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Antineoplastic agents i

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  • I 131 antiferritin immunoglobulin - A radioimmunoconjugate of a rabbit antihuman ferritin IgG labeled with iodine 131 (I-131). Using anti-ferritin IgG as a carrier for I-131 may result in the targeted imaging and/or destruction of cells expressing ferritin. Observed in 35% to 100% of patients with hepatocellular carcinoma, high serum ferritin levels may be due to ferritin production by the tumor cells, or related to the associated iron overload and/or cirrhosis.
  • I 131 monoclonal antibody a33 - A radioimmunoconjugate of a humanized monoclonal antibody (MoAb) A33 labelled with Iodine 131 (I-131). MoAb A33 recognizes A33 antigen, a 43 KDa transmembrane glycoprotein of the immunoglobulin superfamily, highly and homogenously expressed in 95% of colorectal cancers, with only restricted expression in normal colonic mucosa. Using MoAb A33 as a carrier for I-131 results in the targeted imaging and/or destruction of cells expressed A33 antigen.
  • I 131 monoclonal antibody cc49 - A radioimmunoconjugate of the humanized monoclonal antibody CC49 labeled with iodine I 131. Iodine I 131 monoclonal antibody CC49 delivers beta and gamma radiation-emitting I 131 radionuclide specifically to tumor cells that express tumor-associated glycoprotein (TAG)-72, allowing localization of TAG-72-expressing tumor cells with radioimaging devices in diagnostic applications or resulting in specific TAG-72-expressing tumor cell radiocytotoxicity in therapeutic applications. Monoclonal antibody CC49 binds to TAG-72, a pancarcinoma antigen, with high affinity.
  • I 131 monoclonal antibody f19 - A radioimmunoconjugate of a murine monoclonal antibody (MoAb) F19 labelled with Iodine 131 (I-131). MoAb F19 was raised against fibroblast activation protein (FAP), which is highly expressed by tumor stromal cells. Using MoAb F19 as a carrier for I-131 results in the targeted imaging and/or destruction of cells overexpressed FAP.
  • I 131 monoclonal antibody lym-1 - A radioimmunoconjugate of a murine monoclonal antibody, MoAb Lym-1, labeled with iodine 131 (I-131). MoAb Lym-1 recognizes an epitope of the histocompatibility antigen HLA-DR, which is over-expressed on most B-cell lymphomas. I-131 MoAb Lym-1 delivers beta and gamma radiation emitting I-131 nuclide directly to tumor cells that express HLA-DR, thereby allowing imaging and/or treatment of cancers.
  • Iadademstat - An orally available inhibitor of lysine specific histone demethylase 1 (KDM1A; LSD1), with potential antineoplastic activity. Upon administration, iadademstat binds to and inhibits LSD1, a demethylase that suppresses the expression of target genes by converting the di- and mono-methylated forms of lysine at position 4 of histone H3 (H3K4) to mono- and unmethylated H3K4, respectively. LSD1 inhibition enhances H3K4 methylation and increases the expression of tumor suppressor genes. This may lead to an inhibition of cell growth in LSD1-overexpressing tumor cells. In addition, LSD1 demethylates mono- or di-methylated H3K9, which increases gene expression of tumor promoting genes; inhibition of LSD1 promotes H3K9 methylation and decreases transcription of these genes. LSD1, an enzyme belonging to the flavin adenine dinucleotide (FAD)-dependent amine oxidase family, is overexpressed in certain tumor cells and plays a key role in in the regulation of gene expression, tumor cell growth and survival.
  • Ianalumab - A fully human combinatorial antibody library (HuCAL)-derived monoclonal antibody targeting the B-cell-activating factor receptor (BAFF-R), with potential anti-inflammatory and antineoplastic activities. Upon administration, ianalumab targets and binds to BAFF-R, which inhibits both BAFF/BAFF-R interaction and BAFF-R-mediated signaling. This may decrease cell growth in tumor cells expressing BAFF-R. BAFF-R, also known as tumor necrosis factor receptor superfamily member 13C, is overexpressed in certain tumor cell types and autoimmune diseases. In cancer cells, BAFF-R plays a key role in B-cell proliferation and survival. VAY736 was developed using HuCAL technology.
  • Iap inhibitor apg-1387 - A small molecule, second mitochondria-derived activator of caspases (SMAC)-mimetic targeting inhibitor of apoptosis proteins (IAPs) with potential apoptosis-inducing and antineoplastic activities. Upon administration, IAP inhibitor APG-1387 selectively binds to and inhibits the activity of IAPs including X chromosome-linked IAP (XIAP) and cellular IAPs 1 (c-IAP1) and 2 (c-IAP2). This may restore and promote the induction of apoptosis through apoptotic signaling pathways and enhance proteasomal degradation of IAPs. Additionally, APG-1387 may work synergistically with cytotoxic drugs to overcome tumor cell resistance to apoptosis. IAPs are overexpressed by many cancer cell types, suppressing apoptosis by binding and inhibiting active caspases-3, -7 and -9 via their BIR (baculoviral lAP repeat) domains.
  • Iap inhibitor hgs1029 - The hydrochloride salt of a small-molecule inhibitor of IAP (Inhibitor of Apoptosis Protein) family proteins with potential antineoplastic activity. IAP inhibitor HGS1029 selectively inhibits the biological activity of IAP proteins, which may restore apoptotic signaling pathways; this agent may work synergistically with cytotoxic drugs to overcome tumor cell resistance to apoptosis. IAPs are overexpressed by many cancer cell types, suppressing apoptosis by binding and inhibiting active caspases-3, -7 and -9 via their BIR (baculoviral lAP repeat) domains.
  • Iapa-based dendritic cells/cytotoxic t lymphocytes - A cell-based product composed of dendritic cells (DCs) pulsed with tumor-associated antigens (TAAs) and devoid of the inhibitory effect of antigen presentation attenuators (iAPA) combined with cytotoxic T-lymphocytes (CTLs) (iAPA-DC/CTL), with potential immunostimulating and antineoplastic activities. DCs are transduced with a viral vector containing small interfering RNAs (siRNAs) against APAs, which prevents the expression of APA genes and inhibits attenuation of antigen presentation. Upon administration of iAPA-DC/CTL, the DCs are able to efficiently present antigens to the immune system, stimulate the immune system against tumor-associated antigens (TAAs) and hyperactivate TAA-specific CTLs and T-helper cells. Also, the iAPA-based DCs inhibit the activity of the T-regulatory cells (Tregs), thereby abrogating their negative effect on CTL activation and preventing their immunosuppressive activity against TAAs. Altogether, this inhibits tumor cell proliferation. Additionally, the administered CTLs induce direct cancer cell lysis. APAs negatively regulate antigen presentation, activate Tregs and their immunosuppressive activity, affect inflammatory cytokine production by DCs, and negatively regulate the immunostimulatory activity of DCs; they have an overall inhibitory effect on the stimulation of the immune system.
  • Ibandronate sodium - The sodium salt form of ibandronic acid, a synthetic nitrogen-containing bisphosphonate. Ibandronic acid inhibits farnesyl pyrophosphate synthase, resulting in a reduction in geranylgeranyl GTPase signaling proteins and apoptosis of osteoclasts. This agent increases bone mineral density, decreases bone remodeling, inhibits osteoclast-mediated bone resorption, and reduces metastases-related and corticosteroid-related bone pain.
  • Iberdomide - A modulator of the E3 ubiquitin ligase complex containing cereblon (CRL4-CRBN E3 ubiquitin ligase), with immunomodulating and pro-apoptotic activities. Upon administration, iberdomide specifically binds to the cereblon (CRBN) part of the ligase complex, thereby affecting the ubiquitin E3 ligase activity, and targeting certain substrate proteins for ubiquitination. This induces the proteasome-mediated degradation of certain transcription factors, including Ikaros (IKZF1) and Aiolos (IKZF3) which are transcriptional repressors in T-cells. This leads to a reduction of their protein levels, and the modulation of the immune system, including activation of T-lymphocytes. In addition, this leads to a downregulation of other proteins, including interferon regulatory factor 4 (IRF4), which plays a key role in the proliferation of certain cancer cell types. CRBN, the substrate recognition component of the E3 ubiquitin ligase complex, plays a key role in the ubiquitination of certain proteins.
  • Iboctadekin - A recombinant therapeutic agent which is chemically identical to or similar to the endogenous cytokine interleukin-18 (IL-18). Produced primarily by macrophages, IL-18 induces the production of interferon-gamma (IFN-gamma), and enhances the activity of natural killer (NK) and cytotoxic T lymphocytes (CTL). As a potential immunotherapeutic agent, iboctadekin displays antitumor effects in vitro and in animal models.
  • Ibritumomab tiuxetan - An immunoconjugate of the monoclonal antibody ibritumomab conjugated with the linker-chelator tiuxetan, a high affinity, conformationally restricted chelation site for radioisotopes. When bound to indium In 111 or yttrium Y 90, ibritumomab tiuxetan, targeting the CD20 antigen on B cell surfaces, specifically delivers a potentially cytotoxic dose of radiation to B lymphocytes. Ibritumomab is a murine IgG1 kappa monoclonal antibody directed against the CD20 antigen, which is found on the surface of normal and malignant B lymphocytes.
  • Ibrutinib - An orally bioavailable, small-molecule inhibitor of Bruton's tyrosine kinase (BTK) with potential antineoplastic activity. Upon oral administration, ibrutinib binds to and irreversibly inhibits BTK activity, thereby preventing both B-cell activation and B-cell-mediated signaling. This leads to an inhibition of the growth of malignant B cells that overexpress BTK. BTK, a member of the src-related BTK/Tec family of cytoplasmic tyrosine kinases, is required for B cell receptor signaling, plays a key role in B-cell maturation, and is overexpressed in a number of B-cell malignancies. The expression of BTK in tumor cells is also associated with increased proliferation and survival.
  • Ic9-gd2-cd28-ox40-expressing t lymphocytes - Modified T-lymphocytes expressing a 3rd generation chimeric antigen receptor (CAR) specific for the disialoganglioside GD2, which contains the CD3zeta chain, the signaling domains of the co-stimulatory molecules CD28 and CD134 (OX-40) and the suicide gene inducible caspase 9 (iCasp9), with potential immunomodulating and antineoplastic activities. Upon administration, iC9-GD2-CD28-OX40-expressing T lymphocytes target the GD2 antigen on tumor cells, thereby providing selective toxicity towards GD2-expressing tumor cells. iCasp9 consists of a human FK506 drug-binding domain with an F36V mutation (FKBP12-F36V) linked to human caspase 9. If the administered T cells lead to unacceptable side effects, the chemical homodimerizer AP1903 can be administered, which binds to the drug binding FKBP12-F36V domain and activates caspase 9, resulting in the apoptosis of the administered T-cells. The tumor associated antigen GD2 is overexpressed on the surface of almost all tumors of neuroectodermal origin. OX40 and CD28, both T-cell surface-associated co-stimulatory molecules, are required for full T-cell activation.
  • Icotinib hydrochloride - The hydrochloride salt form of icotinib, an orally available quinazoline-based inhibitor of epidermal growth factor receptor (EGFR), with potential antineoplastic activity. Icotinib selectively inhibits the wild-type and several mutated forms of EGFR tyrosine kinase. This may lead to an inhibition of EGFR-mediated signal transduction and may inhibit cancer cell proliferation. EGFR, a receptor tyrosine kinase, has been upregulated in a variety of cancer cell types.
  • Icrucumab - A fully human IgG1 monoclonal antibody directed against human vascular endothelial growth factor receptor 1 (VEGFR-1/FLT-1) with potential antiangiogenesis and antineoplastic activities. Icrucumab specifically binds to and inhibits the activity of VEGFR-1, which may prevent the activation of downstream signaling pathways and so inhibit tumor angiogenesis; the subsequent reduction in tumor nutrient supply may inhibit tumor cell proliferation. Tumor cell overexpression of VEGFR-1 may be associated with tumor angiogenesis and tumor cell proliferation and invasion; VEGFR-1 may modulate VEGFR-2 signaling.
  • Ict-121 dendritic cell vaccine - A cell-based cancer vaccine composed of autologous dendritic cells (DCs) pulsed with purified peptides derived from the tumor-associated antigen (TAA) CD133, with potential immunostimulatory and antineoplastic activities. Upon leukapheresis, monocytes are differentiated into DCs and are mixed with the CD133 peptides. Upon intradermal re-administration of the ICT-121 DC vaccine, the DCs present the CD133 peptides to the immune system, which stimulates the immune system to induce a specific cytotoxic T-lymphocyte (CTL) response against CD133-expressing tumor cells and leads to tumor cell lysis. CD133 is overexpressed on various types of cancer cells; its overexpression is correlated with increased resistance to chemotherapy.
  • Idarubicin - A semisynthetic 4-demethoxy analogue of the antineoplastic anthracycline antibiotic daunorubicin. Idarubicin intercalates into DNA and interferes with the activity of topoisomerase II, thereby inhibiting DNA replication, RNA transcription and protein synthesis. Due to its high lipophilicity, idarubicin penetrates cell membranes more efficiently than other anthracycline antibiotic compounds.
  • Idarubicin hydrochloride - The hydrochloride salt of the anthracycline antineoplastic antibiotic idarubicin. Idarubicin intercalates into DNA and inhibits topoisomerase II, thereby inhibiting DNA replication and ultimately, interfering with RNA and protein synthesis. Due to its high lipophilicity, idarubicin penetrates cell membranes more efficiently than other anthracycline antibiotic compounds
  • Idarubicin-eluting beads - A sustained-release drug delivery embolization system containing small polymeric beads impregnated with the anthracycline antibiotic idarubicin with potential antineoplastic activity. The beads consist of polyvinyl alcohol (PVA) microspheres modified with sulfonic acid groups and loaded with idarubicin. During transarterial chemoembolization (TACE) in the hepatic artery, idarubicin-eluting beads embolize to the tumor vasculature, occlude tumor blood vessels and induce ischemic necrosis of tumor tissue due to mechanical blockage of the tumor vasculature. Simultaneously, idarubicin-eluting beads release cytotoxic idarubicin locally and in a sustained manner. This may result in idarubicin-mediated inhibition of tumor cell proliferation.
