressed by prostate epithelial cells and is overexpressed in prostate cancer. The AKT signaling pathway is often dysregulated in cancer and is associated with tumor cell proliferation, survival and migration. EGFR and VGFR are receptor tyrosine kinases that are mutated or upregulated in many tumor cell types and play a key role in tumor cell proliferation and tumor vascularization.

• Eicosapentaenoic acid-enriched nutritional supplement - A nutritional supplement enriched with eicosapentaenoic acid (EPA), which is an essential, polyunsaturated, 20-carbon omega-3 fatty acid found in fish oil, with potential anti-inflammatory and anti-cachectic activities. Upon oral intake of the EPA-enriched nutritional supplement, EPA is incorporated in cell membrane phospholipids and replaces arachidonic acid. This affects the production of pro-inflammatory mediators, such as tumor necrosis factor-alpha (TNF-a), interleukin-1 (IL-1) and IL-6, through the inhibition of nuclear factor kappa B (NF-kB) activity. This inhibits inflammation and may abrogate the cachexia-mediated decrease of lean body mass (LBM), which may lead to increased body weight. Pro-inflammatory mediators, such as TNF-a, interferon-gamma, and certain interleukins, such as IL-6 and IL-1b, play a key role in cachexia.

• Eif4e antisense oligonucleotide isis 183750 - A second-generation antisense oligonucleotide targeting the eukaryotic translation initiation factor 4E (eIF4E) with potential antitumor activity. Antisense oligonucleotide ISIS EIF4ERx suppresses the expression of eIF4E in fast dividing tumor cells. Blocking the expression of eIF4E results in inhibition of the synthesis of tumor angiogenic factors, thereby leading to the inhibition of cellular proliferation and apoptosis in tumor cells. eIF4E is overexpressed in a variety of cancers, is involved in the mRNA-ribosome binding step of eukaryotic protein synthesis and is the rate-limiting component of the eukaryotic translation apparatus.

• Elacestrant - An orally available, selective estrogen receptor degrader (SERD) and selective estrogen receptor modulator (SERM), with potential antineoplastic and estrogen-like activities. Upon oral administration of higher doses of elacestrant, this agent acts as a SERD, which binds to the estrogen receptor (ER) and induces a conformational change that results in the degradation of the receptor. This may inhibit the growth and survival of ER-expressing cancer cells. At lower doses of this agent, RAD1901 acts as a SERM and has estrogen-like effects in certain tissues, which can both reduce hot flashes and protect against bone loss. In addition, elacestrant is able to cross the blood-brain barrier (BBB).

• Elacytarabine - The lipophilic 5'-elaidic acid ester of the deoxycytidine analog cytosine arabinoside (cytarabine; Ara-C) with potential antineoplastic activity. As a prodrug, elacytarabine is converted intracellularly into cytarabine triphosphate by deoxycytidine kinase and subsequently competes with cytidine for incorporation into DNA, thereby inhibiting DNA synthesis. Compared to cytarabine, elacytarabine shows increased cellular uptake and retention, resulting in increased activation by deoxycytidine kinase to cytarabine triphosphate, decreased deamination and deactivation by deoxycytidine deaminase, and increased inhibition of DNA synthesis. This agent also inhibits RNA synthesis, an effect not seen with cytarabine.

• Elagolix -

• Elesclomol - A small-molecule bis(thio-hydrazide amide) with oxidative stress induction, pro-apoptotic, and potential antineoplastic activities. Elesclomol induces oxidative stress, creating high levels of reactive oxygen species (ROS), such as hydrogen peroxide, in both cancer cells and normal cells. Because tumor cells have elevated levels of ROS compared to normal cells, the increase in oxidative stress beyond baseline levels elevates ROS beyond sustainable levels, exhausting tumor cell antioxidant capacity, which may result in the induction of the mitochondrial apoptosis pathway. Normal cells are spared because the increase in the level of oxidative stress induced by this agent is below the threshold at which apoptosis is induced.

• Elesclomol sodium - The water soluble sodium salt of a small-molecule bis(thio-hydrazide amide) with oxidative stress induction, pro-apoptotic, and potential antineoplastic activities. Elesclomol induces oxidative stress, creating high levels of reactive oxygen species (ROS), such as hydrogen peroxide, in both cancer cells and normal cells. Because tumor cells have elevated levels of ROS compared to normal cells, the increase in oxidative stress beyond baseline levels elevates ROS beyond sustainable levels, exhausting tumor cell antioxidant capacity, which may result in the induction of the mitochondrial apoptosis pathway. Normal cells are spared because the increase in the level of oxidative stress induced by this agent is below the threshold at which apoptosis is induced.

• Elgemtumab - A human monoclonal antibody directed against the human epidermal growth factor receptor HER3 (ErbB3) with potential antineoplastic activity. Elgemtumab binds to and locks HER3 in the inactive conformation and does not interfere with its interaction with neuregulin (NRG). The inactivated form of HER3 blocks the PI3K/Akt signaling pathway, thereby inhibiting cellular proliferation in HER2 or NRG expressing tumor cells. HER3, a member of the epidermal growth factor receptor (EGFR) family of receptor tyrosine kinases, is frequently overexpressed in tumors; it has no active kinase domain but is activated through heterodimerization with other members of the EGFR receptor family, such as HER2.

• Elinafide - A symmetrical dimeric bis-naphthalimide compound and a topoisomerase II inhibitor with antineoplastic activity. Elinafide contains two neutral chromophores joined by a cationic linker and is capable of bis-intercalation at the TpG and CpA steps of the DNA hexanucleotide. Intercalation inhibits topoisomerase II activity and causing DNA stand breakage, thereby leads to inhibition of DNA, RNA, and protein synthesis.

• Elisidepsin - A synthetic cyclic depsipeptide of the kahalalides family with potential antineoplastic activity. PM02734 is a derivative of a natural marine compound extracted from the sacoglossan sea slug, Elysia rufescens. Although the exact mechanism of action has yet to be elucidated, elisidepsin exhibits anti-proliferative activity in a wide variety of cancer types, such as breast, colon, pancreas, lung, and prostate.

• Ellagic acid/annona muricata supplement - A nutritional supplement containing the phytochemical polyphenol, ellagic acid, and an extract of Annona muricata, with potential chemopreventive activity. Although the exact mechanism of action for ellagic acid has yet to be fully elucidated, this agent acts as an anti-oxidant and reduces oxidative stress. This agent also appears to protect the body against certain carcinogens, either through preventing DNA binding or by increasing the rate of their metabolism and deactivation. Certain extracts of Annona muricata, a member of the custard apple plants and belonging to the Annonaceae family, may have antiviral activity, potential targets include human papilloma virus (HPV), and may be cytotoxic against various types of cancer cells.

• Elliptinium - A derivative of the alkaloid ellipticine isolated from species of the plant family Apocynaceae, including Bleekeria vitensis, a plant with anti-cancer properties. As a topoisomerase II inhibitor and intercalating agent, elliptinium stabilizes the cleavable complex of topoisomerase II and induces DNA breakages, thereby inhibiting DNA replication and RNA and protein synthesis.

• Elliptinium acetate - Acetate salt of elliptinium, a derivative of the alkaloid ellipticine isolated from species of the plant family Apocynaceae, including Bleekeria vitensis, a plant with anti-cancer properties. As a topoisomerase II inhibitor and intercalating agent, elliptinium stabilizes the cleavable complex of topoisomerase II and induces DNA breakages, thereby inhibiting DNA replication and RNA and protein synthesis.

• Elmustine - A (2-chloroethy1)nitrosourea derivative related to carmustine, with antineoplastic activity.

• Elotuzumab - A humanized monoclonal antibody directed against the human CS1 (CD2 subset 1, CRACC, SLAMF7) antigen with potential antineoplastic activity. Elotuzumab binds to the CS1 antigen, which may trigger antibody-dependent cellular cytotoxicity (ADCC) in cells expressing CS1. CS1 is a cell surface glycoprotein belonging to the CD2 subset of the immunoglobulin superfamily (IgSF) and is highly expressed by multiple myeloma cells, but minimally expressed by normal cells.

• Elpamotide - A peptide vaccine containing an HLA-A*2402-restricted epitope of vascular endothelial growth factor receptor (VEGFR) 2 with potential immunostimulatory and antineoplastic activities. Upon administration, VEGFR2-169 peptide vaccine may stimulate a cytotoxic T lymphocyte (CTL) response against VEGFR2-expressing tumor cells. VEGFR2, a receptor tyrosine kinase, is overexpressed by a variety of tumor types; overexpression is associated with tumor cell proliferation and tumor angiogenesis. HLA-A*2402 is an MHC class I molecule that presents antigenic peptides to CD8+ T cells; epitope design restricted to epitopes that bind most efficiently to HLA-A*2402 may improve antigenic peptide immunogenicity.

• Elsamitrucin - An heterocyclic antineoplastic antibiotic isolated from the bacterium Actinomycete strain J907-21. Elsamitrucin intercalates into DNA at guanine-cytosine (G-C)-rich sequences and inhibits topoisomerase I and II, resulting in single-strand breaks and inhibition of DNA replication.

• Eltanexor - An orally bioavailable inhibitor of exportin-1 (XPO1; chromosome region maintenance 1 protein homolog; CRM1), with potential antineoplastic activity. Upon administration, eltanexor binds to the XPO1 cargo binding site, which prevents the XPO1-mediated nuclear export of cargo proteins such as tumor suppressor proteins (TSPs), including p53, p73, BRCA1/2, pRB, FOXO, and other growth regulatory proteins and leads to their selective accumulation in the nuclei of tumor cells. As a selective inhibitor of nuclear export (SINE), KPT-8602 restores the nuclear localization and function of tumor suppressing proteins which leads to the induction of apoptosis in tumor cells. XPO1, the major export factor that transports proteins from the nucleus to the cytoplasm, is overexpressed in a variety of cancer cell types while minimally expressed in normal, healthy cells. The export of tumor suppressor proteins into the cytoplasm prevents them from initiating apoptosis and leads to uncontrolled tumor cell proliferation.

• Emactuzumab - A humanized monoclonal antibody directed against the tyrosine kinase receptor colony stimulating factor 1 receptor (CSF1R; CSF-1R; CD115), also known as macrophage colony-stimulating factor receptor (M-CSFR), with potential antineoplastic and immunomodulating activities. Upon administration, emactuzumab binds to CSF1R expressed on macrophages and inhibits the binding of colony-stimulating factor-1 (CSF-1) to CSF1R. This prevents CSF1R activation and CSF1R-mediated signaling in these cells, which blocks the production of inflammatory mediators by macrophages and reduces inflammation. By blocking both the activity of CSF1R-dependent tumor-associated macrophages (TAMs) and the recruitment of TAMs to the tumor microenvironment, emactuzumab enhances T-cell infiltration and antitumor T-cell immune responses, which inhibits the proliferation of tumor cells. TAMs play key roles in immune suppression and promoting inflammation, tumor cell proliferation and survival.