  • Idasanutlin - An orally available, small molecule, antagonist of MDM2 (mouse double minute 2; Mdm2 p53 binding protein homolog), with potential antineoplastic activity. Idasanutlin binds to MDM2 blocking the interaction between the MDM2 protein and the transcriptional activation domain of the tumor suppressor protein p53. By preventing the MDM2-p53 interaction, p53 is not enzymatically degraded and the transcriptional activity of p53 is restored. This may lead to p53-mediated induction of tumor cell apoptosis. MDM2, a zinc finger nuclear phosphoprotein and negative regulator of the p53 pathway, is often overexpressed in cancer cells and has been implicated in cancer cell proliferation and survival.
  • Idecabtagene vicleucel - A preparation of autologous peripheral blood T-lymphocytes (PBTLs) that have been genetically modified to express a chimeric antigen receptor (CAR) specific for the B-cell maturation antigen (BCMA), with potential immunostimulating and antineoplastic activities. Upon administration, idecabtagene vicleucel specifically recognizes and kills BCMA-expressing tumor cells. BCMA, a tumor-specific antigen and a receptor for both a proliferation-inducing ligand (APRIL) and B-cell activating factor (BAFF), is a member of the tumor necrosis factor receptor superfamily (TNFRSF) and plays a key role in plasma survival; it is found on the surfaces of plasma cells and overexpressed on malignant plasma cells.
  • Idelalisib - An orally bioavailable, small molecule inhibitor of the delta isoform of the 110 kDa catalytic subunit of class I phosphoinositide-3 kinase (PI3K) with potential immunomodulating and antineoplastic activities. Idelalisib inhibits the production of the second messenger phosphatidylinositol-3,4,5-trisphosphate (PIP3), preventing the activation of the PI3K signaling pathway and inhibiting tumor cell proliferation, motility, and survival. Unlike other isoforms of PI3K, PI3K-delta is expressed primarily in hematopoietic lineages. The targeted inhibition of PI3K-delta is designed to preserve PI3K signaling in normal, non-neoplastic cells.
  • Idetrexed - An alpha-folate receptor (aFR)-mediated inhibitor of thymidylate synthase (TS), with potential antineoplastic activity. Upon intravenous infusion, idetrexed selectively targets and binds to aFR-expressing tumor cells. Upon uptake by aFR, this agent binds to and inhibits TS. This reduces thymine nucleotide synthesis, inhibits both DNA synthesis and cell division, and leads to tumor cell apoptosis. TS catalyzes the conversion of deoxyuridine monophosphate (dUMP) to deoxythymidine monophosphate (dTMP), an essential precursor for DNA synthesis, and plays a key role in cell growth and division. aFR, a cell-surface receptor glycoprotein, is overexpressed on various tumor cell types, but is minimally expressed by normal, healthy tissue.
  • Idh1 mutant inhibitor ly3410738 - An orally available inhibitor of mutant form of the isocitrate dehydrogenase type 1 (IDH1; IDH-1; IDH1 [NADP+] soluble), including the substitution mutation at arginine (R) in position 132, IDH1(R132), with potential antineoplastic activity. Upon oral administration, IDH1 mutant inhibitor LY3410738 specifically and covalently binds to and modifies a single cysteine (Cys269) in the allosteric binding pocket of mutant forms of IDH1, thereby inactivating IDH1. This inhibits the formation of the oncometabolite 2-hydroxyglutarate (2HG) from alpha-ketoglutarate (a-KG). This depletes 2-HG levels, prevents 2HG-mediated signaling and leads to both an induction of cellular differentiation and an inhibition of cellular proliferation in tumor cells expressing mutant forms of IDH1. In addition, LY3410738 has the ability to cross the blood-brain barrier (BBB). IDH1 mutations, including IDH1(R132) mutations, are highly expressed in certain malignancies, including gliomas; they initiate and drive cancer growth by both blocking cell differentiation and catalyzing the formation of 2HG.
  • Idh1(r132) inhibitor idh305 - An inhibitor of the citric acid cycle enzyme isocitrate dehydrogenase [NADP] cytoplasmic (isocitrate dehydrogenase 1; IDH1) with mutations at residue R132 (IDH1(R132)), with potential antineoplastic activity. Upon administration, IDH305 specifically inhibits IDH1(R132) mutant forms in the cytoplasm, which inhibits the formation of the oncometabolite 2-hydroxyglutarate (2HG). This may lead to both an induction of cellular differentiation and an inhibition of cellular proliferation in IDH1(R132)-expressing tumor cells. IDH1(R132) mutations are highly expressed in certain malignancies, including gliomas; they initiate and drive cancer growth by both blocking cell differentiation and catalyzing the formation of 2HG.
  • Idh1r132h mutation-targeting idh1 peptide vaccine - A peptide vaccine consisting of a 20-mer peptide derived from isocitrate dehydrogenase type 1 (IDH1) containing the point mutation R132H (IDH1R132H), with potential antineoplastic activity. Upon subcutaneous vaccination with the IDH1R132H mutation-targeting IDH1 peptide vaccine, the vaccine stimulates the host immune system to mount a cytotoxic T-lymphocyte (CTL) response against tumor cells that express the IDH1R132H protein. R132H is a point mutation, which contains an amino acid substitution where arginine is replaced by histidine at position 132 of IDH1, and is highly expressed in gliomas as well as other tumor types; this mutation is associated with increased production of the oncometabolite R-2-hydroxyglutarate (2HG).
  • Idh1r132h-specific peptide vaccine pepidh1m - A peptide vaccine consisting of a peptide derived from isocitrate dehydrogenase 1 (IDH1) containing the point mutation R132H (IDH1R132H), with potential antineoplastic activity. Intradermal vaccination with the IDH1R132H-specific peptide vaccine PEPIDH1M may stimulate the host immune system to mount a cytotoxic T lymphocyte (CTL) response against tumor cells that express the IDH1R132H protein. The IDH1 point mutation of amino acid residue 132 is highly expressed in gliomas and is associated with increased production of the oncometabolite R-2-hydroxyglutarate (2HG).
  • Idiotype-pulsed autologous dendritic cell vaccine apc8020 - A cell-based cancer vaccine composed of autologous dendritic cells (DCs) pulsed with tumor-derived clonal immunoglobulin (Ig) with potential immunostimulatory and antineoplastic activities. Upon administration, idiotype-pulsed autologous dendritic cell vaccine APC8020, containing idiotype (Id) protein structures that can be recognized by antibodies and by CD41 T lymphocytes and CD81 T lymphocytes, may stimulate antitumoral cytotoxic T lymphocyte (CTL) and antibody responses against Id-expressing tumor cells. The Id represents the unique antigenic determinants in the variable regions of the clonal Ig.
  • Ido peptide vaccine io102 - A second-generation peptide vaccine derived from the immunomodulatory enzyme indoleamine 2,3-dioxygenase (IDO) with potential immunomodulating and antineoplastic activities. Vaccination with IDO peptide vaccine IO102 may activate the immune system to induce an immune response against IDO-expressing tumor cells. This may restore the proliferation and activation of various immune cells including cytotoxic T-lymphocytes (CTLs), natural killer cells (NKs), and dendritic cells (DCs), and may eradicate IDO-expressing tumor cells through a CTL-mediated response. IDO, a cytosolic enzyme responsible for tryptophan catabolism and conversion of tryptophan into kynurenine, is overexpressed by a variety of tumor cell types and antigen presenting cells (APCs) and plays an important role in immunosuppression mainly through suppression of CTL activation.
  • Ido/tdo inhibitor hti-1090 - An orally available inhibitor of indoleamine 2,3-dioxygenase 1 (IDO1; IDO-1) and the kynurenine-producing hepatic enzyme tryptophan 2,3-dioxygenase (TDO), with potential immunomodulating and antineoplastic activities. Upon administration, IDO1/TDO inhibitor HTI-1090 specifically targets and binds to both IDO1, a cytosolic enzyme responsible for the oxidation of the amino acid tryptophan into the immunosuppressive metabolite kynurenine, and TDO, a hepatic enzyme catalyzing the first step of tryptophan degradation. By inhibiting IDO1 and TDO, HTI-1090 decreases kynurenine levels in tumor cells, restores tryptophan and promotes the proliferation and activation of various immune cells, including dendritic cells (DCs), natural killer (NK) cells and T-lymphocytes. This reduces the number of tumor-associated regulatory T-cells (Tregs) and activates the immune system to induce a cytotoxic T-lymphocyte (CTL) response against the IDO1/TDO-expressing tumor cells, thereby inhibiting the growth of the tumor cells. IDO1 and TDO, both overexpressed by multiple tumor cell types, play important roles in immunosuppression and the promotion of tumor cell survival and proliferation. Tryptophan depletion inhibits T-lymphocyte proliferation and activation, and subsequently suppresses the immune system.
  • Ido/tdo inhibitor ly-01013 - An orally bioavailable, small-molecule inhibitor of indoleamine 2,3-dioxygenase 1 (IDO1; IDO-1) and the kynurenine-producing hepatic enzyme tryptophan 2,3-dioxygenase (TDO), with potential immunomodulating and antineoplastic activities. Upon administration, IDO1/TDO inhibitor LY-01013 specifically targets and binds to both IDO1, a cytosolic enzyme responsible for the oxidation of the amino acid tryptophan into the immunosuppressive metabolite kynurenine, and TDO, a hepatic enzyme catalyzing the first step of tryptophan degradation. By inhibiting IDO1 and TDO, LY-01013 decreases kynurenine levels in tumor cells, restores tryptophan and promotes the proliferation and activation of various immune cells, including dendritic cells (DCs), natural killer (NK) cells and T-lymphocytes. This reduces the number of tumor-associated regulatory T-cells (Tregs) and activates the immune system to induce a cytotoxic T-lymphocyte (CTL) response against the IDO1/TDO-expressing tumor cells, thereby inhibiting the growth of the tumor cells. IDO1 and TDO, both overexpressed by multiple tumor cell types, play important roles in immunosuppression and the promotion of tumor cell survival and proliferation. Tryptophan depletion inhibits T-lymphocyte proliferation and activation, and subsequently suppresses the immune system.
  • Ido1 inhibitor khk2455 - An orally available inhibitor of indoleamine 2,3-dioxygenase 1 (IDO1), with potential immunomodulating and antineoplastic activities. Upon administration, IDO1 inhibitor KHK2455 targets and binds to IDO1, an enzyme responsible for the oxidation of tryptophan into kynurenine. By inhibiting IDO1 and decreasing kynurenine in tumor cells, KHK2455 increases and restores the proliferation and activation of various immune cells, including dendritic cells (DCs), natural killer (NK) cells, and T-lymphocytes. KHK2455 also induces increased interferon (IFN) production, and causes 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, a cytosolic enzyme responsible for tryptophan catabolism and the conversion of tryptophan into kynurenine, is overexpressed by a variety of tumor cell types and antigen presenting cells (APCs); it plays an important role in immunosuppression. Tryptophan depletion inhibits T-lymphocyte proliferation and activation, and subsequently suppresses the immune system.
  • Ido-1 inhibitor ly3381916 - An orally available inhibitor of indoleamine 2,3-dioxygenase 1 (IDO1; IDO-1), with potential immunomodulating and antineoplastic activities. Upon administration, IDO1 inhibitor LY3381916 specifically targets and binds to IDO1, a cytosolic enzyme responsible for the oxidation of the amino acid tryptophan into the immunosuppressive metabolite kynurenine. By inhibiting IDO1 and decreasing kynurenine in tumor cells, LY3381916 restores and promotes the proliferation and activation of various immune cells, including dendritic cells (DCs), natural killer (NK) cells, and T-lymphocytes, and causes a reduction in tumor-associated regulatory T-cells (Tregs). Activation of the immune system, which is suppressed in many cancers, may induce a cytotoxic T-lymphocyte (CTL) response against the IDO1-expressing tumor cells, thereby inhibiting the growth of IDO1-expressing tumor cells. IDO1, overexpressed by multiple tumor cell types, plays an important role in immunosuppression. Tryptophan depletion inhibits T-lymphocyte proliferation and activation, and subsequently suppresses the immune system.
  • Ido1 inhibitor mk-7162 - An orally available inhibitor of indoleamine 2,3-dioxygenase 1 (IDO1), with potential immunomodulating and antineoplastic activities. Upon administration, IDO1 inhibitor MK-7162 specifically targets and binds to IDO1, a cytosolic enzyme responsible for the oxidation of the amino acid tryptophan into the immunosuppressive metabolite kynurenine. By inhibiting IDO1 and decreasing kynurenine in tumor cells, MK-7162 restores and promotes the proliferation and activation of various immune cells, including dendritic cells (DCs), natural killer (NK) cells and T-lymphocytes. This agent may also induce increased interferon (IFN) production, which may lead to a reduction in tumor-associated regulatory T-cells (Tregs). Activation of the immune system, which is suppressed in many cancers, may induce a cytotoxic T-lymphocyte (CTL) response against and inhibit the growth of the IDO1-expressing tumor cells. IDO1, an enzyme overexpressed by multiple tumor cell types, plays an important role in immunosuppression. Tryptophan depletion inhibits T-lymphocyte proliferation and activation, and suppresses the immune system.
  • Ido1 inhibitor pf-06840003 - An orally available hydroxyamidine and inhibitor of indoleamine 2,3-dioxygenase 1 (IDO1), with potential immunomodulating and antineoplastic activities. Upon administration, IDO1 inhibitor PF-06840003 targets and binds to IDO1, an enzyme responsible for the oxidation of tryptophan into kynurenine. By inhibiting IDO1 and decreasing kynurenine in tumor cells, PF-06840003 increases and restores the proliferation and activation of various immune cells, including dendritic cells (DCs), natural killer (NK) cells, and T-lymphocytes; PF-06840003 also induces increased interferon (IFN) production, and causes 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, a cytosolic enzyme responsible for tryptophan catabolism and the conversion of tryptophan into kynurenine, is overexpressed by a variety of tumor cell types and antigen presenting cells (APCs); it plays an important role in immunosuppression. Tryptophan depletion inhibits T-lymphocyte proliferation and activation, and subsequently suppresses the immune system.
  • Ido1/tdo2 inhibitor dn1406131 - An inhibitor of both the enzymes indoleamine 2,3-dioxygenase 1 (IDO1; IDO-1) and tryptophan 2,3-dioxygenase 2 (TDO2; TDO-2), with potential immunomodulating and antineoplastic activities. Upon administration, IDO1/TDO2 inhibitor DN1406131 targets, binds to and inhibits both IDO1 and TDO2, which catalyze the first and rate-limiting step in the production of the immunosuppressive transcription factor aryl hydrocarbon receptor (AhR) ligand kynurenine (KYN). This inhibits the IDO1/TDO2-KYN-AhR pathway. Abrogation of AhR activation prevents the activation of immune-tolerant dendritic cells (DCs) and regulatory T-cells (Tregs) in the tumor microenvironment (TME). This may restore the immune response against tumor cells in which IDO1 and/or TDO2 are overexpressed. The IDO1/TDO2-KYN-AhR pathway is overexpressed in a variety of tumor cell types, plays a key role in immunosuppression and its expression is correlated with poor prognosis.