• Emepepimut-s - A liposome-encapsulated peptide vaccine consisting of a synthetic peptide derived from the mucin 1 (MUC-1) antigen with potential antineoplastic activity. Upon vaccination, MUC-1 peptide vaccine may stimulate the host immune system to mount a cytotoxic T lymphocyte (CTL) response against MUC-1-expressing tumor cells, resulting in growth inhibition. MUC-1 antigen is a high-molecular-weight transmembrane glycoprotein that is overexpressed on the cell surfaces of many epithelial tumor cells as well as on the cell surfaces of some B-cell lymphoma cells and multiple myeloma cells.

• Emibetuzumab - A humanized IgG4 monoclonal antibody directed against human hepatocyte growth factor receptor (HGFR or c-MET) with potential antineoplastic activity. Emibetuzumab binds to c-MET, thereby preventing the binding of HGF to its receptor c-Met and subsequent activation of the HGF/c-Met signaling pathway. This may result in cell death in c-Met-expressing tumor cells. c-Met, a receptor tyrosine kinase overexpressed or mutated in many tumor cell types, plays a key role in cancer cell growth, survival, angiogenesis, invasion, and metastasis.

• Emitefur - An orally available antimetabolite composed of the 1-ethoxymethyl derivative of 5-fluorouracil (5-FU) and the dihydropyrimidine dehydrogenase (DPYD) inhibitor 3-cyano-2,6-dihydroxypyridine (CNDP) in a 1:1 molar ratio, with antineoplastic activity. Upon administration, the prodrug emitefur is converted into 5-FU, while CNDP prevents the degradation of 5-FU by inhibiting DPYD and thereby prolonging the half-life of 5-FU. This increases 5-FU's concentration and thus its antitumor activity through inhibition of DNA and RNA synthesis, as well as inhibition of thymidylate synthase activity. In addition, by inhibiting the formation of 5-FU metabolites, some toxic effects associated with these metabolites may be reduced. DPYD is the rate-limiting enzyme in the catabolism of 5-FU.

• Emofolin sodium - The sodium salt of a synthetic antimetabolite analogue of folate with antineoplastic activity. Emfolin sodium competes for the folate binding site of the enzyme dihydrofolate reductase, resulting in inhibition of tetrahydrofolate synthesis, depletion of nucleotide pools, and inhibition of DNA, RNA and protein synthesis.

• Empesertib - An orally bioavailable, selective inhibitor of the serine/threonine monopolar spindle 1 (Mps1) kinase, with potential antineoplastic activity. Upon administration, empesertib binds to and inhibits the activity of Mps1. This causes inactivation of the spindle assembly checkpoint (SAC), accelerated mitosis, chromosomal misalignment, chromosomal missegregation, mitotic checkpoint complex destabilization, and increased aneuploidy. This leads to the induction of cell death in cancer cells overexpressing Mps1. Mps1, a kinase expressed in proliferating normal tissues and aberrantly overexpressed in a wide range of human tumors, is activated during mitosis and is essential for SAC functioning and controls chromosome alignment.

• Enadenotucirev - A complex, replication-selective, chimeric adenovirus type 11p (Ad11p)/Ad3 oncolytic virus vaccine, with potential antineoplastic and immunomodulating activities. Enadenotucirev has the Ad11p backbone with a large deletion in the E3-region and a small E4-domain (E4orf4) deleted, in addition to a partial E2B substitution by the Ad3 E2B genes. Upon intravenous administration of enadenotucirev, the adenovirus selectively reaches the tumor cells due to the leaky tumor vasculature and replicates in cancer cells; however, it is unable to replicate in normal, healthy cells. This induces a selective adenovirus-mediated cytotoxicity in cancer cells, which leads to cancer lysis. Following the lysis of infected cells, the replicated virus is released and can infect adjacent cells, which both induces further tumor cell oncolysis and may activate, through the release of tumor-associated antigens (TAAs) and inflammatory mediators from the lysed tumor cells, the immune system to mount an anti-tumor immune response. This further kills tumor cells. This may also stimulate long-term anti-tumor immunity. Although the cancer-selectivity of enadenotucirev is not entirely understood, the virus does not efficiently infect normal cells.

• Enadenotucirev-expressing anti-cd40 agonistic monoclonal antibody ng-350a - An oncolytic adenoviral vector, enadenotucirev (EnAd), that expresses a full-length agonistic anti-CD40 monoclonal antibody, with potential immunomodulating and antineoplastic activities. Upon intratumoral administration of NG-350A, enadenotucirev specifically infects and replicates in tumor cells and not in normal, noncancerous tissue, and selectively expresses the agonistic anti-CD40 antibody. The locally expressed anti-CD40 antibody targets and binds to CD40 on a variety of immune cells, including B-cells, T-cells and dendritic cells (DCs) in the tumor microenvironment (TME). This induces CD40-dependent signaling pathways, which activates these immune cells and induces a cytotoxic T-lymphocyte (CTL)-mediated antitumor immune response and leads to tumor cell death. CD40, a cell surface receptor and member of the tumor necrosis factor receptor superfamily (TNFRSF), is expressed on various immune cells and plays a key role in the activation of the immune system.

• Enadenotucirev-expressing fap/cd3 bispecific fap-tac ng-641 - An oncolytic adenoviral vector, a transgene-modified variant of enadenotucirev (EnAd), that expresses a bi-specific T-cell activator molecule FAP-TAc together with immune enhancer molecules C-X-C motif chemokine 9 (CXCL9), C-X-C motif chemokine 10 (CXCL10) and interferon alpha (IFNalpha), with potential immunomodulating and antineoplastic activities. Upon administration of NG-641, EnAd specifically infects and replicates in tumor cells and not in normal, noncancerous tissue, and selectively expresses FAP-TAc. The locally expressed FAP-TAc targets and binds to both fibroblast activating protein (FAP) on cancer associated fibroblasts (CAFs) and CD3 on T-cells. This leads to T-cell activation and T-cell mediated killing of CAFs in tumor stroma. NG-641 also encodes the transgenes CXCL9, CXCL10 and IFNalpha. The production of CXCL9, CXCL10 and IFNalpha leads to the recruitment and further activation of T-cells, enhancing the overall immune response and cancer cell killing. FAP, a cell surface glycoprotein, is overexpressed on tumor-associated fibroblasts but minimally expressed on normal, healthy cells.

• Enapotamab vedotin - An antibody-drug conjugate (ADC), consisting of a human monoclonal antibody directed against AXL receptor tyrosine kinase (AXL; UFO) and conjugated, through a protease-cleavable linker, to the cytotoxic agent monomethyl auristatin E (MMAE), with potential antineoplastic activity. Upon administration, the monoclonal antibody moiety of enapotamab vedotin binds to AXL, which is expressed on the surfaces of a variety of cancer cell types. Upon endocytosis and enzymatic cleavage, MMAE is released into the tumor cell cytosol, where it binds to tubulin and inhibits tubulin polymerization; this may result in G2/M phase arrest and apoptosis. AXL, a member of the TAM (TYRO3, AXL and MER) family of receptor tyrosine kinases and overexpressed by many tumor cell types, plays a key role in tumor cell proliferation, survival, invasion and metastasis; its expression is associated with drug resistance and poor prognosis.

• Enasidenib - An orally available inhibitor of specific mutant forms of the mitochondrial enzyme isocitrate dehydrogenase type 2 (IDH2), with potential antineoplastic activity. Upon administration, enasidenib specifically inhibits various mutant forms of IDH2, including the IDH2 variants R140Q, R172S, and R172K, which inhibits the formation of 2-hydroxyglutarate (2HG). This may lead to both an induction of cellular differentiation and an inhibition of cellular proliferation in IDH2-expressing tumor cells. IDH2, an enzyme in the citric acid cycle, is mutated in a variety of cancers; it initiates and drives cancer growth by blocking differentiation and the production of the oncometabolite 2HG.

• Enavatuzumab - A humanized monoclonal antibody directed against the tumor necrosis factor-like weak inducer of apoptosis receptor (TWEAKR) with potential antineoplastic, immunomodulating and antiangiogenic activities. Enavatuzumab binds to TWEAKR and inhibits TWEAK ligand binding and activation of NF-kappaB-mediated cytokine release, which may result in tumor cell apoptosis. TWEAKR is a cell-surface receptor with homology to tumor necrosis factor receptors. Upon binding with its ligand, TWEAKR has been shown to stimulate cytokine release and cell proliferation, migration, and survival; it may also promote apoptosis under some conditions. This receptor may be overexpressed in a variety of tumors including those of the pancreas, colon, lung, kidney, and breast.

• Encapsulated rapamycin - An orally bioavailable nanoparticle-based formulation composed of sub-micron particles of the macrolide antibiotic rapamycin incorporated into a pH-sensitive poly(methyl methacrylate) polymer, with potential immunomodulating and antineoplastic activities. Upon oral administration of the encapsulated rapamycin, the nanoparticle specifically delivers rapamycin at the tumor site. Rapamycin binds to the immunophilin FK Binding Protein-12 (FKBP-12) to generate a complex that binds to and inhibits the activation of the serine/threonine kinase mammalian target of rapamycin (mTOR), a key regulatory kinase. This may suppress mTORC1 activity. In addition, inhibition of mTOR may modulate central memory CD8 T cells, CD3+/CD56+ natural killer (NK) cells and CD8 T-cell responses. This may kill tumor cells. Compared to the administration of rapamycin alone, this formulation improves oral bioavailability of rapamycin with more consistent rapamycin levels, thereby allowing for administration of lower rapamycin dosage, which improves and minimizes rapamycin's toxicity. Upregulated in some tumors, mTOR is a serine/threonine kinase involved in regulating cellular proliferation, motility, and survival that is located downstream of the PI3K/Akt signaling pathway.

• Encelimab - A humanized, immunoglobulin G4 (IgG4) monoclonal antibody directed against the inhibitory receptor lymphocyte activation gene 3 protein (LAG3; LAG-3), with potential immune checkpoint inhibitory and antineoplastic activities. Upon administration,encelimab binds to LAG3 expressed on tumor-infiltrating lymphocytes (TILs) and blocks its binding with major histocompatibility complex (MHC) class II molecules expressed on tumor cells. This activates antigen-specific T-lymphocytes and enhances cytotoxic T-cell-mediated tumor cell lysis, which leads to a reduction in tumor growth. LAG3, a member of the immunoglobulin superfamily (IgSF), is expressed on various immune cells, and negatively regulates both proliferation and activation of T-cells. Its expression on TILs is associated with tumor-mediated immune suppression.

• Enclomiphene - The trans-isomer of clomiphene citrate (CC). Enclomiphene has a higher rate of clearance and is less active than the cis-isomer, cis-clomiphene. Clomiphene citrate has been evaluated for antineoplastic activity against breast cancer.

• Enclomiphene citrate - The orally bioavailable citrate salt of enclomiphene, the trans-isomer of the nonsteroidal triphenylethylene compound clomiphene, with tissue-selective estrogenic and antiestrogenic activities. As a selective estrogen receptor modulator (SERM), enclomiphene binds to hypothalamic estrogen receptors, blocking the negative feedback of endogenous estrogens and stimulating the release of gonadotropin-releasing hormone (GnRH) from the hypothalamus; released GnRH subsequently stimulates the release of follicle-stimulating hormone (FSH) and luteinizing hormone (LH) from the anterior pituitary, resulting in ovulation. In addition, this agent may bind to estrogen receptors on breast cancer cells, resulting in the inhibition of estrogen-stimulated proliferation in susceptible cell populations.

• Encorafenib - An orally available Raf kinase inhibitor with potential antineoplastic activity. Encorafenib specifically inhibits Raf kinase, a serine/threonine enzyme in the RAF/mitogen-activated protein kinase kinase (MEK)/extracellular signal-related kinase (ERK) signaling pathway. By inhibiting the activation of the RAF/MEK/ERK signaling pathway, the administration of LGX818 may result in a decrease in proliferation of tumor cells. The Raf mutation BRAF V600E is frequently upregulated in a variety of human tumors and results in the constitutive activation of the RAF/MEK/ERK signaling pathway that regulates cellular proliferation and survival.

• Endothelin b receptor blocker enb 003 - An antagonist of the immune checkpoint endothelin B receptor (ETBR; EDNRB), with potential immunomodulating and antineoplastic activities. Upon administration, the ETBR blocker ENB 003 selectively targets and binds to ETBR expressed on tumor cells. This prevents ETBR-mediated signaling and may abrogate the immunosuppressive tumor microenvironment (TME), may enhance a T-cell mediated anti-tumor immune response and may inhibit proliferation of ETBR-expressing tumor cells. ETBR, a G-protein coupled receptor, is overexpressed in a variety of tumor cell types and plays a key role in tumor cell proliferation, invasion, epithelial-mesenchymal transition (EMT) and angiogenesis. It also plays a role in tumor immunosuppression and blocks T-cell trafficking.

• Endothelin receptor type a antagonist ym598 - An orally active synthetic substituted phenylethenesulfonamide. As a selective endothelin A receptor antagonist, YM598 inhibits endothelin-mediated mechanisms involved in tumor cell growth and progression, angiogenesis, and metastasis.

• Enfortumab vedotin - An antibody drug conjugate (ADC) containing a human monoclonal antibody AGS-22 targeting the cell adhesion molecule nectin-4 and conjugated to the cytotoxic agent monomethyl auristatin E (MMAE), via a proprietary enzyme-cleavable linker (AGS-22CE), with potential antineoplastic activity. The monoclonal antibody moiety of enfortumab vedotin selectively binds to nectin-4. After internalization and proteolytic cleavage, MMAE binds to tubulin and inhibits its polymerization, which results in G2/M phase arrest and induces apoptosis in nectin-4 overexpressing tumor cells. Nectin-4, a tumor associated antigen belonging to the nectin family, is overexpressed in a variety of cancers, including breast, bladder, lung and pancreatic cancer.

• Engineered red blood cells co-expressing 4-1bbl and il-15tp rtx-240 - A preparation of allogeneic, off-the-shelf (OTS) red blood cells (RBCs) engineered to express both the co-stimulatory molecule tumor necrosis factor ligand superfamily (TNFSF) member 9 (TNFSF9; 4-1BBL) and a fusion protein composed of the trans-presented cytokine interleukin (IL)-15/IL-15-receptor alpha (IL-15Ra) (IL-15TP) with potential modulating and antineoplastic activities. CD34+ hematopoietic precursor cells (HPC) are collected by apheresis from a healthy O negative donor, purified, and engineered with a lentiviral vector to express 4-1BBL and IL-15TP. The cells are then further expanded and differentiated until the nucleus is ejected, resulting in a mature reticulocyte. Upon administration of the engineered red blood cells co-expressing 4-1BBL and IL-15TP RTX-240, the RBCs express both 4-1BBL and IL-15TP on their cell surfaces. 4-1BBL and IL-15TP bind to and subsequently induce the proliferation and activation of natural killer (NK) cells and T-cells. This enhances the secretion of cytokine interferon-gamma (IFN-g) and results in the induction of an anti-tumor immune response.

• Engineered toxin body targeting cd38 tak-169 - An engineered toxin body (ETB) containing a single chain variable fragment (scFv) from an antibody targeting the cell surface glycoprotein ADP-ribosyl cyclase 1 (CD38) that is fused to a cytotoxic payload composed of the enzymatically active, de-immunized, ribosome-inactivating cytotoxic payload Shiga-like toxin-A subunit (SLTA), with potential antineoplastic activity. Upon administration, the anti-CD38 scFv moiety of TAK-169 specifically targets and binds to CD38-expressing tumor cells. Upon internalization, the SLTA moiety is released and acts as an N-glycosidase, which binds to and removes an adenine nucleobase from the 28S RNA component of the 60S ribosomal subunit.of ribosomes This prevents ribosome activity, This inhibits protein synthesis and leads to apoptosis in CD38-expressing tumor cells. CD38, a type II transmembrane glycoprotein, is present on various immune cells and hematologic malignancies; its expression has been correlated with poor prognosis.

• Engineered toxin body targeting her2 mt-5111 - An engineered toxin body (ETB) composed of a single chain variable fragment (scFv) from an antibody targeting the human epidermal growth factor receptor 2 (HER2; HER-2), fused to the enzymatically active de-immunized, ribosome-inactivating cytotoxic payload Shiga-like toxin-A subunit (SLTA), with potential antineoplastic activity. Upon administration, the scFv moiety of MT-5111 specifically targets and binds to a distinct epitope on HER2-expressing cells. Upon internalization, the SLTA moiety is released and acts as an N-glycosidase, which binds to and cleaves an adenine nucleobase in the 28S RNA component of the 60S subunit of ribosomes and prevents ribosome activity. This inhibits protein synthesis and leads to apoptosis in HER2-expressing tumor cells. HER2, a tumor-associated antigen (TAA), is overexpressed in a variety of tumor cell types.

• Eniluracil/5-fu combination tablet - A combination tablet of ethynyluracil and fluorouracil. Fluorouracil is an antimetabolite fluoropyrimidine analog of the nucleoside pyrimidine with antineoplastic activity. Ethynyluracil is an orally-active fluoropyrimidine analog that inhibits dihydropyrimidine dehydrogenase, the rate-limiting enzyme that catabolizes and inactivates 5-fluorouracil in the liver. This may lead to an increase in the bioavailability and, effectiveness of fluorouracil.

• Enloplatin - A platinum-based alkylating agent with antineoplastic activity. Although its pharmacokinetic properties are similar to that of carboplatin, enloplatin appears to be non-cross resistant with other platinum-based agents, such as cisplatin and carboplatin.

• Enoblituzumab - An Fc-domain optimized, humanized monoclonal antibody directed against cancer stem cells (CSCs), with potential immunomodulating and antineoplastic activities. After binding of enoblituzumab to an as of yet not elucidated target expressed on CSCs and differentiated tumor cells, this agent may induce an antibody-dependent cell-mediated cytotoxicity (ADCC) against CSCs. CSCs are tumor initiating cells that are able to self-renew and are responsible for tumor cell growth and resistance.

• Enobosarm - A non-steroidal agent with anabolic activity. Selective androgen receptor modulator (SARM) GTx-024 is designed to work like testosterone, thus promoting and/or maintaining libido, fertility, prostate growth, and muscle growth and strength. Mimicking testosterone's action, this agent may increase lean body mass, thereby ameliorating muscle wasting in the hypermetabolic state of cancer cachexia.

• Enoticumab - A human monoclonal antibody directed against Delta-like ligand-4 (DLL4) with potential antineoplastic activity. Enoticumab specifically binds to human DLL4, preventing its binding to Notch receptors and inhibiting Notch signaling, which may result in defective tumor vascularization and, so, the inhibition of tumor cell growth. DLL4 is the only Notch ligand selectively expressed on endothelial cells; DLL4/Notch signaling is required for the development of functional tumor blood vessels.

• Enpromate - A synthetic acetylenic carbamate, an alkylating agent, with antineoplastic activity.

• Ensartinib - An orally available small molecule inhibitor of the receptor tyrosine kinase anaplastic lymphoma kinase (ALK) with potential antineoplastic activity. Upon oral administration, ensartinib binds to and inhibits ALK kinase, ALK fusion proteins and ALK point mutation variants. Inhibition of ALK leads to the disruption of ALK-mediated signaling and eventually inhibits tumor cell growth in ALK-expressing tumor cells. ALK belongs to the insulin receptor superfamily and plays an important role in nervous system development. ALK is not expressed in healthy adult human tissue but ALK dysregulation and gene rearrangements are associated with a series of tumors; ALK mutations are associated with acquired resistance to small molecule tyrosine kinase inhibitors.

• Ensituximab - A chimeric monoclonal antibody against human colorectal and pancreatic carcinoma-associated antigens (CPAAs) with potential immunomodulating and anti-tumor activities. Anti-CPAA monoclonal antibody NPC-1C binds to CPAAs, which may activate the immune system to exert a cytotoxic T-lymphocyte (CTL) response and an antibody-dependent cellular cytotoxicity (ADCC) response against CPAA-expressing tumor cells. CPAAs, cell surface proteins, are upregulated on colon and pancreatic tumor cells. NPC-1C contains the variable region of the heavy and light chain of murine NPC-1 and linked in-frame to constant regions of a human IgG1 isotype.

• Enteric-coated trpm8 agonist d-3263 hydrochloride - An enteric-coated orally bioavailable formulation of the hydrochloride salt of a small-molecule agonist for transient receptor potential melastatin member 8 (TRPM8 or Trp-p8) with potential antineoplastic activity. The active ingredient in enteric-coated TRPM8 agonist D-3263 hydrochloride binds to and activates TRPM8, which may result in an increase in calcium and sodium entry; the disruption of calcium and sodium homeostasis; and the induction of cell death in TRPM8-expressing tumor cells. This agent may decrease dihydrotestosterone (DHT) levels, which may contribute to its inhibitory effects on prostate cancer and BPH. TRPM8 is a transmembrane calcium channel protein that is normally expressed in prostate cells and appears to be overexpressed in benign prostatic hyperplasia (BPH) and in prostate cancer.

• Enterococcus gallinarum strain mrx0518 - A live strain of the flagellin-producing Gram-positive bacterium Enterococcus (E.) gallinarum that is isolated from a healthy human gut , with potential immunomodulating and antineoplastic activities. Upon oral administration, MRx0518 modulates the intestinal microbiota and targets both intestinal epithelial cells (IECs), and various immune cells, such as macrophages and dendritic cells (DCs) and is able to induce the production of both pro- and anti-inflammatory mediators, such as interleukin-8 (IL-8), tumor necrosis factor-alpha (TNF-a), IL-1beta, IL-6, IL-23, in these cells and activates the innate immune system. The flagellin produced by MRx0518 interacts with and activates toll-like receptor 5 (TLR5), thereby activating the adaptive immune system and modulating the tumor microenvironment (TME). This activates the immune system to mount a cytotoxic T-lymphocyte (CTL) immune response against tumor cells.