  • Ido1/tdo2 inhibitor m4112 - An inhibitor of both the enzymes indoleamine 2,3-dioxygenase 1 (IDO1; IDO-1) and tryptophan 2,3-dioxygenase 2 (TDO2; TDO-2), with potential immunomodulating and antineoplastic activities. Upon administration, IDO1/TDO2 inhibitor M4112 targets, binds to and inhibits both IDO1 and TDO2, which catalyze the first and rate-limiting step in the production of the immunosuppressive transcription factor aryl hydrocarbon receptor (AhR) ligand kynurenine (Kyn). This inhibits the IDO1/TDO2-Kyn-AhR pathway and abrogates AhR activation. This prevents the activation of immune-tolerant dendritic cells (DCs) and regulatory T-cells (Tregs) in the tumor microenvironment (TME), and may restore the immune response by stimulating a cytotoxic T-lymphocyte (CTL) immune response against tumor cells in which IDO1 and/or TDO2 are overexpressed. The IDO1/TDO2-KYN-AhR pathway is overexpressed in a variety of tumor cell types and plays a key role in immunosuppression. Its expression is correlated with poor prognosis.
  • Idronoxil - A synthetic flavonoid derivative. Idronoxil activates the mitochondrial caspase system, inhibits X-linked inhibitor of apoptosis (XIAP), and disrupts FLICE inhibitory protein (FLIP) expression, resulting in tumor cell apoptosis. This agent also inhibits DNA topoisomerase II by stabilizing the cleavable complex, thereby preventing DNA replication and resulting in tumor cell death.
  • Idronoxil suppository nox66 - A proprietary, suppository-based formulation composed of idronoxil, a synthetic flavonoid derivative, surrounded by a proprietary lipid that protects idronoxil from phase 2 degradation, with potential chemo- and radio-sensitizing activities. Upon administration, idronoxil blocks the activity of ecto-NOX disulfide-thiol exchanger 2 (ENOX2; tNOX), a tumor-specific external NADH oxidase that maintains the transmembrane electron potential across the plasma membrane and is overexpressed in certain cancer cell types while absent in normal, healthy cells. Loss of this potential directly inhibits certain pro-survival signal transduction pathways, such as the PARP1/PI3 kinase/Akt signaling pathway. The inhibition of these pathways prevents resistance to standard chemo- and radio-therapy and makes tumor cells more susceptible to the anti-tumor activity of conventional chemotherapeutic agents and radiotherapy. The formulation prevents detoxification of idronoxil to an inactive form by bypassing phase 2 metabolism; this increases idronoxil's bioavailability as compared to idronoxil alone.
  • Ieramilimab - A humanized monoclonal antibody directed against the inhibitory receptor lymphocyte activation gene-3 (LAG-3), with potential immunomodulating and antineoplastic activities. Upon administration, Ieramilimab binds to LAG-3 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. LAG-3, a member of the immunoglobulin superfamily (IgSF) and expressed on various immune cells, negatively regulates cellular proliferation and activation of T-cells. Its expression on TILs is associated with tumor-mediated immune suppression.
  • Ifabotuzumab - A non-fucosylated monoclonal antibody directed against the ephrin receptor A3 (EphA3), with potential antineoplastic activity. Upon administration, ifabotuzumab selectively binds to tumor cells expressing EphA3. This blocks both EphA3 activation and EphA3-mediated signaling, and induces apoptosis in EphA3-expressing tumor cells. In addition, ifabotuzumab can stimulate antibody dependent cell-mediated cytotoxicity (ADCC) against EphA3-expressing tumor cells. This agent also prevents tumor cell proliferation by inhibiting both EphA3 signaling and proliferation of endothelial cells in the tumor vasculature. The cell-surface receptor EphA3, a member of the ephrin family of receptor tyrosine kinases (RTKs) that are involved in mammalian development, is overexpressed by a variety of tumor types but is not expressed in normal healthy adult tissues. It plays an important role in tumor cell proliferation. Non-fucosylation of the antibody enhances its ADCC activity.
  • Ifetroban - An orally bioavailable thromboxane (TxA2) and prostaglandin H2 (PGH2) (TP) receptor antagonist, with anti-thrombotic, anti-hypertensive, anti-asthmatic and potential anti-metastatic activities. Upon administration, ifetroban targets and binds to TxA2 and PGH2 receptors, thereby preventing the activity of both TxA2 and PGH2 and disrupting their downstream signaling pathways. This prevents platelet activation, aggregation and thrombosis. It also prevents vascular constriction and causes vasodilation. In addition, as cancer cells use platelets to metastasize to different parts of the body, ifetroban can reduce the stickiness of the platelets and prevent metastasis. TxA2 causes vascular contraction and platelet activation.
  • Ifosfamide - A synthetic analogue of the nitrogen mustard cyclophosphamide with antineoplastic activity. Ifosfamide alkylates and forms DNA crosslinks, thereby preventing DNA strand separation and DNA replication. This agent is a prodrug that must be activated through hydroxylation by hepatic microsomal enzymes.
  • Igf-1r antisense oligodeoxynucleotide-treated autologous glioma cells - Autologous glioma cells treated ex vivo with an 18-mer antisense oligodeoxynucleotide of insulin-like growth factor receptor 1 (IGF-1R/AS ODN), with potential antineoplastic activity. IGF-1R/AS ODN pre-treated glioma cells encapsulated in small Lucite diffusion chambers are implanted into a subcutaneous pocket in the patient's abdominal rectus sheath. Within the diffusion chambers, IGF-1R/AS ODN binds to IGF-1R mRNA, and shuts down the translation of IGF-1R in the glioma cells. Downregulation of IGF-1R induces apoptosis and causes the release of exosomes, which contain tumor-associated antigens (TAAs). The diffusion of exosomes and IGF-1R/AS ODN from the Lucite chambers may active the patient's immune system and mount a cytotoxic T-lymphocyte (CTL) response against cells expressing these TAAs. IGF-1R, a receptor tyrosine kinase, is overexpressed in a variety of tumor cell types and is essential for tumor cell growth, transformation and survival.
  • Igf-1r inhibitor pl225b - An orally bioavailable inhibitor of the insulin-like growth factor 1 receptor (IGF-1R) with potential antineoplastic activity. IGF-1R inhibitor PL225B selectively binds to and inhibits the activities of IGF-1R, which may result in both the inhibition of tumor cell proliferation and the induction of tumor cell apoptosis in IGF-1R-overexpressing tumor cells. IGF-1R, a receptor tyrosine kinase overexpressed in a variety of human cancers, plays a significant role in the stimulation of cellular proliferation, oncogenic transformation, and suppression of apoptosis.
  • Igf-1r/ir inhibitor kw-2450 - An orally bioavailable inhibitor of insulin-like growth factor 1 receptor (IGF-1R) and insulin receptor (IR) tyrosine kinases with potential antineoplastic activity. IGF-1R/IR inhibitor KW-2450 selectively binds to and inhibits the activities of IGF-1R and IR, which may result in the inhibition of tumor cell proliferation and the induction of tumor cell apoptosis. IGF-R1 and IR tyrosine kinases, overexpressed in a variety of human cancers, play significant roles in the stimulation of cellular proliferation, oncogenic transformation, and suppression of apoptosis.
  • Igf-methotrexate conjugate - A conjugate containing the antimetabolite and antifolate agent methotrexate conjugated to insulin-like growth factor (IGF), with potential antineoplastic activity. After intravenous administration, the IGF moiety of the IGF-methotrexate conjugate binds to and is internalized by IGF receptors (IGFR) on the surface of tumor cells. Following cell entry, the methotrexate then binds to and inhibits the enzyme dihydrofolate reductase, which catalyzes the conversion of dihydrofolate to tetrahydrofolate. This results in both the inhibition of DNA and RNA synthesis and the induction of death in rapidly dividing cells. Binding to IGFR can localize the cytotoxic effect of methotrexate in tumor cells. This may increase its efficacy while decreasing its toxicity to normal, healthy cells. IGFR is overexpressed on many types of cancer cells and has been implicated in metastasis and resistance to apoptosis.
  • Il-10 immunomodulator mk-1966 - An agent that downregulates the activity of the anti-inflammatory cytokine human interleukin-10 (IL-10), with potential immunomodulating and antineoplastic activities. Upon administration, IL-10 immunomodulator MK-1966 blocks the activity of IL-10 and may abrogate the IL-10-induced immunosuppressive tumor microenvironment. This activates cell-mediated immunity against cancer cells, increases cytokine production, including interferon-gamma (IFN-g), decreases T regulatory cell (Treg) activity, and induces a tumor-specific cytotoxic CD8+ T-cell-mediated immune response, which enhances tumor cell death.
  • Il-12-expressing hsv-1 nsc 733972 - A genetically engineered, replication selective, infected cell protein (ICP) 34.5 gene-deleted, oncolytic human simplex virus type 1 (HSV-1) expressing the human immunostimulating cytokine interleukin-12 (IL-12), with potential antineoplastic activity. Upon intratumoral administration of HSV-1 expressing IL-12 NSC 733972, the IL-12-expressing HSV-1 preferentially infects and replicates in tumor cells of neuronal origin causing viral-mediated tumor cell lysis. The released virus particles, in turn, infect and replicate in neighboring tumor cells. In addition, the IL-12-expressing HSV-1 promotes the secretion of IL-12 by the tumor cells. IL-12 promotes the activation of natural killer cells, which induces both the secretion of interferon-gamma and a cytotoxic T-lymphocyte (CTL) response against the tumor cells. This results in both immune-mediated tumor cell death and further inhibition of tumor cell proliferation. Deletion of the gene encoding for ICP34.5 imparts tumor selectivity by preventing replication in healthy cells.
  • Il-12-expressing mesenchymal stem cell vaccine gx-051 - Human mesenchymal stem cells (MSCs) transduced with a retroviral vector encoding a modified form of the cytokine interleukin-12 (IL-12), with potential immunomodulating and antineoplastic activities. Upon intratumoral administration, IL-12-expressing MSC vaccine GX-051 secretes IL-12. IL-12 activates the immune system by both promoting the secretion of interferon-gamma, which activates natural killer cells (NKs), and inducing cytotoxic T-cell responses, which may result in both decreased cell proliferation and increased cell death in tumor cells.
  • Il-12sc, il-15sushi, ifna and gm-csf mrna-based immunotherapeutic agent sar441000 - An immunotherapeutic agent utilizing mRNA to encode the cytokines interleukin-12sc (IL-12sc), interleukin-15sushi (IL-15sushi), interferon alpha (IFNa) and granulocyte-macrophage colony-stimulating factor (GM-CSF), with potential immunomodulating and antineoplastic activities. Upon intratumoral administration of IL-12sc, IL-15sushi, IFNa and GM-CSF mRNA-based immunotherapeutic agent SAR441000, mRNA is picked up by nearby cells, translated and released into the local tumor microenvironment (TME). Secretion of these cytokines activate the immune system by promoting the activation of natural killer cells (NKs) and inducing cytotoxic T-lymphocyte (CTL) responses, which may result in an immune-mediated destruction of tumor cells.
  • Il13ralpha2-specific hinge-optimized 41bb-co-stimulatory car truncated cd19-expressing autologous t-lymphocytes - A preparation of ex vivo expanded, genetically modified autologous central memory-enriched T-cells (Tcm) transduced with a replication incompetent, self-inactivating (SIN) lentiviral vector expressing a hinge-optimized, chimeric antigen receptor (CAR) specific for interleukin-13 receptor alpha 2 (IL13Ra2), and containing the cluster of differentiation 137 (CD137; 4-1BB) co-stimulatory signaling domain fused to the signaling domain of the T cell antigen receptor complex zeta chain (CD3-zeta), and a truncated form of human cluster of differentiation 19 (CD19t), with potential immunostimulating and antineoplastic activities. Upon intratumoral or intracavitary administration, IL13Ra2-specific, hinge-optimized, 41BB-co-stimulatory CAR/truncated CD19 expressing T-lymphocytes are directed to, and induce selective toxicity and cytolysis in IL13Ra2-expressing tumor cells. IL13Ra2, overexpressed by a variety of tumor cell types, is associated with increased tumor cell proliferation, migration and invasiveness. The costimulatory signaling domain enhances both proliferation of T-cells and antitumor activity. Hinge optimization prevents the recognition and clearance of the CAR by endogenous Fc receptors (FcRs). CD19t is used as a surface marker to both quantify and track the gene modified T-cells in vivo.
  • Il13ralpha2-specific hinge-optimized 4-1bb-co-stimulatory car/truncated cd19-expressing autologous tn/mem cells - A preparation of ex vivo expanded, genetically modified autologous na├»ve and memory T-cells (TN/MEM) transduced with a replication incompetent, self-inactivating (SIN) lentiviral vector expressing a hinge-optimized, chimeric antigen receptor (CAR) specific for interleukin-13 receptor alpha 2 (IL13Ra2), and containing the cluster of differentiation 137 (CD137; 4-1BB) co-stimulatory signaling domain fused to the signaling domain of the T-cell antigen receptor complex zeta chain (CD3-zeta), and a truncated form of human cluster of differentiation 19 (CD19t), with potential immunostimulating and antineoplastic activities. Upon intratumoral or intracavitary administration, IL13Ra2-specific hinge-optimized 4-1BB-co-stimulatory CAR/truncated CD19-expressing autologous TN/MEM cells are directed to, and induce selective toxicity and cytolysis in, IL13Ra2-expressing tumor cells. IL13Ra2, overexpressed by a variety of tumor cell types, is associated with increased proliferation, migration and invasiveness of tumor cells. The co-stimulatory signaling domain enhances both proliferation of T-cells and antitumor activity. Hinge optimization prevents the recognition and clearance of the CAR by endogenous Fc receptors (FcRs). CD19t is used as a surface marker to both track and quantify the modified T-cells in vivo.