• Entinostat - A synthetic benzamide derivative with potential antineoplastic activity. Entinostat binds to and inhibits histone deacetylase, an enzyme that regulates chromatin structure and gene transcription. This agent appears to exert dose-dependent effects in human leukemia cells including cyclin-dependent kinase inhibitor 1A (p21/CIP1/WAF1)-dependent growth arrest and differentiation at low drug concentrations; a marked induction of reactive oxygen species (ROS); mitochondrial damage; caspase activation; and, at higher concentrations, apoptosis. In normal cells, cyclin-dependent kinase inhibitor 1A expression has been associated with cell-cycle exit and differentiation.

• Entolimod - A polypeptide derived from the Salmonella filament protein flagellin with potential radioprotective and anticancer activities. As a toll-like receptor 5 (TLR5) agonist, entolimod binds to and activates TLR5 thereby stimulating tumor necrosis factor production and activating nuclear factor kappa B (NF-kB). This induces NF-kB-mediated signaling pathways and inhibits the induction of apoptosis. This may prevent apoptosis in normal, healthy cells during radiotherapy of cancerous cells and may allow for increased doses of ionizing radiation. In addition, entolimod may inhibit radiation-independent proliferation in TLR5-expressing tumor cells.

• Entospletinib - An orally available inhibitor of spleen tyrosine kinase (Syk), with potential antineoplastic activity. Upon oral administration of entospletinib, this agent may inhibit the activity of Syk, which inhibits B-cell receptor (BCR) signaling and leads to an inhibition of 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 hematopoeitic malignancies.

• Entrectinib - An orally bioavailable inhibitor of the tyrosine kinases tropomyosin receptor kinases (Trk) A, B and C, C-ros oncogene 1 (ROS1) and anaplastic lymphoma kinase (ALK), with potential antineoplastic activity. Upon administration, entrectinib binds to and inhibits TrkA, TrkB, TrkC, ROS1 and ALK. Inhibition of these kinases may result in a disruption of TrkA-, TrkB-, TrkC-, ROS1-, and ALK-mediated signaling. This leads to an induction of apoptosis and an inhibition of tumor cell proliferation in tumor cells that express these kinases. TrkA, TrkB, TrkC, ROS1 and ALK are overexpressed in a variety of cancer cell types.

• Envafolimab - An injectable formulation of a monoclonal antibody directed against programmed cell death-1 ligand 1 (PD-L1; cluster of differentiation 274; CD274), with immune checkpoint inhibitory and potential antineoplastic activities. Upon subcutaneous administration, envafolimab binds to PD-L1, blocking its binding to and activation of its receptor programmed death 1 (PD-1), which may enhance the T-cell-mediated immune response to neoplasms and reverse T-cell inactivation. 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 expressed on activated T-cells, is a negative regulator of the immune system that limits the expansion and survival of CD8+ T cells.

• Enzalutamide - An orally bioavailable, organic, non-steroidal small molecule targeting the androgen receptor (AR) with potential antineoplastic activity. Through a mechanism that is reported to be different from other approved AR antagonists, enzalutamide inhibits the activity of prostate cancer cell ARs, which may result in a reduction in prostate cancer cell proliferation and, correspondingly, a reduction in the serum prostate specific antigen (PSA) level. AR over-expression in prostate cancer represents a key mechanism associated with prostate cancer hormone resistance.

• Enzastaurin hydrochloride - The hydrochloride salt of enzastaurin, a synthetic macrocyclic bisindolemaleimide with potential antineoplastic activity. Binding to the ATP-binding site, enzastaurin selectively inhibits protein kinase C beta, an enzyme involved in the induction of vascular endothelial growth factor (VEGF)-stimulated neo-angiogenesis. This agent may decrease tumor blood supply and so tumor burden.

• Ep2/ep4 antagonist tpst-1495 - An orally bioavailable, dual antagonist of the human prostaglandin E2 receptor subtypes 2 (EP2) and 4 (EP4), with potential immunomodulating and antineoplastic activities. Upon oral administration, the EP2/EP4 antagonist TPST-1495 selectively targets and binds to EP2 and EP4, inhibiting the binding of the immunosuppressive prostaglandin E2 (PGE2) to EP2 and EP4. This prevents the activation of EP2 and EP4, and inhibits PGE2-EP2/EP4-mediated signaling. This inhibits PGE2-driven immune suppression by preventing the PGE2-mediated inhibition of anti-tumor immune effector cells in the tumor microenvironment (TME), such as natural killer (NK) cells, T-lymphocytes, dendritic cells (DCs) and M1 macrophages, and blocking the PGE2-mediated increase in suppressive immune cells, such as myeloid derived suppressor cells (MDSCs), M2 macrophages, and regulatory T cells (Tregs). This inhibits the proliferation of tumor cells in which the PGE2-EP2/4 signaling pathway is over-activated. EP2 and EP4, G protein-coupled receptors (GPCRs) that are overexpressed in certain types of cancers, promote tumor cell proliferation, invasion, survival, and metastasis.

• Ep4 antagonist inv-1120 - A small molecule and antagonist of the prostaglandin E2 receptor subtype 4 (PTGER4; EP4), with potential immunomodulating and antineoplastic activities. Upon administration, the EP4 antagonist INV-1120 selectively targets and binds to EP4, inhibiting the binding of the immunosuppressive prostaglandin E2 (PGE2) to EP4. This prevents the activation of EP4 and inhibits PGE2-EP4-mediated signaling, thereby inhibiting proliferation of tumor cells in which the PGE2-EP4 signaling pathway is over-activated. In addition, EP4 inhibition prevents the activity of tumor-associated myeloid cells (TAMCs) in the tumor microenvironment (TME) by inhibiting interleukin-23 (IL-23) production and the IL-23-mediated expansion of Th17 cells. EP4, a prostanoid receptor, is a G protein-coupled receptor that is expressed in certain types of cancers; it promotes tumor cell proliferation and invasion.

• Ep4 antagonist ono-4578 - An orally bioavailable antagonist of the prostaglandin E2 receptor subtype 4 (PTGER4; EP4), with potential analgesic, immunomodulating and antineoplastic activities. Upon administration, the EP4 antagonist ONO-4578 selectively targets and binds to EP4, inhibiting the binding of the immunosuppressive prostaglandin E2 (PGE2) to EP4. This prevents the activation of EP4 and inhibits PGE2-EP4-mediated signaling, thereby inhibiting proliferation of tumor cells in which the PGE2-EP4 signaling pathway is over-activated. In addition, EP4 inhibition prevents the activity of tumor-associated myeloid cells (TAMCs) in the tumor microenvironment (TME) by inhibiting interleukin-23 (IL-23) production and the IL-23-mediated expansion of Th17 cells. EP4, a prostanoid receptor, is a G protein-coupled receptor that is expressed in certain types of cancers; it promotes tumor cell proliferation and invasion.

• Epacadostat - An orally available hydroxyamidine and inhibitor of indoleamine 2,3-dioxygenase (IDO1), with potential immunomodulating and antineoplastic activities. Epacadostat targets and binds to IDO1, an enzyme responsible for the oxidation of tryptophan into kynurenine. By inhibiting IDO1 and decreasing kynurenine in tumor cells, INCB024360 increases and restores the proliferation and activation of various immune cells, including dendritic cells (DCs), NK cells, and T-lymphocytes, as well as interferon (IFN) production, and a reduction in tumor-associated regulatory T cells (Tregs). Activation of the immune system, which is suppressed in many cancers, may inhibit the growth of IDO1-expressing tumor cells. IDO1 is overexpressed by a variety of tumor cell types and DCs.

• Epcam-specific car-expressing autologous t-lymphocytes - A preparation of autologous T-lymphocytes that have been genetically modified to express a chimeric antigen receptor (CAR) specific for the antigen epithelial cell adhesion molecule (EpCAM), with potential immunostimulating and antineoplastic activities. Upon administration, the EpCAM-specific CAR-expressing autologous T-lymphocytes specifically recognize and bind to EpCAM-expressing tumor cells, resulting in tumor cell lysis. EpCAM, a cell surface protein, is expressed by a variety of tumor cells.

• Epcoritamab - A bispecific monoclonal antibody, with potential immunomodulating and antineoplastic activities. Epcoritamab contains two antigen-recognition sites: one for human CD3, a T-cell surface antigen, and one for human CD20, a tumor-associated antigen (TAA) that is exclusively expressed on B-cells during most stages of B-cell development and is often overexpressed in B-cell malignancies. Upon administration, epcoritamab binds to both T-cells and CD20-expressing B-lineage tumor cells. The resulting cross-linkage may trigger a potent cytotoxic T-lymphocyte (CTL) response against the CD20-expressing tumor B-cells.

• Epha2-targeting bicycle toxin conjugate bt5528 - A bicyclic peptide targeting Ephrin receptor A2 (EphA2) and conjugated, through an inert sarcosine spacer chain and a valine-citrulline cleavable linker, to the cytotoxic agent monomethyl auristatin E (MMAE), an auristatin derivative and a potent inhibitor of microtubule polymerization, with potential antineoplastic activity. Upon administration of the EphA2-targeting bicycle toxin conjugate BT5528, this agent targets and binds to EphA2-expressing tumor cells. After internalization and enzymatic cleavage of the immunoconjugate within the tumor cell cytosol, free MMAE binds to tubulin and inhibits its polymerization, which may result in G2/M phase arrest and tumor cell apoptosis. The cell-surface receptor EphA2, a member of the ephrin family of receptor tyrosine kinases (RTKs) involved in mammalian development, is overexpressed by a variety of different cancer cell types. EphA2 expression is associated with poor prognosis.

• Epha2-targeting dopc-encapsulated sirna - A liposomal formulation consisting of short-interfering RNAs (siRNAs) directed against ephrin type-A receptor 2 (EphA2) and encapsulated into 1,2-dioleoyl-sn-glycero-3-phosphatidylcholine (DOPC) neutral liposomes, with potential antineoplastic activity. Upon internalization, EphA2-targeting DOPC-encapsulated siRNA can hybridize to EphA2 DNA and mRNA, thereby interfering with both the transcription and translation of EphA2, and thus inhibiting tumor cell growth. The cell-surface receptor EphA2, a member of the ephrin family of receptor tyrosine kinases (RTKs) involved in mammalian development, is overexpressed by a variety of different cancer cell types and plays an important role in tumor growth.

• Epipodophyllotoxin analog gl331 - An epipodophyllotoxin analogue possessing antineoplastic properties. GL331 binds to and inhibits topoisomerase II, resulting in the accumulation of single- or double-strand DNA breaks, the inhibition of DNA replication and transcription, and apoptotic cell death. (NCI)

• Epipropidine - An epoxide and alkylating agent with antineoplastic activity. Epipropidone is not used clinically due to its unstable nature.

• Epirubicin - A 4'-epi-isomer of the anthracycline antineoplastic antibiotic doxorubicin. Epirubicin intercalates into DNA and inhibits topoisomerase II, thereby inhibiting DNA replication and ultimately, interfering with RNA and protein synthesis. This agent also produces toxic free-radical intermediates and interacts with cell membrane lipids causing lipid peroxidation.

• Epirubicin hydrochloride - The hydrochloride salt of the 4'-epi-isomer of the anthracycline antineoplastic antibiotic doxorubicin. Epirubicin intercalates into DNA and inhibits topoisomerase II, thereby inhibiting DNA replication and ultimately, interfering with RNA and protein synthesis. This agent also produces toxic free-radical intermediates and interacts with cell membrane lipids causing lipid peroxidation.

• Epitinib succinate - The succinate salt form of epitinib, an orally available epidermal growth factor receptor (EGFR) inhibitor, with potential antineoplastic activity. Upon administration, epitinib inhibits the activity of EGFR, thereby preventing EGFR-mediated signaling. This may lead to induction of cell death and inhibition of tumor growth in EGFR-overexpressing tumor cells. EGFR is a receptor tyrosine kinase (RTK) that is overexpressed in certain tumor types and plays a key role in tumor cell proliferation and vascularization.

• Epitiostanol - An androgenic anabolic steroid having potent anti-estrogenic effect, which inhibits the progression of estrogen-stimulated cancers such as breast cancer. (NCI)

• Epothilone analog utd1 - A genetically engineered epothilone analog with potential antineoplastic activity. Upon administration, epothilone analog UTD1 binds to tubulin, induces microtubule polymerization and stabilizes microtubules against depolymerization, which may result in the inhibition of cell division, the induction of G2/M arrest, and apoptosis. Compared to first-generation epothilones, this agent exhibits greater safety and enhanced activity against certain multidrug-resistant (MDR) tumors.

• Epothilone kos-1584 - A second-generation epothilone with potential antineoplastic activity. Epothilone KOS-1584 binds to tubulin and induces microtubule polymerization and stabilizes microtubules against depolymerization, which may result in the inhibition of cell division, the induction of G2/M arrest, and apoptosis. Compared to first-generation epothilones, this agent exhibits greater safety and efficacy with an enhanced pharmaceutical profile, including enhanced water solubility and tumor penetration, and reduced CNS exposure. In addition, epothilone KOS-1584 is a poor substrate for the P-glycoprotein (P-gp) drug efflux pump.

• Epratuzumab - A recombinant, humanized monoclonal antibody directed against CD22, a cell surface glycoprotein present on mature B-cells and on many types of malignant B-cells. After binding to CD22, epratuzumab's predominant antitumor activity appears to be mediated through antibody-dependent cellular cytotoxicity (ADCC).

• Epratuzumab-cys-tesirine - An antibody-drug conjugate (ADC) composed of a cysteine-engineered version of epratuzumab (hLL2), a humanized anti-CD22 monoclonal antibody derived from the murine immunoglobulin (Ig) G2a monoclonal antibody LL2 (EPB-2), site-specifically conjugated to the cross-linking cytotoxic agent tesirine (SG3249), a cathepsin B-cleavable valine-alanine pyrrolobenzodiazepine dimer (PBD), with potential antineoplastic activity. Upon administration of epratuzumab-cys-tesirine, the epratuzumab moiety targets and binds to the B cell-specific CD22 receptor and is rapidly internalized. Upon cleavage, the imine groups of tesirine target and bind to the N2 positions of guanines on opposite strands of DNA. This induces interstrand cross-links in the minor groove of DNA and inhibits DNA replication, which inhibits the proliferation of CD22-overexpressing tumor cells. CD22, a cell surface glycoprotein, is expressed on mature B-cells and on most malignant B-cells.

• Eps8 peptide-specific dendritic cells - A preparation of dendritic cells (DCs) pulsed with peptides derived from epidermal growth factor receptor (EGFR) pathway substrate 8 (EPS8), with potential immunostimulating and antineoplastic activities. Upon administration of the EPS8 peptide-specific DCs, the immune system is exposed to the EPS8 antigens. This results in the induction of a specific cytotoxic T-lymphocyte (CTL) response against EPS8-expressing tumor cells and tumor cell lysis. EPS8, a tumor-associated antigen (TAA), is overexpressed in a variety of tumor cell types but rarely in normal tissues. As a substrate for the EGFR kinase, it plays a key role in tumor progression through the EGFR-dependent pathway. Its expression is correlated with a poor prognosis.

• Er alpha proteolysis-targeting chimera protein degrader arv-471 - An orally available hetero-bifunctional molecule and selective estrogen receptor (ER) alpha-targeted protein degrader, using the proteolysis targeting chimera (PROTAC) technology, with potential antineoplastic activity. ARV-471 is composed of an ER alpha ligand attached to an E3 ligase recognition moiety. Upon oral administration, ARV-471 targets and binds to the ER ligand binding domain on ER alpha. E3 ligase is recruited to the ER by the E3 ligase recognition moiety and ER alpha is tagged by ubiquitin. This causes ubiquitination and degradation of ER alpha by the proteasome. This decreases ER alpha protein levels, decreases the expression of ER alpha-target genes and halts ER-mediated signaling. This results in an inhibition of proliferation in ER alpha-overexpressing tumor cells. In addition, the degradation of the ER alpha protein releases the ARV-471 and can bind to additional ER alpha target proteins. ER alpha is overexpressed in a variety of cancers and plays a key role in cancer cell proliferation.

• Era36 modulator icaritin - A metabolite of icariin, a principal flavonoid glycoside in Herba Epimedii (a traditional Chinese medicine herb used in treating osteoporosis) with potential antineoplastic activity. ERa36 modulator icaritin selectively binds to a novel variant of estrogen receptor alpha, a36, and mediates a membrane-initiated "nongenomic" signaling pathway, which is linked to activate signaling pathways like the MAPK/ERK and the PI3K/Akt pathways. This agent induces cell cycle arrest at G1, or G2/M arrest depending upon the dose. Consistently with G1 arrest, icaritin increases protein expressions of pRb, p27(Kip1) and p16(Ink4a), while decreasing phosphorylated pRb, Cyclin D1 and CDK4. 40% of ER-negative breast cancer tumors express high levels of ERa36, and this subset of patients is less likely to benefit from tamoxifen treatment compared with those with ERa66-positive/ERa36-negative tumors.

• Erastin analogue prlx 93936 - A structural analogue of erastin with potential antineoplastic activity. Erastin analogue PRLX 93936 appears to inhibit mitochondrial outer membrane protein VDACs (voltage-dependent anion channels) 2 and 3, resulting in an oxidative, non-apoptotic cell death. Erastin analogue PRLX 93936 exhibits greater lethality in cell lines harboring mutations in the GTPase protein oncogenes HRAS and KRAS or the serine-threonine protein kinase oncogene BRAF than in non-tumorigenic cell lines. VDACs 2 and 3 are up-regulated in a wide variety of tumor cell lines.

• Erbulozole - A water soluble congener of tubulozole and a tubulin binding agent with potential antimitotic and antineoplastic activities. Erbulozole targets and binds to tubulin, thereby preventing the polymerization of tubulin. This may lead to an inhibition of cell division and induction of apoptosis.

• Erdafitinib - An orally bioavailable, pan fibroblast growth factor receptor (FGFR) inhibitor with potential antineoplastic activity. Upon oral administration, erdafitinib binds to and inhibits FGFR, which may result in the inhibition of FGFR-related signal transduction pathways and thus the inhibition of tumor cell proliferation and tumor cell death in FGFR-overexpressing tumor cells. FGFR, upregulated in many tumor cell types, is a receptor tyrosine kinase essential to tumor cell proliferation, differentiation and survival.

• Eribulin - An analogue of halichondrin B, a substance derived from a marine sponge (Lissodendoryx sp.) with antineoplastic activity. Eribulin binds to the vinca domain of tubulin and inhibits the polymerization of tubulin and the assembly of microtubules, resulting in inhibition of mitotic spindle assembly, induction of cell cycle arrest at G2/M phase, and, potentially, tumor regression.

• Eribulin mesylate - The mesylate salt of a synthetic analogue of halichondrin B, a substance derived from a marine sponge (Lissodendoryx sp.) with antineoplastic activity. Eribulin binds to the vinca domain of tubulin and inhibits the polymerization of tubulin and the assembly of microtubules, resulting in inhibition of mitotic spindle assembly, induction of cell cycle arrest at G2/M phase, and, potentially, tumor regression.

• Erk 1/2 inhibitor astx029 - An orally bioavailable inhibitor of the extracellular signal-regulated kinases (ERK) 1 and 2, with potential antineoplastic activity. Upon administration, ASTX029 specifically binds to and inhibits both ERK 1 and 2, thereby preventing the activation of mitogen-activated protein kinase (MAPK)/ERK-mediated signal transduction pathways. This results in the inhibition of ERK-dependent tumor cell proliferation and survival. The MAPK/ERK pathway is often upregulated in a variety of tumor cell types and plays a key role in the proliferation, differentiation and survival of tumor cells.

• Erk inhibitor - Any agent that targets and inhibits the activity of extracellular signal-regulated kinase (ERK).

• Erk inhibitor cc-90003 - An orally available inhibitor of extracellular signal-regulated kinase (ERK), with potential antineoplastic activity. Upon oral administration, CC-90003 inhibits ERK activity, and prevents the activation of ERK-mediated signal transduction pathways. This results in the inhibition of ERK-dependent tumor cell proliferation and survival. The mitogen-activated protein kinase (MAPK)/ERK pathway is often upregulated in a variety of tumor cell types and plays a key role in tumor cell proliferation, differentiation and survival.

• Erk inhibitor gdc-0994 - An orally available inhibitor of extracellular signal-regulated kinase (ERK), with potential antineoplastic activity. Upon oral administration, GDC-0994 inhibits both ERK phosphorylation and activation of ERK-mediated signal transduction pathways. This prevents ERK-dependent tumor cell proliferation and survival. The mitogen-activated protein kinase (MAPK)/ERK pathway is upregulated in a variety of tumor cell types and plays a key role in tumor cell proliferation, differentiation and survival.

• Erk inhibitor ltt462 - An orally available inhibitor of extracellular signal-regulated kinase (ERK), with potential antineoplastic activity. Upon oral administration, LTT462 binds to and inhibits ERK, thereby preventing the activation of ERK-mediated signal transduction pathways. This results in the inhibition of ERK-dependent tumor cell proliferation and survival. The mitogen-activated protein kinase (MAPK)/ERK pathway is upregulated in numerous tumor cell types and plays a key role in tumor cell proliferation, differentiation and survival.

• Erk inhibitor mk-8353 - An orally available inhibitor of extracellular signal-regulated kinase (ERK), with potential antineoplastic activity. Upon oral administration, MK-8353 inhibits both ERK phosphorylation and activation of ERK-mediated signal transduction pathways; thereby, preventing ERK-dependent tumor cell proliferation and survival. The mitogen-activated protein kinase (MAPK)/ERK pathway is often upregulated in a variety of tumor cell types and plays a role in tumor cell proliferation, differentiation and survival.