  • Il-2 recombinant fusion protein alt-801 - A recombinant protein consisting of the cytokine interleukin-2 (IL-2) fused to a humanized soluble T-cell receptor (TCR) directed against a tumor suppressor p53-derived antigen with potential immunopotentiating and antineoplastic activities. The TCR moiety of IL-2 recombinant fusion protein ALT-801 binds to tumor cells displaying p53 epitope/MHC complexes; subsequently, the tumor cell-localized IL-2 moiety may stimulate natural killer (NK) cell and T cell cytotoxic immune responses against p53-expressing tumor cells.
  • Il-2/9/15 gamma chain receptor inhibitor bnz-1 - A pegylated peptide antagonist that binds to the common gamma chain (gc; IL2RG; CD132) of the signaling receptor for the pro-inflammatory cytokines interleukin (IL)-2, IL-9, and IL-15, with potential immunomodulating and antineoplastic activities. Upon administration, IL-2/9/15 gc receptor inhibitor BNZ-1 specifically targets and binds to the IL binding site on the gc receptor and blocks IL-2, IL-9 and IL-15 binding, thereby inhibiting IL-2-, IL-9-, and IL-15-mediated signaling and downstream pathways. This may inhibit proliferation of tumor cells that are dependent on IL-2/9/15 signaling for their growth. IL-2/9/15 are upregulated in certain tumor cell types and play a key role in tumor progression and survival.
  • Il-2/lptn gene-modified allogeneic neuroblastoma tumor cell vaccine - A cancer vaccine consisting of allogeneic neuroblastoma tumor cells have been genetically modified to secrete the human cytokine interleukin-2 (IL-2) and the human chemokine lymphotactin (Lptn) with potential immunostimulating and antineoplastic activities. Upon administration, IL-2 and Lptn are secreted by the IL-2/Lptn gene-modified allogeneic neuroblastoma tumor cell vaccine, potentially enhancing the cytotoxic T lymphocyte (CTL) response elicited by vaccine neuroblastoma tumor-associated antigens (TAAs) against host neuroblastoma tumor cells. Produced by activated progenitor T cells, Lptn belongs to the C chemokine subfamily and is a potent chemotactic factor for lymphocytes; IL-2 stimulates natural killer (NK) cells and may enhance a vaccine-elicited CTL immune response against tumor cells.
  • Il4-pseudomonas exotoxin fusion protein mdna55 - A fusion protein consisting of the cytokine interleukin-4 (IL-4) linked to a truncated form of Pseudomonas exotoxin with potential antineoplastic activity. Upon specific, high-affinity binding to IL-4 receptors located on the tumor cell surface., IL4-Pseudomonas exotoxin fusion protein MDNA55 is internalized; the exotoxin moiety then binds to translation elongation factor 2 (EF-2), which may result in ADP ribosylation, deactivation of EF-2, inhibition of protein synthesis, and tumor cell apoptosis. The Pseudomonas exotoxin moiety of this agent has been engineered to reduce non-specific binding to cells expressing its receptor, the multiligand cell surface receptor alpha 2-macroglobulin receptor/low-density lipoprotein receptor-related protein (alpha 2MR/LRP). IL-4R is a type I transmembrane protein that binds IL-4 and IL-13 and may be overexpressed by cancers such as renal cell carcinoma and glioma.
  • Ilginatinib - An orally bioavailable, small molecule inhibitor of Janus-associated kinase 2 (JAK2) and Src-family kinases, with potential antineoplastic activity. Ilginatinib competes with ATP for binding to JAK2 as well as the mutated form JAK2V617F, thereby inhibiting the activation of JAK2 and downstream molecules in the JAK2/STAT3 (signal transducer and activator of transcription 3) signaling pathway that plays an important role in normal development, particularly hematopoiesis. In addition, ilginatinib inhibits the Src family tyrosine kinases. This eventually leads to the induction of tumor cell apoptosis. JAK2 is the most common mutated gene in bcr-abl-negative myeloproliferative disorders (MPDs); JAK2V617F is a constitutively activated kinase that activates the JAK/STAT signaling pathway and dysregulates cell growth and function, and its expression transforms hematopoietic cells to cytokine-independent growth.
  • Ilixadencel - An off-the-shelf immune primer consisting of allogeneic monocyte-derived dendritic cells (MoDCs) that have been stimulated with a combination of activating factors to produce pro-inflammatory factors including tumor necrosis factor-alpha (TNF-alpha), interleukin-1 beta (IL-1 beta), interleukin-12, p70 (IL-12 p70), C-C motif chemokine 4 (CCL4; macrophage inflammatory protein 1-beta; MIP-1-beta), C-C motif chemokine 5 (CCL5; RANTES), and C-X-C motif chemokine 10 (CXCL10), with potential immunostimulating and antineoplastic activities. Upon intratumoral injection of ilixadencel, the dendritic cells (DCs) release type 1 T-helper cell (Th1)-associated chemokines, including CCL4, CCL5 and CXCL10, that may recruit natural killer (NK)-cells and pre-DCs into the tumor microenvironment (TME). The interaction between NK cells and ilixadencel DCs may induce NK-cell-mediated killing of tumor cells, resulting in release of tumor-associated-antigens (TAAs). The production of interferon-gamma (IFN-gamma) by activated NK-cells and TNF-alpha/beta released by ilixadencel DCs will induce maturation and promote cross-presentation of TAAs by recruited endogenous "bystander" DCs. Migration of these antigen-loaded and matured "bystander" DCs to the tumor-draining lymph node will lead to a Th1-polarized activation of tumor-specific T-cells.
  • Iloprost - A prostacyclin analogue with potential chemopreventive activity. Iloprost binds to the prostacyclin receptor in various target cells, thereby causing vasodilation, inhibition of platelet aggregation, and decreased tumor cell adhesion to endothelium among other effects. Prostacyclin is a naturally occurring eicosanoid with anti-inflammatory, antineoplastic, and anti-metastatic properties. (NCI05)
  • Ilorasertib - An orally bioavailable, adenosine triphospate mimetic, and inhibitor of Aurora kinases, vascular endothelial growth factor receptors (VEGFRs) and platelet-derived growth factor receptor (PDGFRs), with potential antineoplastic activity. Upon administration, ilorasertib selectively binds to and inhibits Aurora kinases A, B and C, which may disrupt both the assembly of the mitotic spindle apparatus and chromosome segregation, and inhibit both cellular division and proliferation in Aurora kinase-overexpressing tumor cells. In addition, ilorasertib selectively binds to and inhibits VEGFRs and PDGFRs, which may result in the inhibition of both angiogenesis and tumor cell proliferation in VEGFR/PDGFR-overexpressing tumor cells. This agent also inhibits the Src family of cytoplasmic tyrosine kinases. Aurora kinases A, B and C, are serine/threonine kinases that play essential roles in mitotic checkpoint control and are overexpressed by a wide variety of tumor cell types. Both VEGFRs and PDGFRs are receptor tyrosine kinase families whose members may be upregulated in various tumor cell types.
  • Imalumab - A human, recombinant monoclonal antibody (MoAb) against macrophage migration inhibitory factor (MIF), with potential immunomodulating, anti-inflammatory and antineoplastic activities. Upon intravenous administration, imalumab binds to MIF, blocking its activity and preventing the MIF-mediated secretion of certain cytokines, including interleukin-1 beta and tumor necrosis factor-alpha. This may lead to an inhibition of cancer cell proliferation in MIF-overexpressing tumor cells. MIF, a pro-inflammatory cytokine overexpressed in some cancers, plays a key role in inflammation, immune responses and cancer cell proliferation.
  • Imaradenant - An orally bioavailable antagonist of the adenosine A2A receptor (A2AR; ADORA2A), with potential immunomodulating and antineoplastic activities. Upon administration, imaradenant selectively binds to and inhibits A2AR expressed on T-lymphocytes. This blocks tumor-released adenosine from interacting with A2AR and prevents the adenosine/A2AR-mediated inhibition of T-lymphocytes. This results in the proliferation and activation of T-lymphocytes, and stimulates a T-cell-mediated immune response against tumor cells. A2AR, a G protein-coupled receptor, is highly expressed on the cell surfaces of T-cells and, upon activation by adenosine, inhibits T-cell proliferation and activation. Adenosine is often overproduced by cancer cells and plays a key role in immunosuppression.
  • Imatinib - An antineoplastic agent that inhibits the Bcr-Abl fusion protein tyrosine kinase, an abnormal enzyme produced by chronic myeloid leukemia cells that contain the Philadelphia chromosome. Imatinib also inhibits the receptor tyrosine kinases for platelet-derived growth factor (PDGF) and stem cell factor (SCF)/c-kit; the SCF/c-kit receptor tyrosine kinase is activated in gastrointestinal stromal tumor (GIST). This agent inhibits proliferation and induces apoptosis in cells that overexpress these oncoproteins.
  • Imatinib mesylate - The mesylate salt of imatinib, a tyrosine kinase inhibitor with antineoplastic activity. Imatinib binds to an intracellular pocket located within tyrosine kinases (TK), thereby inhibiting ATP binding and preventing phosphorylation and the subsequent activation of growth receptors and their downstream signal transduction pathways. This agent inhibits TK encoded by the bcr-abl oncogene as well as receptor TKs encoded by the c-kit and platelet-derived growth factor receptor (PDGFR) oncogenes. Inhibition of the bcr-abl TK results in decreased proliferation and enhanced apoptosis in malignant cells of Philadelphia-positive (Ph+) hematological malignancies such as CML and ALL; effects on c-kit TK activity inhibit mast-cell and cellular proliferation in those diseases overexpressing c-kit, such as mastocytosis and gastrointestinal stromal tumor (GIST).
  • Imetelstat - A synthetic lipid-conjugated, 13-mer oligonucleotide N3'-P5'-thio-phosphoramidate with potential antineoplastic activity. Complementary to the template region of telomerase (hTR) RNA, imetelstat acts as a competitive enzyme inhibitor that binds and blocks the active site of the enzyme (a telomerase template antagonist), a mechanism of action which differs from that for the antisense oligonucleotide-mediated inhibition of telomerase activity through telomerase mRNA binding. Inhibition of telomerase activity in tumor cells by imetelstat results in telomere shortening, which leads to cell cycle arrest or apoptosis.
  • Imetelstat sodium - The sodium salt of imetelstat, a synthetic lipid-conjugated, 13-mer oligonucleotide N3' P5'-thio-phosphoramidate with potential antineoplastic activity. Complementary to the template region of telomerase RNA (hTR), imetelstat acts as a competitive enzyme inhibitor that binds and blocks the active site of the enzyme (a "telomerase template antagonist"), a mechanism of action which differs from that for the antisense oligonucleotide-mediated inhibition of telomerase activity through telomerase mRNA binding. Inhibition of telomerase activity in tumor cells by imetelstat results in telomere shortening, which leads to cell cycle arrest or apoptosis.
  • Imexon - A 2-cyanoaziridine derivative with antitumor activity in multiple myeloma. Although its mechanism of action is not clearly known, imexon may induce apoptosis via a pathway involving cleaved caspase-3, caspase-9, and/or caspase-8. Other cytotoxic mechanisms of action of this agent may involve thiol depletion, generation of reactive oxygen species (ROS), and decreases in the mitochondrial membrane potential.
  • Imgatuzumab - A glycoengineered monoclonal antibody directed against the epidermal growth factor receptor (EGFR) with potential antineoplastic activity. Imgatuzumab binds to the extracellular domain of EGFR, preventing the activation and subsequent dimerization of the receptor; the decrease in receptor activation and dimerization may result in an inhibition of downstream ERK and JNK signaling pathways and so inhibition of EGFR-dependent tumor cell proliferation and metastasis. EGFR, a member of the epidermal growth factor family of extracellular protein ligands, may be overexpressed on the cell surfaces of various solid tumor cell types.
  • Imidazole mustard - A synthetic derivative of imidazole with potent antineoplastic properties. Imidazole mustard alkylates DNA, preferentially at guanine residues, resulting in DNA interstrand crosslinks and inhibition of DNA replication and RNA and protein synthesis.
  • Imidazole-pyrazole - A synthetic agent, also known as IMPY, with antineoplastic properties. IMPY inhibits ribonucleotide reductase, an enzyme that converts ribonucleotides to deoxyribonucleotides during DNA synthesis; this agent specifically binds the smaller, nonheme-iron subunit of the enzyme.
  • Imifoplatin - A platinum (Pt)-based agent belonging to the phosphaplatin family comprised of Pt complexed to a pyrophosphate ligand, with potential antineoplastic activity. Although the exact mechanisms through which imifoplatin exerts its effect have yet to be fully elucidated, this agent, upon intravenous administration, binds to certain transmembrane proteins and activates several genes involved in tumor suppression and apoptosis. This leads to the activation of various signal transduction pathways, induces S/G2 phase cell cycle, and causes tumor cell apoptosis. In addition, imifoplatin may inhibit angiogenesis. Unlike conventional Pt-based chemotherapeutics, imifoplatin does not bind to DNA and is able to overcome drug resistance, which occurs with conventional Pt-based chemotherapeutics; it also has a more favorable side effect profile and is more stable in plasma.
  • Imipramine blue - A triphenylmethane-based dye and an inhibitor of nicotinamide adenine dinucleotide phosphate (NADP+) oxidase 4 (NOX4), with potential anti-invasive and anti-oxidative activities. Upon administration, imipramine blue (IB) inhibits the activity of NOX4 and prevents NOX4-mediated cell signaling. This prevents the formation of NOX4-mediated reactive oxygen species (ROS), abrogates the ROS-induced inhibition of protein tyrosine phosphatase (PTP) activation, and induces both G2/M cell cycle arrest and apoptosis. NOX4, an enzyme belonging to the NOX family of proteins, promotes the production of ROS and plays a key role in the suppression of PTP activation; it is upregulated in a variety of cancers.
  • Imiquimod - A synthetic agent with immune response modifying activity. As an immune response modifier (IRM), imiquimod stimulates cytokine production, especially interferon production, and exhibits antitumor activity, particularly against cutaneous cancers. Imiquimod's proapoptotic activity appears to be related to Bcl-2 overexpression in susceptible tumor cells.
  • Immediate-release onapristone - An immediate-release (IR) 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.
  • Immediate-release tablet afuresertib - An immediate-release (IR) tablet formulation containing afuresertib, an inhibitor of the serine/threonine protein kinase Akt (protein kinase B) with potential antineoplastic activity. Upon oral administration of the IR formulation, afuresertib binds to and inhibits the activity of Akt, which may result in the inhibition of PI3K/Akt signaling pathway, decreased tumor cell proliferation and the induction of tumor cell apoptosis in Akt-expressing tumor cells. Activation of the PI3K/Akt signaling pathway is frequently associated with tumorigenesis and dysregulated PI3K/Akt signaling may contribute to tumor resistance to a variety of antineoplastic agents.
  • Immune checkpoint inhibitor asp8374 - An immune checkpoint inhibitor with potential immunomodulating and antineoplastic activities. Although the exact target is undisclosed, ASP8374 inhibits the activity of an immune checkpoint protein, which ultimately leads to the activation of a cytotoxic T-lymphocyte (CTL)-mediated immune response against cancer cells.
  • Immunocytokine nhs-il12 - A fusion protein consisting of the heavy-chains of the human antibody NHS76, raised against DNA released by necrotic tumor cells, and fused to two molecules of a genetically modified human interleukin-12 (IL-12) with potential immunostimulating and antineoplastic activities. Upon administration, the antibody moiety of immunocytokine NHS-IL12 binds to DNA released from necrotic tumor cells located primarily at the core of necrotic solid tumors, thereby delivering the IL-12 moiety. In turn, the IL-12 moiety of this agent stimulates the host immune system to mount an immune response against tumor cells, thereby inhibiting tumor growth. IL-12 is a proinflammatory cytokine with numerous immunoregulatory functions and may augment host immune responses to tumor cells. By targeting tumor cells, NHS-IL-12 may reduce the toxicity associated with systemic administration of recombinant human IL-12.
  • Immunocytokine nhs-il2-lt - A fusion protein consisting of a mouse-human chimeric antibody directed against DNA released by necrotic tumor cells fused to two molecules of a genetically modified human interleukin-2 (IL-2) with potential antineoplastic activity. Upon administration, the antibody moiety of immunocytokine NHS-IL2-LT binds to DNA released by necrotic tumor cells located primarily at the core of necrotic solid tumors, delivering the IL-2 moiety. In turn, the IL-2 moiety of this agent activates the immune system to mount a cytotoxic T lymphocyte response against nearby tumor cells.
  • Immunomodulator ohr/avr118 - A broad-spectrum peptide nucleic acid formulation comprised of breakdown products of casein, peptone, RNA and serum albumin, with potential anti-inflammatory, immunomodulatory, anti-anorectic and anti-cachexia activities. AVR118 mainly contains two peptides, peptide A and peptide B, in approximately a 1:1 ratio: peptide A (31 a. a.) is derived from bovine casein; peptide B (21 a. a.) is covalently linked via phosphodiester bond to a diadenosine unit. In addition, AVR118 contains nucleosides, nucleoside diphosphates and nucleoside monophosphates. Upon subcutaneous injection of AVR118, this agent affects the synthesis of many pro-inflammatory chemokines and cytokines, especially monocyte chemotactic protein-1 (MCP-1), interleukin (IL)-8, IL-1 beta, IL-6, and tumor necrosis factor-alpha (TNF-alpha). In particular, AVR118 stimulates macrophages to produce these mediators while in highly activated macrophages this agent inhibits their synthesis. This way, AVR118 may prevent the excessive release of cytokines seen during chemotherapy. Controlling the release of pro-inflammatory mediators may ultimately improve appetite and mood, increase strength and weight gain, and decrease fatigue.
  • Immunomodulatory agent cc-11006 - A proprietary, orally available, small molecule and thalidomide analog, with potential immunomodulating and antineoplastic activity. CC-11006 appears to have a similar mechanism to thalidomide and may modulate the expression of proinflammatory and regulatory cytokines.
  • Immunomodulatory oligonucleotide hyb2055 - A second generation synthetic oligonucleotide with immunomodulatory and potential antineoplastic activities. HYB2055 consists of unmethylated CpG dinucleotide motifs that are present abundantly in bacterial and parasitic DNA, and a novel DNA structure, called an immunomer that contributes to metabolic stability of the agent. Upon infections, CpG-containing DNA released from pathogenic organisms triggers host immune responses, which are mediated by the action of intracellular toll-like receptor 9 (TLR9), a pattern recognition receptor. This agent mimics bacterial DNA and selectively activates TLR9, thereby initiating immune signaling pathways, and leading to activation of B-cells and dendritic cells and induction of Th1-type cytokine production.
  • Immunotherapeutic combination product cmb305 - An immunotherapeutic combination product composed of LV305, an engineered lentiviral vector that both targets dendritic cells (DCs) and contains nucleic acids encoding the human tumor-associated cancer-testis antigen NY-ESO-1 (CTAG1), and G305, a cancer vaccine comprised of an NY-ESO-1 recombinant protein and glucopyranosyl lipid adjuvant (GLA)-stable emulsion (GLA-SE), with potential synergistic immunostimulatory and antineoplastic activities. Upon intradermal administration of LV305, the DC-targeting lentiviral vector targets and binds to dermal DCs via the DC-specific intercellular adhesion molecule-3-grabbing non-integrin (DC-SIGN) receptor. Upon internalization of the vector, the NY-ESO-1 protein is expressed, which stimulates DC maturation, and activates the immune system to mount a cytotoxic T-lymphocyte (CTL) response against NY-ESO-1-expressing cells; this may result in tumor cell lysis. Upon the sequential intramuscular injection of G305, the adjuvant portion of G305 binds to toll-like receptor 4 (TLR-4) expressed on various immune cells, including DCs, monocytes, macrophages and B-cells. The activated DCs present the NY-ESO-1 antigen to CD4-positive Th1 T-lymphocytes. The induction of antigen-specific CD4-positive T-lymphocytes further induces a CTL response against NY-ESO-1-expressing tumor cells. In addition, G305 induces an NY-ESO-1-specific antibody response. NY-ESO-1, expressed in normal testes and on the surfaces of various tumor cells, plays a key role in tumor cell proliferation and survival.
  • Immunotherapeutic gsk1572932a - An immunotherapeutic containing a proprietary adjuvant system combined with a melanoma-associated antigen peptide MAGE-A3 epitope with potential immunomodulating and antineoplastic activities. Intramuscular administration with GSK1572932A may stimulate the immune system to exert both humoral and cellular immune responses against MAGE-A3-expressing tumor cells. MAGE-A3, a tumor associated antigen (TAA), is overexpressed in a variety of tumor cell types, including non-small cell lung cancer (NSCLC), melanoma, head and neck cancer, and bladder cancer.
  • Immunotherapy regimen mkc-1106-mt - An immunotherapy regimen containing three components: a plasmid encoding portions of the two melanoma-associated antigens Melan A (also called MART-1) and tyrosinase and two synthetic analogs of Melan-A and tyrosinase antigen epitopes with potential immunostimulating and antitumor activities. First, the plasmid is injected directly into lymph nodes in order to sensitize or prime antigen-presenting cells (APCs) and central memory T cells in lymph nodes to plasmid-expressed Melan A and tyrosinase. After several priming injections with plasmids, the Melan A and tyrosinase synthetic epitope analogs are injected directly into lymph nodes; upon binding to major histocompatibility complex (MHC) molecules on APC cell surfaces, these synthetic epitope analogs may stimulate a "primed" cytotoxic T lymphocyte (CTL) response against melanoma tumor cells, resulting in tumor cell lysis. Melan-A and tyrosinase are overexpressed by melanoma tumor cells.
  • Immunotoxin cmd-193 - A humanized immunotoxin directed against the Lewis Y antigen conjugated with calicheamicin, a hydrophobic enediyne antibiotic, with potential antineoplastic activity. CMD193 binds to the Lewis Y antigen, a tetrasaccharide expressed on the cell surfaces of many tumor cell types. Upon binding, CMD-193 is internalized, thereby delivering the attached calicheamicin to Lewis Y antigen-expressing tumor cells. Calicheamicin binds non-covalently to the minor groove of DNA and prompts conformational changes and DNA oxidation, thereby inhibiting DNA synthesis and inducing apoptosis.
  • Immunotoxin d2c7-(scdsfv)-pe38kdel - A recombinant immunotoxin fusion protein consisting of single-chain variable-region antibody fragments (scFvs), which contain disulfide stabilized heavy- (Vh) and light- (Vl) chain variable regions of the monoclonal antibody D2C7 (D2C7-scdsFv), targeting both the wild-type form (EGFRwt) and the in-frame deletion mutant form (EGFRvIII) of epidermal growth factor receptor (EGFR), and fused, via a 15-amino acid peptide linker to domains II and III of the Pseudomonas exotoxin A (PE38KDEL) (D2C7-(scdsFv)-PE38KDEL), with potential antineoplastic activity. Upon intratumoral administration by convection-enhanced delivery, the scFv moiety of immunotoxin anti-EGFR scFv monoclonal antibody fragment immunotoxin D2C7-(scdsFv)-PE38KDEL targets and binds to a specific amino acid epitope present in the extracellular domain of both the EGFRwt and EGFRvIII proteins. This binding facilitates the internalization of the immunotoxin by tumor cells. Inside the cells, the exotoxin portion of the fusion protein binds to translation elongation factor 2 (EF-2), and deactivates EF-2 through ADP ribosylation. This results in the inhibition of protein synthesis, the induction of apoptosis and a reduction in cell proliferation of EGFRwt/EGFRvIII-expressing tumor cells. Compared to intact IgG antibodies and single-chain antibodies, scFvs are smaller with increased tumor-penetrating capacity which may enhance therapeutic efficacy. The EGFR gene, a transmembrane receptor tyrosine kinase, and its mutant form, EGFRvIII, which contains a deletion of exons 2-7 of the EGFR gene, are frequently amplified and overexpressed in a variety of cancers. KDEL increases the toxin's intracellular retention, thereby enhancing its cytotoxicity.
  • Imt-1012 immunotherapeutic vaccine - A multi-peptide cancer vaccine with potential immunostimulating and antineoplastic activities. IMT-1012 immunotherapeutic vaccine contains twelve different synthetic peptides or tumor associated antigens (TAAs), including cyclin I (CCNI), cyclin-dependent kinase CDC2, EDDRI and TACE/ADAM17, each of which is involved in a different pathway associated with tumor growth, survival, and metastasis. Each antigen in the vaccine elicits a specific cytotoxic T-lymphocyte (CTL) immune response against tumor cells expressing that antigen. This multi-antigen/multi-pathway targeting strategy provides broad immunotherapeutic coverage with respect to tumor complexity and heterogeneity and may result in enhanced vaccine efficacy.
  • Inactivated oncolytic virus particle gen0101 - An inactivated, non-replicating particle of hemagglutinating virus of Japan (HVJ), an oncolytic virus of the paramyxovirus family, with potential immunostimulating and antineoplastic activities. Upon intracutaneous administration, GEN0101 targets and binds to the cytosolic nucleic acid receptor retinoic acid-inducible gene I (RIG-I). This induces RIG-I-mediated signaling and a potent innate immune response against tumor cells, leading to the activation of natural killer (NK) cells and cytotoxic T-lymphocytes (CTL), and apoptosis in tumor cells. GEN0101 also activates dendritic cells (DCs) to produce cytokine interleukin-6 (IL-6), suppressing the function of regulatory T cells (Treg), a negative regulator of immune responses. The suppression of Treg activity helps maintain the induced immune responses.
  • Inalimarev - A cancer vaccine comprised of a recombinant vaccinia viral vector encoding the carcinoembryonic antigen (CEA), MUC-1 (mucin-1), a transmembrane glycoprotein secreted by glandular tissues, and TRICOM, comprised of the three co-stimulatory molecule transgenes B7-1, ICAM-1 and LFA-3. Upon administration, inalimarev may enhance CEA and MUC-1 presentation to antigen presenting cells (APC) and may activate a cytotoxic T lymphocyte (CTL) response against CEA- and MUC-1-expressing tumor cells.
  • Incomplete freund's adjuvant - A water-in-oil emulsion that stimulates the T-cell immune response to antigens and may be used in various types of cancer vaccines.
  • Incyclinide - A chemically-modified tetracycline with potential antineoplastic activity. Incyclinide inhibits matrix metalloproteinases (MMPs), thereby inducing extracellular matrix degradation, and inhibiting angiogenesis, tumor growth and invasion, and metastasis. This agent also causes mitochondrial depolarization in tumor cells and induces both cellular apoptosis and tissue necrosis.
  • Indatuximab ravtansine - An immunoconjugate consisting of a monoclonal antibody directed against a highly-expressed myeloma cell surface antigen covalently attached to the maytansinoid DM4, a derivative of the cytotoxic agent maytansine (DM1), with potential antineoplastic activity. Indatuximab ravtansine binds to an unspecified cell surface antigen highly expressed on myeloma cells; upon internalization the DM4 moiety is released, binding to tubulin and disrupting microtubule assembly/disassembly dynamics, which may result in the inhibition of cell division and cell growth of myeloma tumor cells.
  • Indibulin - A synthetic small molecule with antimitotic and potential antineoplastic activities. Indibulin binds to a site on tubulin that is different from taxane- or Vinca alkaloid-binding sites, destabilizing tubulin polymerization and inducing tumor cell cycle arrest and apoptosis. This agent has been shown to be active against multidrug-resistant (MDR) and taxane- resistant tumor cell lines.
  • Indicine-n-oxide - A natural pyrrolizidine alkaloid with antineoplastic properties. Indicine-N-oxide alkylates and crosslinks DNA.
  • Indisulam - A novel sulfonamide compound with potential antineoplastic activity. Indisulam inhibits cyclin-dependent kinases (CDK), which regulate cell cycle progression and are usually over-expressed in cancerous cells. Inhibition of CDK results in G1/S phase arrest of the cell cycle, and may lead to induction of apoptosis and inhibition of tumor cell proliferation. In addition, indisulam also inhibits carbonic anhydrases (CA), especially isoforms IX and XII that are involved in aqueous humor production and are highly overexpressed in some types of cancers. Inhibition of CA IX and XII results in interference with ion exchange and pH in hypoxic tumor tissue and preventing chemoresistance to weakly basic antineoplastic agents.
  • Individualized mva-based vaccine tg4050 - An off-the-shelf (OTS) individualized vaccine comprised of a modified Vaccinia virus Ankara (MVA) viral vector encoding tumor-specific neoantigens (TSNAs), with potential immunostimulatory and antineoplastic activities. Following administration of the individualized MVA-based vaccine TG4050, the neoantigens are expressed and presented to the immune system, which induces the activation of a specific cytotoxic T-lymphocyte (CTL) immune response against tumor cells expressing the patient-specific neoantigens.