• Erk1/2 inhibitor asn007 - An orally bioavailable inhibitor of the extracellular signal-regulated kinases 1 (ERK1) and 2 (ERK2), with potential antineoplastic activity. Upon oral administration, ASN007 specifically binds to and inhibits the serine/threonine-protein kinase activities of both ERK1 and ERK2, thereby preventing the phosphorylation of ERK1/2 substrates and the activation of mitogen-activated protein kinase (MAPK)/ERK-mediated signal transduction pathways. This results in the inhibition of ERK-dependent proliferation and survival of tumor cells. The MAPK/ERK pathway, also known as the RAS/RAF/MEK/ERK pathway, is hyperactivated in a variety of tumor cell types due to mutations in upstream targets. It plays a key role in the proliferation, differentiation and survival of tumor cells.

• Erk1/2 inhibitor hh2710 - An orally bioavailable inhibitor of the extracellular signal-regulated kinases 1 (ERK1) and 2 (ERK2), with potential antineoplastic activity. Upon oral administration, ERK1/2 inhibitor HH2710 specifically targets, binds to and inhibits the activity of the serine/threonine-protein kinases ERK1 and ERK2, thereby preventing the phosphorylation of ERK1/2 substrates and the activation of mitogen-activated protein kinase (MAPK)/ERK-mediated signal transduction pathways. This results in the inhibition of ERK-dependent proliferation and survival of tumor cells. The MAPK/ERK pathway, also known as the RAS/RAF/MEK/ERK pathway, is hyperactivated in a variety of tumor cell types due to mutations in upstream targets. It plays a key role in the proliferation, differentiation and survival of tumor cells.

• Erk1/2 inhibitor jsi-1187 - An orally bioavailable inhibitor of the extracellular signal-regulated kinases 1 (ERK1) and 2 (ERK2), with potential antineoplastic activity. Upon oral administration, ERK1/2 inhibitor JSI-1187 specifically targets, binds to and inhibits the activity of the serine/threonine-protein kinases ERK1 and ERK2, thereby preventing the phosphorylation of ERK1/2 substrates and the activation of mitogen-activated protein kinase (MAPK)/ERK-mediated signal transduction pathways. This results in the inhibition of ERK-dependent proliferation and survival of tumor cells. The MAPK/ERK pathway, also known as the RAS/RAF/MEK/ERK pathway, is hyperactivated in a variety of tumor cell types due to mutations in upstream targets. It plays a key role in the proliferation, differentiation and survival of tumor cells.

• Erk1/2 inhibitor ko-947 - An inhibitor of the extracellular signal-regulated kinases (ERK) 1 and 2, with potential antineoplastic activity. Upon intravenous administration, KO-947 specifically binds to and inhibits both ERK 1 and 2, thereby preventing the activation of mitogen-activated protein kinase (MAPK)/ERK-mediated signal transduction pathways. This results in the inhibition of ERK-dependent tumor cell proliferation and survival. The MAPK/ERK pathway is often upregulated in a variety of tumor cell types and plays a key role in the proliferation, differentiation and survival of tumor cells.

• Erk1/2 inhibitor ly3214996 - An orally available inhibitor of extracellular signal-regulated kinase (ERK) 1 and 2, with potential antineoplastic activity. Upon oral administration, LY3214996 inhibits both ERK 1 and 2, thereby preventing the activation of mitogen-activated protein kinase (MAPK)/ERK-mediated signal transduction pathways. This results in the inhibition of ERK-dependent tumor cell proliferation and survival. The MAPK/ERK pathway is often upregulated in a variety of tumor cell types and plays a key role in tumor cell proliferation, differentiation and survival.

• Erlotinib - A quinazoline derivative with antineoplastic properties. Competing with adenosine triphosphate, erlotinib reversibly binds to the intracellular catalytic domain of epidermal growth factor receptor (EGFR) tyrosine kinase, thereby reversibly inhibiting EGFR phosphorylation and blocking the signal transduction events and tumorigenic effects associated with EGFR activation.

• Erlotinib hydrochloride - The hydrochloride salt of a quinazoline derivative with antineoplastic properties. Competing with adenosine triphosphate, erlotinib reversibly binds to the intracellular catalytic domain of epidermal growth factor receptor (EGFR) tyrosine kinase, thereby reversibly inhibiting EGFR phosphorylation and blocking the signal transduction events and tumorigenic effects associated with EGFR activation.

• Ertumaxomab - A murine monoclonal antibody with two antigen-recognition sites: one for CD3, an antigen expressed on mature T cells, and one for HER-2-neu, a tumor-associated antigen that promotes tumor growth. Ertumaxomab attaches to CD3-expressing T cells and HER-2-neu-expressing tumor cells, selectively cross-linking tumor and immunologic cells which results in the recruitment of cytotoxic T cells to the T cell/tumor cell aggregate.

• Erythrocyte-encapsulated l-asparaginase suspension - A suspension of erythrocytes encapsulating L-asparaginase with potential antineoplastic activity. Upon administration of erythrocyte-encapsulated L-asparaginase suspension, L-asparagine is hydrolyzed to L-aspartic acid and ammonia in plasma, thereby depleting tumor cells of asparagine. Due to low asparagine synthetase activity in tumor cells, de novo synthesis of asparagine is suppressed within tumor cells. Shortage of asparagine prevents synthesis of important proteins necessary for tumor cell growth. Encapsulation of asparaginase in erythrocytes decreases the immunogenicity of exogenous protein, enhances its circulation time and may limit toxicity.

• Esorubicin - A synthetic derivative of the anthracycline antineoplastic antibiotic doxorubicin with potential antineoplastic activity. Esorubicin intercalates into DNA and inhibits topoisomerase II, thereby inhibiting DNA replication and ultimately, interfering with RNA and protein synthesis. This agent exhibits less cardiotoxicity than the parent antibiotic doxorubicin, but may cause more severe myelosupression compared to other compounds within the anthracycline class.

• Esorubicin hydrochloride - A hydrochloride salt of esorubicin, a derivative of the anthracycline antineoplastic antibiotic doxorubicin, with potential antineoplastic activity. Esorubicin intercalates into DNA and inhibits topoisomerase II, thereby inhibiting DNA replication and ultimately, interfering with RNA and protein synthesis. This agent exhibits less cardiotoxicity than the parent antibiotic doxorubicin, but may cause more severe myelosupression compared to other compounds within the anthracycline class.

• Esperamicin a1 - An enediyne antineoplastic antibiotic hybrid containing an anthranilate moiety. Esperamicin A1 is isolated from the bacterium Actinomadura verrucosospora. The anthranilate component of esperamicin A1 intercalates DNA and the benzene diradical intermediate of the enediyne core binds to the minor groove of DNA, resulting in single- and double-stranded breaks in DNA and apoptosis.

• Essiac - An herbal formula containing burdock root (Arctium lappa), Turkey rhubarb root (Rheum palmatum), sheep sorrel (Rumex acetosella), and slippery elm bark (Ulmus fulva) with potential immunostimulating, anti-inflammatory and anti-tumor activities. The extract's chemical profile, their respective concentrations and the mechanism of action of Essiac are largely unknown due to the proprietary nature of the formula and product inconsistency. Several chemical classes in Essiac are consistently represented and may attribute to its therapeutic effect, including anthraquinone derivatives such as rhein and emodin, high molecular polysaccharides, and lignans such as arctigenin. However, all these chemicals are unlikely to occur in high concentrations in Essiac, and its potential therapeutic effect may be attributed to a potential synergistic effect of these various compounds.

• Estradiol valerate - The parenterally-administered synthetic valerate ester of estradiol, a steroid sex hormone vital to the maintenance of fertility and secondary sexual characteristics in females. As the primary, most potent estrogen hormone produced by the ovaries, estradiol binds to and activates specific nuclear receptors. This agent exhibits mild anabolic and metabolic properties, and increases blood coagulability.

• Estramustine - A synthetic molecule combining estradiol and nornitrogen mustard through a carbamate link. Estramustine and its major metabolite estramustine bind to microtubule-associated proteins (MAPs) and tubulin, thereby inhibiting microtubule dynamics and leading to anaphase arrest in a dose-dependent fashion. This agent also exhibits anti-androgenic effects.

• Estramustine phosphate sodium - The orally available disodium salt, monohydrate, of estramustine phosphate, a synthetic molecule that combines estradiol and nornitrogen mustard through a carbamate link. Estramustine and its major metabolite estramustine bind to microtubule-associated proteins (MAPs) and tubulin, thereby inhibiting microtubule dynamics and leading to anaphase arrest in a dose-dependent fashion. This agent also exhibits anti-androgenic effects.

• Estrogen receptor agonist gtx-758 - An orally available, nonsteroidal selective estrogen receptor (ER) alpha agonist with potential antineoplastic activity. Upon administration of GTx-758, this agent suppresses the secretion of the gonadotropins follicle-stimulating hormone (FSH) and luteinizing hormone (LH) by the pituitary gland through feedback inhibition. In males, the inhibition of LH secretion prevents the synthesis of androgens, including testosterone, by the testes. This may result in suppressed total serum testosterone to the levels observed in castration.

• Etalocib - A second-generation selective leukotriene B4 receptor (LTB4R) antagonist with potential antineoplastic activity. Although the exact underlying mechanism through which LY293111 exerts its effects has not been fully elucidated, this agent selectively binds to and blocks LTB4Rs, thereby inhibiting the downstream signalling pathway. LY29311 has been shown to induce apoptosis and inhibits cellular proliferation in LTB4R expressing cells, such as pancreatic cancer cells.

• Etanercept - A recombinant soluble dimeric fusion protein consisting of the extracellular ligand-binding region of recombinant human tumor necrosis factor (rhTNF) receptor attached to the constant (Fc) region of human immunoglobulin G (FcIgG). The receptor moiety of etanercept binds to circulating TNF (2 molecules of TNF per receptor) and inhibits its attachment to endogenous TNF cell surface receptors, thereby rendering TNF inactive and inhibiting TNF-mediated mechanisms of inflammation.

• Etanidazole - A 2-nitroimidazole with radiosensitizing properties. Etanidazole depletes glutathione and inhibits glutathione transferase, thereby enhancing the cytotoxicity of ionizing radiation. This agent may also be useful as an imaging agent for identifying hypoxic, drug-resistant regions of primary tumors or metastases.

• Etaracizumab - A humanized monoclonal IgG1 antibody directed against the vitronectin receptor alpha v beta 3 integrin. Etaracizumab blocks the binding of ligands, such as vitronectin, to alpha v beta 3 integrin, resulting in inhibition of angiogenesis and metastasis. Alpha v beta 3 integrin is a cell adhesion and signaling receptor that is expressed on the surface of tumor vessel endothelial cells, some tumor cells, and a number of other cell types.

• Etarotene - An ethylsulfonyl derivative of arotinoic acid with differentiation inducing and potential antineoplastic activities. Like other retinoic acid agents, etarotene binds to and activates retinoic acid receptors (RARs), thereby inducing changes in the expression of certain genes leading to cell differentiation and decreased cell proliferation in susceptible cells.

• Ethaselen - An orally bioavailable organoselenium inhibitor of thioredoxin reductase 1 (TrxR1), with potential antineoplastic activity. Upon oral administration, ethaselen specifically binds to the selenocysteine-cysteine redox pair in the C-terminal active site of TrxR1 and inhibits its activity, which may result in growth inhibition and the induction of apoptosis in TrxR1 overexpressing tumor cells. TrxR1, upregulated in many cancer cell types, plays a key role in various redox-dependent cellular pathways, regulates transcription factor activity, inhibits apoptosis, and promotes cell growth and survival.