  • Indocyanine green-labeled polymeric micelles onm-100 - A micellar polymer tracer labeled with the near-infrared (NIR) fluorescent imaging dye indocyanine green (ICG), with potential fluorescent imaging activity. Upon administration, the ICG-labeled polymeric micelles ONM-100 accumulate in tumor tissue. The micelles dissociate and subsequently fluoresce upon exposure to the acidic conditions of the tumor microenvironment (TME), allowing the visualization of tumors using infrared-based cameras.
  • Indole-3-carbinol - A naturally occurring, orally available cleavage product of the glucosinolate glucobrassicanin, a natural compound present in a wide variety of plant food substances including members of the family Cruciferae with antioxidant and potential chemopreventive properties. Indole-3-carbinol scavenges free radicals and induces various hepatic cytochrome P450 monooxygenases. Specifically, this agent induces the hepatic monooxygenase cytochrome P4501A1 (CYP1A1), resulting in increased 2-hydroxylation of estrogens and increased production of the chemoprotective estrogen 2-hydroxyestrone.
  • Indoleamine 2,3-dioxygenase peptide vaccine - A peptide vaccine against the immunomodulatory enzyme indoleamine 2,3-dioxygenase (IDO), with potential immunomodulating and antineoplastic activities. Vaccination with indoleamine 2,3-dioxygenase peptide vaccine may activate the immune system to induce an immune response against IDO-expressing cells. This may increase and restore the proliferation and activation of various immune cells, including dendritic cells (DCs), natural killer (NK) cells, and T-lymphocytes, and may eradicate IDO-expressing tumor cells. IDO, a cytosolic enzyme responsible for tryptophan catabolism and conversion of tryptophan into kynurenine, is overexpressed by a variety of tumor cell types and antigen presenting cells (APCs) and plays an important role in immunosuppression; Tryptophan depletion inhibits T-lymphocyte proliferation and activation, and suppresses the immune system.
  • Indomethacin - A synthetic nonsteroidal indole derivative with anti-inflammatory activity and chemopreventive properties. As a nonsteroidal anti-inflammatory drug (NSAID), indomethacin inhibits the enzyme cyclooxygenase, thereby preventing cyclooxygenase-mediated DNA adduct formation by heterocyclic aromatic amines. This agent also may inhibit the expression of multidrug-resistant protein type 1, resulting in increased efficacies of some antineoplastic agents in treating multi-drug resistant tumors. In addition, indomethacin activates phosphatases that inhibit the migration and proliferation of cancer cells and downregulates survivin, which may result in tumor cell apoptosis.
  • Indoximod - A methylated tryptophan with immune checkpoint inhibitory activity. Indoximod inhibits the enzyme indoleamine 2,3-dioxygenase (IDO), which degrades the essential amino acid tryptophan, and may increase or maintain tryptophan levels important to T cell function. Tryptophan depletion is associated with immunosuppression involving T cell arrest and anergy.
  • Indoximod prodrug nlg802 - An orally bioavailable prodrug of indoximod, a methylated tryptophan, with immune checkpoint inhibitory and antineoplastic activities. Upon oral administration, the indoximod prodrug NLG802 is converted to indoximod. Indoximod targets, binds to and inhibits the enzyme indoleamine 2,3-dioxygenase (IDO; IDO1), which converts the essential amino acid tryptophan into the immunosuppressive metabolite kynurenine. By increasing tryptophan levels and decreasing kynurenine levels, indoximod restores and promotes the proliferation and activation of various immune cells, including dendritic cells (DCs), natural killer (NK) cells, and T-lymphocytes, and causes a reduction in tumor-associated regulatory T-cells (Tregs). Activation of the immune system, which is suppressed in many cancers, may induce a cytotoxic T-lymphocyte (CTL) response against IDO1-expressing tumor cells, thereby inhibiting their growth. IDO1, overexpressed by multiple tumor cell types, plays an important role in immunosuppression. Tryptophan depletion inhibits T-lymphocyte proliferation and activation, and subsequently suppresses the immune system. NLG802 elicits increased plasma concentrations of indoximod and improves its efficacy, compared to the direct administration of indoximod.
  • Indusatumab vedotin - An antibody-drug conjugate (ADC) containing a monoclonal antibody directed against guanylyl cyclase C (GCC or GUCY2C) conjugated to monomethylauristatin E (MMAE), an auristatin derivative and a potent microtubule inhibitor, with potential antineoplastic activity. The monoclonal antibody moiety of indusatumab vedotin selectively binds to GCC, a transmembrane receptor normally found on intestinal cells and dopamine neurons in the brain, but is also overexpressed on the surface of gastrointestinal cancers. Upon internalization and proteolytic cleavage, MMAE binds to tubulin and inhibits its polymerization, resulting in G2/M phase arrest and tumor cell apoptosis in GCC-expressing tumor cells.
  • Inebilizumab - A humanized immunoglobulin IgG1 kappa monoclonal antibody directed against the B-cell-specific membrane protein CD-19 with potential immunostimulating and antineoplastic activities. Inebilizumab binds to CD19, which may result in a cytotoxic T-lymphocyte (CTL) response and antibody-dependent cellular cytotoxicity (ADCC) to CD19-expressing B-cells. The Fc portion of inebilizumab does not contain a fucose sugar moiety, which may contribute to its enhanced ADCC activity. CD19 is a membrane antigen that is widely expressed during B-cell development, from pro-B-cell to early plasma cell stages.
  • Inecalcitol - An analog of calcitriol and a vitamin D3 receptor (VDR) agonist, with potential antineoplastic activity. Upon administration, inecalcitol targets and binds to VDR. This activates VDR and VDR-mediated signal transduction pathways. This modulates the VDR-mediated expression of certain genes, including the expression of anti-cancer genes, enhances cellular differentiation, induces tumor cell apoptosis and inhibits tumor cell growth. VDR plays a central role in calcium homeostasis and in the growth of certain cancer cells.
  • Infigratinib - An orally bioavailable pan inhibitor of human fibroblast growth factor receptors (FGFRs) with potential antiangiogenic and antineoplastic activities. Infigratinib selectively binds to and inhibits the activities of FGFRs, which may result in the inhibition of tumor angiogenesis and tumor cell proliferation, and the induction of tumor cell death. FGFRs are a family of receptor tyrosine kinases which may be upregulated in various tumor cell types and may be involved in tumor cell differentiation and proliferation, tumor angiogenesis, and tumor cell survival.
  • Infigratinib mesylate - The mesylate salt of infigratinib, an orally bioavailable pan-inhibitor of human fibroblast growth factor receptors (FGFRs) with potential antiangiogenic and antineoplastic activities. Upon administration, infigratinib selectively binds to and inhibits the activities of FGFRs, which may result in the inhibition of tumor angiogenesis and tumor cell proliferation, and the induction of tumor cell death. FGFRs are a family of receptor tyrosine kinases which may be upregulated in various tumor cell types and may be involved in tumor cell differentiation and proliferation, tumor angiogenesis, and tumor cell survival.
  • Infliximab - A recombinant chimeric, mouse-human monoclonal antibody directed against tumor necrosis factor alpha (TNF-alpha), a protein involved in inflammation, cell survival, and apoptosis. Infliximab may be pro- apoptotic or anti-apoptotic, depending on cell type.
  • Ingenol mebutate - A selective small-molecule activator of protein kinase C (PKC) isolated from the plant Euphorbia peplus with potential antineoplastic activity. Ingenol mebutate activates various protein kinase C (PKC) isoforms, thereby inducing apoptosis in some tumor cells, including myeloid leukemia cells, melanoma cells, and basal cell carcinoma cells. The PKC family consists of signaling isoenzymes that regulate many cell processes including proliferation, differentiation, and apoptosis.
  • Ingenol mebutate gel - A topical, aqueous gel formulation containing the mebutate salt form of ingenol, a selective small-molecule activator of protein kinase C (PKC) that is isolated from the sap of Euphorbia species, with potential antineoplastic activity. Upon topical application of the ingenol mebutate gel, ingenol activates various PKC isoforms, which induces apoptosis in certain tumor cells, including myeloid leukemia cells, melanoma cells, and basal cell carcinoma cells. The PKC family consists of signaling isoenzymes that regulate many cell processes, including proliferation, differentiation, and apoptosis.
  • Iniparib - A small molecule iodobenzamide with potential cytotoxic and antineoplastic activities. Although the mechanism of action is unknown, iniparib appears to be cytotoxic in cells with DNA alterations or DNA damage, like that found in tumor cells with mutations in the ataxia telangiectasia mutated (ATM) gene. ATM encodes a serine/threonine protein kinase and mutations of the gene are associated with ataxia telangiectasia and contribute to certain cancers such as T-cell acute lymphoblastic leukemia, B-cell chronic lymphocytic leukemia and B-cell non-Hodgkin lymphomas.
  • Inkt cell agonist abx196 - A synthetic glycolipid agonist for natural killer T-cells (NKTs) expressing an invariant (alpha, beta) T-cell receptor (iNKTs), with potential immunomodulating and antineoplastic activities. Upon infusion of the iNKT cell agonist ABX196, this agent targets and binds to iNKTs, thereby activating iNKTs. In turn, iNKTs recognize CD1d-restricted lipid ligands, which are expressed on certain tumor cells, and secrete large amounts of various cytokines. This may activate the immune system against tumor cells. Additionally, iNKTs directly target and lyse tumor cells.
  • Innate immunostimulator rbbx-01 - A recombinant 19 kDa protein derived from the Apicomplexa protozoan Eimeria with potential immunostimulating and antitumor activities. Upon administration, innate immunostimulator rBBX-01 activates dendritic cells (DCs), stimulates the Toll-like receptor 11 (TLR-11)-mediated release of interleukin-12 (Il-12) from DCs, and induces a T-helper 1 (Th1) type immune response, which may induce an immune response against tumor cells. Infection with Eimeria, a coccidian commonly infecting the intestine, may be negatively correlated with tumorigenesis.
  • Ino-1001 - A isoindolinone derivative and potent inhibitor of the nuclear enzyme poly (ADP-ribose) polymerase (PARP) with chemosensitization and radiosensitization properties. INO-1001 inhibits PARP, which may result in inhibition of tumor cell DNA repair mechanisms and, so, tumor cell resistance to chemotherapy and radiation therapy. PARP enzymes are activated by DNA breaks and have been implicated in the repair of DNA single-strand breaks (SSB).
  • Inodiftagene vixteplasmid - A recombinant DNA plasmid carrying the gene for diphtheria toxin-A (dT-A) chain under the regulation of the H19 promoter, with potential antineoplastic activity. Upon intravesical administration, dT-A chain expression is triggered by the presence of H19 transcription factors that are upregulated in tumor cells. The dT-A chain binds to nicotinamide adenine dinucleotide (NAD) and inactivates the ADP-ribosylation of elongation factor 2 (EF2), resulting in the inhibition of protein synthesis and cell death leading to tumor cell destruction. Inodiftagene Vixteplasmid does not carry the gene for the diphtheria toxin-B (dT-B) chain, thereby preventing the transfer of the toxic dT-A chain between cells. H19, a paternally imprinted, oncofetal gene, is highly expressed in embryonic and certain malignant tissues, but minimally expressed in normal, adult tissues.
  • Inos dimerization inhibitor asp9853 - An orally bioavailable small molecule inhibitor of inducible nitric oxide synthase (iNOS) with potential antineoplastic activity. Upon administration, ASP9853 inhibits iNOS dimerization, which results in decreased nitric oxide (NO) production. iNOS expression is upregulated in certain cancers and may invoke a chronic inflammatory state in tumor cells that promotes metastatic growth.
  • Inosine 5'-monophosphate dehydrogenase inhibitor ff-10501-01 - An orally bioavailable inhibitor of inosine 5'- monophosphate dehydrogenase (IMPDH), with potential antineoplastic activity. Upon administration, IMPDH inhibitor FF-10501-01 competitively inhibits the enzyme IMPDH, thereby preventing the conversion of inosine monophosphate to xanthosine monophosphate. This inhibits the synthesis of guanine nucleotides, deprives cancer cells of guanosine triphosphate (GTP), disrupts DNA and RNA synthesis, and decreases tumor cell proliferation. Tumor cells are highly susceptible to IMPDH inhibition because they are rapidly dividing cells that are dependent on rapid DNA synthesis, which requires a high concentration of nucleotides. IMPDH, an enzyme that catalyzes the rate-limiting step in the synthesis of guanosine triphosphate (GTP), is overexpressed in numerous tumor cell types.
  • Inosine monophosphate dehydrogenase inhibitor avn944 - An orally available, synthetic small molecule with potential antineoplastic activity. AVN944 inhibits inosine monosphosphate dehydrogenase (IMPDH), an enzyme involved in the de novo synthesis of guanosine triphosphate (GTP), a purine molecule required for DNA and RNA synthesis. Inhibition of IMPDH deprives cancer cells of GTP, resulting in disruption of DNA and RNA synthesis, inhibition of cell proliferation, and the induction of apoptosis. AVN944 appears to have a selective effect on cancer cells in that deprivation of GTP in normal cells results in a temporary slowing of cell growth only. IMPDH is overexpressed in some cancer cells, particularly in hematological malignancies.
  • Inositol - A natural sugar found in cell membrane phospholipids, plasma lipoproteins, and (as the phosphate form) in the nucleus with potential chemopreventive properties. As one of a number of intracellular phosphate compounds, inositol is involved in cell signaling and may stimulate tumor cell differentiation.
  • Inotuzumab ozogamicin - A CD22-targeted cytotoxic immunoconjugate composed of a humanized IgG4 anti-CD22 antibody covalently linked to N-acetyl-gamma-calicheamicin dimethyl hydrazide (CalichDMH) with potential antineoplastic activity. Inotuzumab ozogamicin is rapidly internalized upon binding of the antibody moiety to B cell-specific CD22 receptors, delivering the conjugated CalichDMH intracellularly; the CalichDMH moiety binds to the minor groove of DNA in a sequence-specific manner, resulting in double-strand DNA breaks and apoptosis. CalichDMH is a derivative of gamma calicheamicin, a cytotoxic antibiotic produced by the bacterium Micromonospora echinospora.
  • Inproquone - A benzoquinone-based antineoplastic agent. Inproquone was never marketed.
  • Integrin alpha-2 inhibitor e7820 - A small molecule and aromatic sulfonamide derivative with potential antiangiogenic and antitumor activities. E7820 inhibits angiogenesis by suppressing integrin alpha 2, a cell adhesion molecule expressed on endothelial cells. Inhibition of integrin alpha 2 leads to an inhibition of cell-cell interactions, endothelial cell-matrix interactions, vascular endothelial cell proliferation and angiogenesis.
  • Integrin receptor antagonist glpg0187 - A small molecule integrin receptor antagonist (IRA) with potential antineoplastic activity. Upon administration, GLPG0187 binds to and blocks the activity of 5 RGD-integrin receptor subtypes, including alphavbeta1, alphavbeta3, alphavbeta5, alphavbeta6 and alpha5beta1. This may result in the inhibition of endothelial cell-cell interactions and endothelial cell-matrix interactions, and the prevention of angiogenesis and metastasis in tumor cells expressing these integrin receptors. Integrin receptors are transmembrane glycoproteins expressed on the surface of tumor vessel endothelial cells and some types of cancer cells, and play a crucial role in endothelial cell adhesion and migration.
  • Interferon alfacon-1 - An analogue of consensus interferon which contains an additional methionyl amino acid residue. Consensus interferon (also known as interferon alfacon-1, rCon-IFN, and CIFN) is a genetically engineered synthetic interferon created from the most common amino acid sequences from the naturally occurring alpha interferons. Alpha interferons bind to specific cell-surface receptors, resulting in the transcription and translation of genes whose protein products have antiviral, antiproliferative, anticancer, and immune-modulating effects.
  • Interferon alfa-n1 - A highly purified alpha interferon produced by a human lymphoid cell line. Interferon alpha-n1 consists of multiple alpha interferon subtypes, at least two of which are glycosylated. In contrast, recombinant alpha interferons are individual non-glycosylated proteins produced from individual alpha interferon genes. Alpha interferons bind to specific cell-surface receptors, resulting in the transcription and translation of genes whose proteins have antiviral, antiproliferative, anticancer, and immune-modulating effects.
  • Interferon alfa-n3 - A formulated therapeutic analog of the endogenous alpha interferon containing multiple interferon species with antiviral and antitumor properties. Interferons bind to specific cell-surface receptors, leading to the transcription and translation of genes with an interferon-specific response element, thereby inducing: antiviral effects (the most important being inhibition of viral protein synthesis); antiproliferative effects (including inhibition of cellular growth and alteration of cellular differentiation); anticancer effects (including interference with oncogene expression); and immune-modulating effects (including activation of natural killer cells, alteration of cell surface antigen expression, and augmentation of lymphocyte and macrophage cytotoxicity).
  • Interferon beta-1a - A recombinant form of the endogenous cytokine human interferon (IFN) beta-1a, with antiproliferative, antiviral and immunomodulating activities. Upon administration, interferon beta-1a targets and binds to specific type I IFN receptors, which eventually results in the transcription and translation of genes containing an interferon-specific response element and leads to the production of various anti-viral proteins and modulates the production of various immune-modulating proteins. This reduces the production of certain pro-inflammatory cytokines while upregulating the anti-inflammatory cytokine interleukin 10 (IL-10), upregulates the expression of major histocompatibility (MHC) I proteins which allows for increased presentation of peptides derived from viral antigens, and activates CD8+ T cells as well as other immune cells. Endogenous IFN-beta-1a is produced following viral infection and it plays a key role in innate immune response against viral pathogens.
  • Interferon beta-secreting mesenchymal stem cells - Human autologous mesenchymal stem cells (MSCs) harvested from the bone marrow of healthy individuals and transduced with a retroviral vector encoding the human cytokine interferon beta (IFNb), with potential immunomodulating and antineoplastic activities. Upon administration of IFNb-secreting MSCs, the cells are attracted and specifically migrate to tumor sites and become part of the tumor microenvironment. Since the MSCs express IFNb, these cells selectively deliver high levels of IFNb to the tumor site. In turn, IFNb binds to IFN-specific cell surface receptors and modulates the transcription and translation of certain genes whose protein products are involved in tumor cell proliferation. This decreases tumor cell growth.
  • Interferon-gamma-expressing adenovirus vaccine asn-002 - A replication-defective adenoviral serotype 5 vector encoding a recombinant form of the human cytokine interferon-gamma (IFN-g), with potential antineoplastic and immunoregulatory activities. Upon intratumoral administration, the sustained expression of IFN-g by IFN-g-expressing adenovirus vaccine ASN-002 promotes a T-helper type 1 (Th1) immune response and inhibits the Th2-mediated cytokine production observed in many cutaneous lymphomas. IFN-g also mediates interleukin-12 (IL-12) production by antigen-presenting cells (APCs); activates macrophages, cytotoxic T-cells, and natural killer (NK) cells; upregulates major histocompatibility complex (MHC) molecules; and stimulates antibody-dependent cellular cytotoxicity (ADCC). Altogether, these IFN-g-mediated effects may result in both an inhibition of tumor cell proliferation and tumor cell death. Compared to IFN-g injections, the prolonged local production of IFN-g at the tumor site allows for higher efficacy and a reduction of systemic toxicity.
  • Interleukin-12 gene - The DNA sequence that encodes the protein cytokine interleukin-12 (IL-12). When introduced as the complementary DNA (cDNA) form into tumor cells by, for example, a genetically engineered adenovirus vector, the transfected IL-12 cDNA expresses IL-12 which activates antitumoral natural killer (NK) cells and CD8+ T-cells and stimulates the secretion of interferon-gamma (IFN-gamma), potentially inhibiting tumor cell metastasis. This gene therapy may also result in IL-12-mediated inhibition of vascular endothelial growth factor (VEGF) and enhancement of matrix metalloproteinases (MMPs).
  • Interleukin-12-fc fusion protein df6002 - A fusion protein composed of human interleukin-12 (IL-12) fused to a Fc fragment, with potential immunomodulatory and antineoplastic activities. Upon administration of IL-12-Fc fusion protein DF6002, the IL-12 moiety binds to the IL-12 receptor. This may activate the immune system by promoting the secretion of interferon-gamma, activating natural killer cells (NKs), and inducing cytotoxic T-lymphocyte (CTL) responses, which may result in both decreased tumor cell proliferation and enhanced immune-mediated destruction of tumor cells.
  • Interleukin-15 agonist fusion protein shr1501 - A human Fc fusion protein composed of the cytokine interleukin (IL)-15 cross-linked with the high-affinity binding sushi domain of IL-15 receptor alpha (IL-15Ra), with potential antineoplastic activity. Upon administration, SHR-1501 activates and increases the levels of natural killer (NK) cells and memory CD8+ T-cells without stimulating regulatory T-cells (Tregs). The memory T-cells enhance the secretion of the cytokine interferon-gamma (IFN-g), which further potentiates the immune response against tumor cells. This may increase tumor cell killing and decrease tumor cell proliferation. IL-15 regulates CD8+ T and NK cell development, activation and proliferation. SHR1501 is more potent than unmodified IL-15 and does not require endogenous IL-15Ra for its action. The Fc moiety allows for an extended half-life of SHR-1501 while cross linking IL-15 with IL-15Ra sushi domain improves stability.
  • Interleukin-15 fusion protein bj-001 - A human fusion protein composed of the cytokine interleukin (IL)-15 linked with an integrins-targeting moiety, with potential antineoplastic activity. Upon subcutaneous administration, the integrins-targeting moiety of BJ-001 targets tumor cells that overexpress integrins such as alpha v beta 3 (avb3), alpha v beta 5 (avb5) and alpha v beta 6 (avb6) and the IL-15 moiety binds to the IL-2/IL-15 receptor beta-common gamma chain (IL-2Rbetagamma) receptor on natural killer (NK) cells and CD8+ T-lymphocytes. This activates and increases the levels of NK cells and memory CD8+ T-cells. The memory T-cells enhance the secretion of the cytokine interferon-gamma (IFN-g), which further potentiates the immune response against tumor cells. This may increase tumor cell killing and decrease tumor cell proliferation. IL-15 regulates CD8+ T- and NK cell development, activation and proliferation. Integrins are involved in tumor growth, angiogenesis, and metastasis and they are overexpressed in a variety of tumor cell types. The linkage of the two moieties may limit the effects of IL-15 to the local tumor microenvironment (TME), increasing efficacy while reducing systemic toxicities.
  • Interleukin-15/interleukin-15 receptor alpha complex-fc fusion protein xmab24306 - An interleukin (IL)-15/IL-15-receptor alpha (IL-15Ra) complex fused to a bispecific Fc domain, with potential antineoplastic activity. Upon administration, XmAb24306 stimulates the proliferation of natural killer (NK) cells and memory CD8+ T-cells. The memory T-cells enhance the secretion of the cytokine interferon-gamma (IFN-g), which further potentiates the immune response against tumor cells. This may increase tumor cell killing and decrease tumor cell proliferation. IL-15 regulates CD8+ T and NK cell development, activation and proliferation. XmAb24306 does not require endogenous IL-15Ra for its activation.
  • Interleukin-15/interleukin-15 receptor alpha sushi+ domain fusion protein so-c101 - A human fusion protein consisting of the cytokine interleukin (IL)-15 and the high-affinity binding sushi+ domain of IL-15 receptor alpha (IL-15Ra), with potential antineoplastic activities. Upon administration, SO-C101 activates and increases the levels of natural killer (NK) cells and memory CD8+ T-cells. The memory T-cells enhance the secretion of the cytokine interferon-gamma (IFN-g), which further potentiates the immune response against tumor cells. This may increase tumor cell killing and decrease tumor cell proliferation. IL-15 regulates CD8+ T and NK cell development, activation and proliferation. SO-C101 is more potent than unmodified IL-15 and does not require endogenous IL-15Ra for its action.
  • Interleukin-2 gene - The DNA sequence that encodes the protein cytokine interleukin-2 (IL-2). When introduced as the complementary DNA (cDNA) form into tumor cells by, for example, a genetically engineered adenovirus vector, the transfected IL-2 cDNA expresses IL-2 which may activate antitumoral natural killer cells and elicit an antitumoral cytotoxic T-cell response, resulting in an inhibition of tumor progression.
  • Interleukin-2 liposome - A formulation in which liposomes are loaded with the cytokine interleukin-2 (IL-2). By activating cytotoxic T-lymphocytes, such as lymphokine-activated killer cells, and increasing levels of the cytotoxic cytokines interferon-gamma (IFN-gamma) and transforming growth factor-beta (TGF-beta), IL-2 may exhibit antitumoral activity. Liposomal formulations of IL-2 may promote entry of the cytokine into target tumor cells and may be used as an immunoadjuvant in cancer vaccine therapy.
  • Intermediate-affinity interleukin-2 receptor agonist alks 4230 - A selective effector cell activator protein and agonist of the intermediate-affinity interleukin-2 (IL-2) receptor with potential immunostimulating and antineoplastic activity. Upon administration, intermediate-affinity interleukin-2 receptor agonist ALKS 4230 binds to and signals through the intermediate-affinity IL-2 receptor complex; this may selectively stimulate and activate natural killer (NK) cells and memory CD8 T-cells, leading to tumor cell elimination, while circumventing the activation of immunosuppressive cells that may prevent the anti-tumor response. IL-2 is a cytokine signaling molecule that plays a critical role in the immune response.
  • Intetumumab - A pan alpha-v human monoclonal antibody that recognizes alpha-v beta-1, alpha-v beta-3, alpha-v beta-5, and alpha-v beta-6 integrins with antiangiogenic and antitumor activities. Intetumumab competitively binds to and blocks both alpha-v beta-3 and alpha-v beta-5 integrins, resulting in inhibition of integrin-mediated tumor angiogenesis and tumor growth. Integrins facilitate the adhesion of stimulated endothelial cells to the extracellular matrix (ECM); trigger the secretion of ECM-rearranging proteases; and propagate signaling events that promote the survival and differentiation of cells in newly formed vasculature.
  • Intoplicine - A benzopyridoindole derivative with antineoplastic property. Intoplicine inhibits activities of both topoisomerase I and II via intercalating DNA helix, thereby hindering the movements of enzymes along DNA molecules during DNA transcription and replication, respectively. Furthermore, this agent stabilizes DNA-enzyme complexes during unwinding processes by both topoisomerases, leading to double- and single-stranded DNA breaks. Consequently, these effects bring about cell growth inhibition and apoptosis of tumor cells.
  • Inulin - A naturally occurring, indigestible and non-absorbable oligosaccharide produced by certain plants with prebiotic and potential anticancer activity. Inulin stimulates the growth of beneficial bacteria in the colon, including Bifidobacteria and Lactobacilli, thereby modulating the composition of microflora. This creates an environment that protects against pathogens, toxins and carcinogens, which can cause inflammation and cancer. In addition, fermentation of inulin leads to an increase in short-chain fatty acids and lactic acid production, thereby reducing colonic pH, which may further control pathogenic bacteria growth and may contribute to inulin's cancer protective properties.
  • Iobenguane i-131 - An I 131 radioiodinated synthetic analogue of the neurotransmitter norepinephrine. Iobenguane localizes to adrenergic tissue and, in radioiodinated forms, may be used to image or eradicate tumor cells that take up and metabolize norepinephrine.
  • Iodine i 124 monoclonal antibody a33 - A radioimmunoconjugate of a humanized monoclonal antibody (MoAb) A33 labelled with Iodine 124 (I-124). MoAb A33 recognizes A33 antigen, a 43 KDa transmembrane glycoprotein of the immunoglobulin superfamily, highly and homogenously expressed in 95% of colorectal cancer metastases, with only restricted expression in normal colonic mucosa. I-124 MoAb A33 delivers beta particle emitting I-124 nuclide directly to metastatic colorectal tissues, thereby this agent could be used in kinetics studies or radioimmunotherapy.
  • Iodine i 124 monoclonal antibody m5a - A radioimmunoconjugate comprised of M5A, a humanized monoclonal antibody directed against carcinoembryonic antigen-related cell adhesion molecule 5 (CEA or CEACAM5), labeled with iodine I 124 (I-124) with potential radiolocalization applications. Upon administration, the antibody moiety of iodine I 124 monoclonal antibody M5A specifically binds to cells expressing CEA. Upon binding, the radioisotope moiety can be detected using positron-emission tomography (PET), thereby allowing the imaging and quantification of CEA-expressing tumor cells. CEA, a tumor associated antigen and a member of the CEA family of proteins, plays a key role in cell migration, cell invasion, and cell adhesion and is overexpressed by a variety of cancer types.