• Ethinyl estradiol - A semisynthetic estrogen. Ethinyl estradiol binds to the estrogen receptor complex and enters the nucleus, activating DNA transcription of genes involved in estrogenic cellular responses. This agent also inhibits 5-alpha reductase in epididymal tissue, which lowers testosterone levels and may delay progression of prostatic cancer. In addition to its antineoplastic effects, ethinyl estradiol protects against osteoporosis. In animal models, short-term therapy with this agent has been shown to provide long-term protection against breast cancer, mimicking the antitumor effects of pregnancy.

• Ethylchlorformate - A substance used to treat tumor cells for synthesis of a tumor-specific immunotherapeutic agent, ethyl chloroformate polymerized tumor protein, for use in Immunotherapy.

• Ethylchlorformate vaccine - A tumor vaccine comprised of ethylchlorformate polymerized tumor protein, obtained by treating tumor cells with ethylchloroformate to produce a tumor-specific immunotherapeutic agent. (NCI)

• Ethyleneimine - A monofunctional alkylating agent with potential antineoplastic activity. Reacting with DNA mainly at guanine and adenine residues, ethylenimine alkylates DNA, thereby producing DNA interstrand crosslinks and DNA breaks, and interfering with DNA replication and cell division.

• Ethylnitrosourea - A nitrosourea with potential antineoplastic activity. Used experimentally as a mutagen and carcinogen, ethylnitrosourea alkylates DNA and proteins, thereby damaging DNA and inducing point mutations.

• Etidronate-cytarabine conjugate mbc-11 - A synthetic conjugate composed of the bisphosphonate etidronate linked to the cytostatic agent and antimetabolite cytarabine, with potential antineoplastic and antiresorptive activities. Upon intravenous administration of the etidronate-cytarabine conjugate MBC-11, the etidronate moiety targets bone and the two moieties are released upon hydrolysis. Etidronate binds to hydroxyapatite crystals in bone tissues and prevents its resorption. This prevents bone destruction and induces bone cell mineralization. In addition, the bone-targeting nature of this agent allows for the accumulation of cytarabine in bone tissue, where it is able to exert its antitumor effect locally by competing with cytidine for incorporation into DNA, thereby inhibiting DNA synthesis, while reducing systemic exposure. This leads to a destruction of bone-associated tumor cells, an inhibition of tumor cell proliferation and bone metastasis, and prevents tumor-mediated bone destruction.

• Etigilimab - A monoclonal antibody targeting the human co-inhibitory molecule and immune checkpoint inhibitor T-cell immunoreceptor with immunoglobulin (Ig) and immunoreceptor tyrosine-based inhibitory motif (ITIM) domains (TIGIT), with potential immune checkpoint inhibitory activity. Upon administration, etigilimab binds to TIGIT expressed on various immune cells, including T-cells, and prevents the interaction of TIGIT with its ligands CD112 (nectin-2; poliovirus receptor related-2; PVRL2) and CD155 (poliovirus receptor; PVR; nectin-like protein 5; NECL-5). This enhances the interaction of CD112 and CD155 with the costimulatory receptor CD226 (DNAX Accessory molecule-1; DNAM-1), which is expressed on immune cells, such as natural killer (NK) cells and CD8-positive T-cells, and leads to CD226 dimerization and CD226-mediated signaling. This activates the immune system to exert a T-cell-mediated immune response against cancer cells. TIGIT, a member of the Ig super family and an immune inhibitory receptor, plays a key role in the suppression of T-cell proliferation and activation; it is involved in tumor cell immune evasion and the inhibition of antiviral immune responses.

• Etirinotecan pegol - An extended-release (ER) formulation composed of irinotecan, which is a semisynthetic derivative of camptothecin and a topoisomerase I-inhibitor prodrug, that is conjugated, via a proprietary biodegradable ester-based linker, to polyethylene glycol (PEG), with antineoplastic activity. Upon administration of etirinotecan pegol (EP), the agent penetrates into the leaky tumor vasculature and accumulates in the tumor. The linker slowly hydrolyzes and releases irinotecan, which leads to sustained exposure of the tumor to irinotecan. In turn, irinotecan is converted to the biologically active metabolite 7-ethyl-10-hydroxy-camptothecin (SN38) by a carboxylesterase. SN38 inhibits topoisomerase I activity by stabilizing the cleavable complex of topoisomerase I and DNA; this results in DNA breaks that inhibit DNA replication and trigger apoptosis. Pegylation provides improved systemic exposure, increases drug penetration into tumors and decreases drug clearance, thereby increasing the duration of therapeutic effects while lowering the toxicity profile.

• Etoglucid - An epoxide compound with potential antineoplastic alkylating activity. Etoglucid is able to crosslink DNA via its epoxide group, resulting in disruption of DNA function and cell cycle arrest.

• Etoposide - A semisynthetic derivative of podophyllotoxin, a substance extracted from the mandrake root Podophyllum peltatum. Possessing potent antineoplastic properties, etoposide binds to and inhibits topoisomerase II and its function in ligating cleaved DNA molecules, resulting in the accumulation of single- or double-strand DNA breaks, the inhibition of DNA replication and transcription, and apoptotic cell death. Etoposide acts primarily in the G2 and S phases of the cell cycle.

• Etoposide phosphate - A phosphate salt of a semisynthetic derivative of podophyllotoxin. Etoposide binds to the enzyme topoisomerase II, inducing double-strand DNA breaks, inhibiting DNA repair, and resulting in decreased DNA synthesis and tumor cell proliferation. Cells in the S and G2 phases of the cell cycle are most sensitive to this agent.

• Etoposide toniribate - A prodrug of etoposide, a semisynthetic derivative of podophyllotoxin extracted from the mandrake root Podophyllum peltatum, with potential antineoplastic activity. Upon intravenous administration of etoposide toniribate, etoposide is released after enzymatic cleavage of CAP7.1 by specific carboxylesterases (CE) 1 and 2, which are upregulated in certain tumor cell types. Etoposide acts primarily in the G2 and S phases of the cell cycle. This drug binds to and inhibits topoisomerase II, an enzyme elevated in tumor cells. This results in the accumulation of double-strand DNA breaks, the inhibition of DNA replication and transcription and the induction of apoptotic cell death. The tumor-specific activation of etoposide increases its efficacy while lowering its systemic toxicity.

• Etoprine - A lipophilic, diaminopyrimidine folate antagonist with potential antineoplastic activity. Etoprine inhibits dihydrofolate reductase, resulting in decreased cellular folate metabolism. This may eventually result in a reduction of cellular growth and the induction of apoptosis. In addition, this agent inhibits histamine-N-methyltransferase, resulting in decreased histamine catabolism. Lipid-soluble etoprine is capable of crossing the blood-brain barrier.

• Etoricoxib - A synthetic, nonsteroidal anti-inflammatory drug (NSAID) with antipyretic, analgesic, and potential antineoplastic properties. Etoricoxib specifically binds to and inhibits the enzyme cyclooxygenase-2 (COX-2), resulting in inhibition of the conversion of arachidonic acid into prostaglandins. Inhibition of COX-2 may induce apoptosis and inhibit tumor cell proliferation and angiogenesis.

• Ets-family transcription factor inhibitor tk216 - A proprietary biologic that inhibits the transcriptional-promoting activity of E26 transformation-specific (Ets, E-twenty-six) family transcription factors, with potential antineoplastic activity. Although the exact mechanism(s) of action through which this agent exerts its effect has yet to be fully elucidated, upon administration, Ets-family transcription factor inhibitor TK216 inhibits transcriptional activation mediated by Ets family proteins, including the oncogenic Ewing sarcoma breakpoint region 1/Friend leukemia virus integration 1 (EWSR1/FLI1; EWS/FLI1) fusion protein. This agent may both inhibit the malignant downstream effects mediated by genomic rearrangements that result in the overexpression of Ets family transcription factors and decrease tumor cell growth and proliferation. A chromosomal translocation t(11;22)(q24;q12) fuses the EWSR1 gene and the FLI1 gene and encodes the EWSR1/FLI1 fusion protein, which is an oncoprotein expressed by peripheral primitive neuroectodermal (pPNET) tumors.

• Everolimus - A derivative of the natural macrocyclic lactone sirolimus with immunosuppressant and anti-angiogenic properties. In cells, everolimus binds to the immunophilin FK Binding Protein-12 (FKBP-12) to generate an immunosuppressive complex that binds to and inhibits the activation of the mammalian Target of Rapamycin (mTOR), a key regulatory kinase. Inhibition of mTOR activation results in the inhibition of T lymphocyte activation and proliferation associated with antigen and cytokine (IL-2, IL-4, and IL-15) stimulation and the inhibition of antibody production. (NCI05)

• Everolimus tablets for oral suspension - Tablets for oral suspension containing everolimus, a derivative of the natural macrocyclic lactone sirolimus, with immunosuppressive and antineoplastic activities. After suspension of the everolimus tablets in water and oral administration, this agent inhibits the activation of the serine/threonine kinase mammalian target of rapamycin (mTOR) by binding to mTOR's cytosolic receptor immunophilin FK Binding Protein-12 (FKBP-12). Inhibition of the mTOR complex may result in the inhibition of the phosphatidylinositol 3 kinase/Akt/mTOR pathway and an inhibition in the expression of vascular endothelial cell growth factor (VEGF) and hypoxia-inducible factor. Ultimately, this may result in decreased tumor cell proliferation and tumor angiogenesis. This pediatric formulation can dissolve easily in a small volume of water making it easier to swallow and is available in smaller dose increments thereby allowing for greater dosing flexibility.

• Evofosfamide - A hypoxia-activated prodrug of the cytotoxin bromo-isophosphoramide mustard (Br-IPM) conjugated with 2-nitroimidazole, with potential antineoplastic activity. When exposed to hypoxic conditions, such as those found in hypoxic tumors, the 2-nitroimidazole moiety of evofosfamide is reduced. This releases the DNA-alkylating Br-IPM moiety, which introduces intra- and inter-strand DNA crosslinks in nearby cells; the crosslinks inhibit both DNA replication and cell division, and may lead to apoptosis of cells in the tumor. The inactive form of the prodrug is stable under normoxic conditions, which may limit systemic toxicity.

• Ex vivo-activated autologous lymph node lymphocytes - Autologous human lymph node T-lymphocytes, with potential immunostimulatory and antineoplastic activity. Upon collection of immune cells from the tumor-draining lymph node, the human lymph node lymphocytes are activated with anti-CD3/anti-CD28 microbeads, cultured with recombinant, human interleukin-2 (IL-2), expanded and isolated ex vivo. Upon reintroduction into the patient, the ex vivo-activated autologous lymph node lymphocytes recognize and lyse the tumor cells.

• Ex vivo-expanded autologous t cells ima101 - A preparation of autologous cytotoxic T-lymphocytes, specifically recognizing certain tumor-associated antigens (TAAs), with potential antineoplastic activity. The endogenous T-cells are isolated, expanded ex vivo, and reintroduced back into the patient. Upon administration, the ex vivo-expanded autologous T-cells IMA101 target and kill tumor cells. The T-cells are analyzed beforehand for their ability to specifically recognize certain TAAs, based on a proprietary antigen warehouse.

• Ex vivo-expanded her2-specific t cells - T cells specific for the human epidermal growth factor receptor 2 (HER2) with potential immunopotentiating activity. T cells directed against HER2, overexpressed on many tumor cells, are collected from HER2-expressing tumor tissue, expanded ex vivo and, then re-introduced in the patient. Re-introduction of ex vivo-expanded HER2-specific T cells may enhance the cytotoxic T cell response against tumor cells overexpressing HER2, resulting in inhibition of tumor growth.

• Exatecan mesylate - A semisynthetic, water-soluble derivative of camptothecin with antineoplastic activity. Exatecan mesylate inhibits topoisomerase I activity by stabilizing the cleavable complex between topoisomerase I and DNA and inhibiting religation of DNA breaks, thereby inhibiting DNA replication and triggering apoptotic cell death. This agent does not require enzymatic activation and exhibits greater potency than camptothecin and other camptothecin analogues.

• Exatecan mesylate anhydrous - The anhydrous, mesylate salt form of exatecan, a semisynthetic, water-soluble derivative of camptothecin, with antineoplastic activity. Upon administration, exatecan mesylate inhibits topoisomerase I activity by stabilizing the cleavable complex between topoisomerase I and DNA and inhibiting re-ligation of DNA breaks, thereby inhibiting DNA replication and triggering apoptotic cell death.

• Exemestane - A synthetic androgen analogue. Exemestane binds irreversibly to and inhibits the enzyme aromatase, thereby blocking the conversion of cholesterol to pregnenolone and the peripheral aromatization of androgenic precursors into estrogens.

• Exicorilant - An orally available, selective glucocorticoid receptor (GR) antagonist, with potential antineoplastic activity. Upon oral administration, exicorilant competitively and selectively binds to GRs, inhibiting the activation of GR-mediated proliferative and anti-apoptotic gene expression pathways. The GR, a member of the nuclear receptor superfamily of ligand-dependent transcription factors, is overexpressed in certain tumor types and may be associated with tumor cell proliferation and treatment resistance. Inhibition of GR activity may potentially slow tumor cell growth and disease progression in certain cancers.

• Exisulind - An inactive metabolite of the nonsteroidal, anti-inflammatory agent sulindac. After oral administration, sulindac undergoes extensive biotransformation including irreversible oxidation to sulindac sulfone. Approximately, one half of an administered dose of sulindac is eliminated through the urine, mostly as the conjugated sulfone metabolite.

• Expanded/activated gamma delta t-cells - A preparation of gamma delta T-lymphocytes derived from donor T-cells that have been expanded and activated ex-vivo and further depleted of alpha and beta T-cell receptors (TCRs), with potential immunomodulating and antineoplastic activities. Upon administration, these expanded/activated gamma delta (EAGD) T-cells secrete interferon-gamma (IFN-g) and exert direct killing of tumor cells. In addition, these cells activate the immune system to exert a cytotoxic T-lymphocyte (CTL) response against tumor cells. Gamma delta T-lymphocytes play a key role in the activation of the immune system and do not require major histocompatibility complex (MHC)-mediated antigen presentation to exert their cytotoxic effect.

• Extended release flucytosine - An extended release (ER) oral tablet that contains flucytosine (5-FC), a fluorinated cytosine analog, with antifungal activity and potential anti-cancer activity. Following oral administration of ER 5-FC, the 5-FC is deaminated to its active metabolite 5-fluorouracil (5-FU). 5-FU replaces uracil during RNA synthesis, which consequently inhibits downstream protein synthesis. In addition, 5-FU is metabolized further to 5-fluorodeoxyuridylic acid monophosphate, which inhibits thymidylate synthetase. Inhibition of this enzyme interrupts nucleotide synthesis, DNA replication and cell proliferation. Negative regulation of protein synthesis, DNA replication and cell proliferation can lead to cell death. Following ingestion of ER 5-FC, intravenous injection of a retroviral vector encoding cytosine deaminase (TC 511) at a tumor site may result in higher local concentrations of 5-FU and its metabolites, and increased tumor cell death than other 5-FU treatment regimens.

• Extended release metformin hydrochloride - An extended-release (ER) tablet composed of the hydrochloride salt form of the biguanide metformin, with antihyperglycemic and potential prostate-cancer protective and antineoplastic activities. Upon oral administration, metformin targets and inhibits complex I (NADPH:ubiquinone oxidoreductase) of the mitochondrial respiratory chain and increases the cellular adenosine monophosphate (AMP) to adenosine triphosphate (ATP) ratio leading to activation of AMP-activated protein kinase (AMPK). This modulates AMPK-mediated transcription of target genes, which prevents hepatic gluconeogenesis, decreases intestinal absorption of glucose, enhances insulin sensitivity and fatty acid oxidation, and increases glucose uptake and utilization in target tissues. This lowers blood glucose levels. Metformin may exert antineoplastic effects through AMPK-mediated or AMPK-independent inhibition of mammalian target of rapamycin (mTOR), which is up-regulated in many cancer tissues. It also reduces cyclin D1. This inhibits cancer cell proliferation. Furthermore, this agent also inhibits tumor cell migration and invasion by inhibiting matrix metalloproteinase-9 (MMP-9) expression which is mediated through the suppression of transcription activator protein-1 (AP-1) activation. Also, metformin reduces hyperinsulinemia which may contribute to an anti-tumor effect. Metformin may increase the prostate-specific antigen (PSA) doubling time and may lower serum PSA levels.

• Extended-release onapristone - An extended-release (ER) formulation of onapristone, an orally bioavailable progesterone receptor (PR) antagonist, with antineoplastic activity. Onapristone binds to the PR and inhibits both PR activation and the associated expression of PR-responsive genes. This may inhibit PR-mediated proliferative effects in cancer cells overexpressing PR. PR is expressed on certain cancer cell types and plays a key role in proliferation and survival.

• Ezabenlimab - A monoclonal antibody directed against the negative immunoregulatory human cell surface receptor programmed cell death protein 1 (PD-1; PDCD1), with immune checkpoint inhibitory and antineoplastic activities. Upon administration, ezabenlimab selectively binds to and blocks the activation of PD-1, an immunoglobulin (Ig) superfamily transmembrane protein, by its ligands programmed cell death ligand 1 (PD-L1), which is overexpressed on certain cancer cells, and programmed cell death ligand 2 (PD-L2), which is primarily expressed on antigen-presenting cells (APCs). This results in the activation of T-cells and T-cell-mediated immune responses against tumor cells. Activated PD-1 negatively regulates T-cell activation and plays a key role in in tumor evasion from host immunity.

• Ezh1/2 inhibitor hh2853 - An orally bioavailable inhibitor of the histone lysine methyltransferases enhancer of zeste homolog 1 (EZH1) and 2 (EZH2), with potential antineoplastic activity. Upon oral administration, EZH1/2 inhibitor HH2853 inhibits the activity of both wild-type and mutated forms of EZH1 and EZH2. Inhibition of EZH1/2 specifically prevents the methylation of lysine 27 on histone H3 (H3K27). This decrease in histone methylation alters gene expression patterns associated with cancer pathways, enhances transcription of certain target genes, and results in decreased proliferation of EZH1/2-expressing cancer cells. EZH1/2, histone lysine methyltransferase (HMT) class enzymes and catalytic subunits of the polycomb repressive complex 2 (PRC2), are overexpressed or mutated in a variety of cancer cells and play key roles in tumor cell proliferation, progression, stem cell self-renewal and migration.

• Ezh2 inhibitor - Any agent that inhibits the histone lysine methyltransferase EZH2.

• Ezh2 inhibitor cpi-0209 - An orally available selective inhibitor of the histone lysine methyltransferase (HMT) enhancer of zeste homolog 2 (EZH2), with potential antineoplastic activity. Upon oral administration, EZH2 inhibitor CPI-0209 selectively targets, binds to and inhibits the activity of EZH2. Inhibition of EZH2 specifically prevents the methylation of histone H3 on lysine 27 (H3K27). This decrease in histone methylation alters gene expression patterns associated with cancer pathways and results in decreased proliferation of EZH2-expressing cancer cells. EZH2, an HMT class enzyme and the catalytic subunit of the polycomb repressive complex 2 (PRC2), is overexpressed or mutated in a variety of cancer cells and plays a key role in tumor cell proliferation; its expression is correlated with tumor initiation, progression, stem cell self-renewal, migration and angiogenesis.

• Ezh2 inhibitor cpi-1205 - An orally available selective inhibitor of the histone lysine methyltransferase EZH2, with potential antineoplastic activity. Upon oral administration, CPI-1205 selectively inhibits the activity of both wild-type and mutated forms of EZH2. Inhibition of EZH2 specifically prevents the methylation of histone H3 on lysine 27 (H3K27). This decrease in histone methylation alters gene expression patterns associated with cancer pathways and results in decreased proliferation of EZH2-expressing cancer cells. EZH2, a histone lysine methyltransferase (HMT) class enzyme and the catalytic subunit of the polycomb repressive complex 2 (PRC2), is overexpressed or mutated in a variety of cancer cells and plays a key role in tumor cell proliferation; its expression is correlated with tumor initiation, progression, stem cell self-renewal, migration and angiogenesis.

• Ezh2 inhibitor pf-06821497 - An orally available selective inhibitor of the histone lysine methyltransferase (HMT) enhancer of zeste homolog 2 (EZH2), with potential antineoplastic activity. Upon oral administration, EZH2 inhibitor PF-06821497 selectively targets, binds to and inhibits the activity of EZH2. Inhibition of EZH2 specifically prevents the methylation of histone H3 on lysine 27 (H3K27). This decrease in histone methylation alters gene expression patterns associated with cancer pathways and results in decreased proliferation of EZH2-expressing cancer cells. EZH2, an HMT class enzyme and the catalytic subunit of the polycomb repressive complex 2 (PRC2), is overexpressed or mutated in a variety of cancer cells and plays a key role in tumor cell proliferation; its expression is correlated with tumor initiation, progression, stem cell self-renewal, migration and angiogenesis.

• Ezh2 inhibitor shr2554 - An orally available selective inhibitor of the histone lysine methyltransferase (HMT) enhancer of zeste homolog 2 (EZH2), with potential antineoplastic activity. Upon oral administration, EZH2 inhibitor SHR2554 selectively targets, binds to and inhibits the activity of EZH2. Inhibition of EZH2 specifically prevents the methylation of histone H3 on lysine 27 (H3K27). This decrease in histone methylation alters gene expression patterns associated with cancer pathways and results in decreased proliferation of EZH2-expressing cancer cells. EZH2, an HMT class enzyme and the catalytic subunit of the polycomb repressive complex 2 (PRC2), is overexpressed or mutated in a variety of cancer cells and plays a key role in tumor cell proliferation; its expression is correlated with tumor initiation, progression, stem cell self-renewal, migration and angiogenesis.

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