  • Iodine i 125-anti-egfr-425 monoclonal antibody - A radioimmunoconjugate consisting of a murine IgG2a monoclonal antibody directed against the human epidermal growth factor receptor (EGFR) labeled with iodine I 125 with potential antineoplastic activity. Iodine I 125 anti-EGFR-425 monoclonal antibody binds specifically to the epidermal growth factor receptor (EGFR). Upon binding to EGFR-expressing tumor cells, this agent is internalized, selectively delivering a potentially cytotoxic dose of gamma radiation. EGFR is a receptor tyrosine kinase that may be overexpressed on the cell surfaces of various solid tumors.
  • Iodine i 131 anti-fibronectin antibody fragment l19-sip - An iodine 131 radioimmunoconjugate of a small immunoprotein (SIP), derived from the variable region fragment of human monoclonal antibody L19, that is directed against the extra-domain B (ED-B) of fibronectin, with potential radioimmunotherapeutic activity. The SIP moiety of iodine I 131 anti-fibronectin antibody fragment L19-SIP binds to the ED-B domain of fibronectin on tumor cells in the tumor neovasculature. Upon internalization, the I 131 radionuclide may selectively detect or deliver cytotoxic radiation to fibronectin-expressing tumor cells. ED-B of fibronectin, a naturally occurring marker of tissue remodeling and angiogenesis, is expressed in the majority of aggressive solid human tumors, whereas it is not detectable in normal vessels and tissues.
  • Iodine i 131 apamistamab - A radioimmunoconjugate consisting of BC8, a murine IgG1 anti-CD45 monoclonal antibody labeled with iodine 131 (I-131), with radioimmunotherapeutic properties. Using monoclonal antibody BC8 as a carrier for I-131 results in the targeted destruction of cells expressing CD45. CD45 is tyrosine phosphatase expressed on virtually all leukocytes, including myeloid and lymphoid precursors in bone marrow and mature lymphocytes in lymph nodes; it is also expressed on most myeloid and lymphoid leukemic cells, but not on mature erythrocytes or platelets.
  • Iodine i 131 derlotuximab biotin - An iodine 131 labeled radioimmunoconjugate of monoclonal antibody (MOAB) TNT-1/B with radioimaging and antineoplastic properties. MOAB TNT-1/B was developed for radioimmunotherapy of solid tumors, designated as Tumor Necrosis Treatment (TNT). TNT exploits the presence of degenerating and necrotic cells within tumors by utilizing MOAbs directed against universal, intracellular nucleosomal determinants consisting of histone H1 and DNA. This MOAB was conjugated with biotin (B) molecules, which increase pharmacokinetic performance of the monoclonal antibody. Upon administration, iodine I 131 derlotuximab biotin delivers I 131 to tumor cells and results in the targeted imaging and/or destruction of cells with exposed necrotic antigens.
  • Iodine i 131 ethiodized oil - A cytotoxic radioconjugate consisting of lipiodol, an iodinated ethyl ester derived from poppy seed oil, labeled with iodine 131 (I-131). I-131 Lipiodol accumulates in hepatocellular carcinoma and hepatoblastoma tumor cells, resulting in targeted cytotoxicity to tumor cells while sparing surrounding normal cells and tissues.
  • Iodine i 131 ipa - A radioconjugate consisting of the tumor-specific amino acid derivative 4-iodo-L-phenylalanine labeled with iodine I 131, a beta emitting radionuclide, with potential antineoplastic activity. Upon administration, iodine I 131 IPA actively crosses the blood-brain barrier and accumulates specifically in gliomas, via the amino acid transport system l-amino acid transporter 1 (LAT1) over-expressed in malignant glioma cells. where it delivers a cytotoxic dose of beta radiation. Cells that are exposed to radiation may also release potent toxins into the intracellular environment, leading to radiation-induced biological bystander effects (RIBBE) and killing cells not directly exposed to the radiation. Iodine I 131 IPA may also act synergistically with external irradiation due to its radiosensitizing property.
  • Iodine i 131 mip-1095 - A radioconjugate composed of MIP-1095, a urea-based ligand for the tumor-associated antigen (TAA) prostate-specific membrane antigen (PSMA) radiolabeled with iodine I 131 (I131), with potential antineoplastic activity. Upon administration of iodine I 131 MIP-1095, the MIP-1095 moiety selectively targets and binds to the extracellular domain of PSMA, thereby delivering cytotoxic iodine I 131 specifically to PSMA-expressing cancer cells. PSMA is a transmembrane glycoprotein that is highly expressed by malignant prostate epithelial cells and certain other tumor cells.
  • Iodine i 131 monoclonal antibody 81c6 - A radioimmunoconjugate consisting of 81C6, a murine IgG2 anti-tenascin monoclonal antibody labeled with iodine 131 (I-131), with radioimaging and radioimmunotherapeutic activities. Using monoclonal antibody 81C6 as a carrier for I-131 results in the targeted imaging and/or destruction of cells expressing tenascin. Tenascin is an extracellular matrix protein which is overexpressed in gliomas and other cancers.
  • Iodine i 131 monoclonal antibody cc49-deltach2 - A radioimmunoconjugate consisting of the humanized CH2 domain-deleted monoclonal antibody CC49 and iodine I 131 with antineoplastic activity. Monoclonal antibody CC49-deltaCH2 targets the tumor-associated glycoprotein 72 (TAG-72) that is expressed by a wide range of human neoplasms including colorectal, gastric, pancreatic, ovarian, endometrial, breast, non-small cell lung, and prostate cancers. Iodine I 131 monoclonal antibody CC49-deltaCH2 binds to tumor cells expressing TAG-72, selectively delivering a cytotoxic dose of beta and gamma radiation.
  • Iodine i 131 monoclonal antibody f16sip - A fully human monoclonal antibody (MoAb) against human A1 domain of tenascin-C, in small immunoprotein (SIP) format conjugated with iodine 131 with potential antineoplastic activity. Iodine I 131 MoAb F16SIP binds to tenascin-C on the vascular tissues and delivers cytotoxic radiation to the tumors, thereby minimizing systemic radiotoxicity. Tenascin-C is a glycoprotein of the extracellular matrix, and the large isoform of this matrix protein is expressed and restricted around vascular structures in the tumor stroma of a variety of different tumors.
  • Iodine i 131 monoclonal antibody g-250 - A radioimmunoconjugate comprised of the chimeric monoclonal antibody G-250 conjugated with iodine I 131 with potential antineoplastic activity. The antibody moiety of iodine I 131 chimeric monoclonal antibody G-250 binds to G-250, a renal-cell carcinoma-associated antigen, delivering cytotoxic iodine I 131 specifically to renal carcinoma cells that express G-250.
  • Iodine i 131 monoclonal antibody muj591 - A radioimmunoconjugate of a mouse monoclonal antibody (MoAb) J591 labeled with Iodine 131 (I-131). MoAb muJ591 recognizes the extracellular domain of the prostate-specific membrane antigen (PSMA) and reacts with tumor vascular endothelium. Using MoAb muJ591 as a carrier for I-131 results in the targeted imaging and/or destruction of cells overexpressed PSM.
  • Iodine i 131 omburtamab - A radioimmunoconjugate consisting of the iodine 131-radiolabeled murine IgG1 monoclonal antibody 8H9 directed against the surface immunomodulatory glycoprotein 4Ig-B7-H3 with potential radioimaging and radioimmunotherapeutic uses. Iodine I 131 monoclonal antibody 8H9 binds to 4Ig-B7-H3 (human B7-H3 with 4 Ig-like domains) and may be used to radioimage and/or destroy tumor cells that express tenascin. 4Ig-B7-H3 inhibits T-cell activation and the production of effector cytokines such as interferon-gamma and interleukin-4; it is expressed on the cell membranes of a wide variety of tumors of neuroectodermal, mesenchymal and epithelial origin and is highly expressed on monocyte-derived dendritic cells (mdDCs). In vitro, it has been shown that monoclonal antibody-mediated masking of 4Ig-B7-H3 on neuroblastoma cells resulted in the enhancement of natural killer (NK)-mediated lysis of target cells.
  • Iodine i 131 rituximab - A radioimmunoconjugate comprised of rituximab, a recombinant chimeric monoclonal antibody directed against the CD20 antigen, and labeled with iodine I 131 with potential antineoplastic activity. The antibody moiety of iodine I 131 rituximab binds to the CD20 antigen thereby delivering cytotoxic iodine I 131 specifically to cancer cells expressing CD20. The CD20 antigen, a hydrophobic transmembrane protein, is expressed on normal pre-B and mature B lymphocytes.
  • Iodine i 131 tenatumomab - A radioimmunoconjugate of tenatumomab, a murine monoclonal antibody targeting the tumor-associated antigen (TAA) tenascin-C (TNC), labeled with iodine I 131, with potential antineoplastic activity. The antibody moiety of iodine I 131 tenatumomab binds to TNC, thereby delivering a cytotoxic dose of iodine I 131 specifically to tumors expressing TNC. TNC, an extracellular matrix protein, is upregulated in a variety of tumor cell types; it plays a key role in invasion, tumor cell proliferation and immune evasion.
  • Iodine i 131 tm-601 - An iodine 131 (I 131) radioconjugate of the synthetic chlorotoxin (CTX) TM-601 with potential antiangiogenic and antineoplastic activities. CTX is a 36 amino acid neurotoxin found in the venom of the giant yellow scorpion Leiurus quinquestriatus that preferentially binds malignant cells of neuroectodermal origin. The recombinant version of this peptide, TM-601, is expressed in and purified from E. coli and then covalently linked to I 131 to produce 131I-TM-601. 131I-TM-601 binds to tumor cells of neuroectodermal origin and is internalized; administered once, it may be used as a radioimaging agent; repeated administration may result in a tumor-specific, cumulative radiocytotoxic dose of I 131. In addition, TM-601 alone, similar to native CTX, may inhibit angiogenesis due to its ability to bind to and inhibit matrix metalloproteinase 2 (MMP-2), an endopeptidase involved in tissue remodeling processes such as angiogenesis.
  • Iodine i 131 tositumomab - A monoclonal antibody directed against the CD20 protein expressed on the surface of B-lymphocytes and radiolabeled with the radioisotope iodine I 131 with potential antineoplastic activity. Iodine I 131 tositumomab binds to and selectively delivers cyctotoxic radiation to CD20-expressing B-lymphocytes, thereby minimizing systemic radiotoxicity.
  • Iodine i-131 - A radioactive isotope of iodine with an atomic mass of 131, a half life of eight days, and potential antineoplastic activity. Selectively accumulating in the thyroid gland, iodine I 131 emits beta and gamma particles, thereby killing thyroid cells and decreasing thyroid hormone production.
  • Ioflubenzamide i-131 - An iodine 131-radiolabeled small-molecule benzamide compound with potential antineoplastic activity. The benzamide moiety of 131-I-MIP-1145 binds to melanin, selectively delivering a cyotoxic dose of gamma and beta radiation to melanin-expressing tumor cells. Melanin pigments, polymer derivatives of the amino acid tyrosine, are over-expressed in approximately 40% of melanomas.
  • Ionomycin - A polyether antibiotic isolated from Streptomyces conglobatus sp. nov. Trejo with antineoplastic activity. Ionomycin is a calcium ionophore that increases intracellular Ca++ levels, possibly relating to endonuclease activation of lymphocytes and decreased ratio of Bcl-2 to Bax and ultimately apoptosis. In addition, this agent is used to investigate the role of intracellular calcium in cellular processes. (NCI)
  • Ipafricept - A proprietary fusion protein comprised of the cysteine-rich domain of frizzled family receptor 8 (Fzd8) fused to the human immunoglobulin Fc domain with potential antineoplastic activity. Upon intravenous administration, ipafricept competes with the membrane-bound Fzd8 receptor for its ligand, Wnt proteins, thereby antagonizing Wnt signaling. This may result in the inhibition of Wnt-driven tumor growth. Fzd8, a member of the Frizzled family of G protein-coupled receptors, is one of the components in the Wnt/beta-catenin signaling pathway that plays key roles in embryogenesis and cancer growth.
  • Ipatasertib - An orally bioavailable inhibitor of the serine/threonine protein kinase Akt (protein kinase B) with potential antineoplastic activity. Ipatasertib binds to and inhibits the activity of Akt in a non-ATP-competitive manner, which may result in the inhibition of the PI3K/Akt signaling pathway and tumor cell proliferation and the induction of tumor cell apoptosis. Activation of the PI3K/Akt signaling pathway is frequently associated with tumorigenesis and dysregulated PI3K/Akt signaling may contribute to tumor resistance to a variety of antineoplastic agents.
  • Ipilimumab - A recombinant human immunoglobulin (Ig) G1 monoclonal antibody directed against the human T-cell receptor cytotoxic T-lymphocyte-associated antigen 4 (CTLA4), with immune checkpoint inhibitory and antineoplastic activities. Ipilimumab binds to CTLA4 expressed on T-cells and inhibits the CTLA4-mediated downregulation of T-cell activation. This leads to a cytotoxic T-lymphocyte (CTL)-mediated immune response against cancer cells. CTLA4, an inhibitory receptor and member of the immunoglobulin superfamily, plays a key role in the downregulation of the immune system.
  • Ipomeanol - A natural toxic furan isolated from a fungus-infected sweet potato (Ipomoea batatas) with potential antineoplastic activity. Ipomeanol is activated by mixed function oxidases in vivo to its epoxide form, an alkylating agent that covalently binds cell macromolecules. This agent causes cell death by a p53-independent mechanism.
  • Iproplatin - A synthetic second-generation platinum-containing compound related to cisplatin. Iproplatin binds to and forms DNA crosslinks and platinum-DNA adducts, resulting in DNA replication failure and cell death. Although less prone to glutathione inactivation compared to cisplatin, resistance to this agent has been observed in vitro due to repair of platination damage by tumor cells.
  • Ipsc-derived cd16/il-15rf-expressing anti-cd19 car-nk cells ft596 - An allogeneic, off-the-shelf, chimeric antigen receptor (CAR)-natural killer (NK) cell product derived from a clonal master induced pluripotent stem cell (iPSC) line, and engineered to express a NK cell-specific anti-CD19 CAR, a high-affinity, non-cleavable CD16 (hnCD16) Fc receptor, and a recombinant fusion of IL-15 and IL-15 receptor alpha (IL-15RF), with potential immunostimulatory and antineoplastic activities. Upon administration, iPSC-derived CD16/IL-15RF-expressing Anti-CD19 CAR-NK Cells FT596 recognize, bind to and induce selective cytotoxicity in CD19-expressing tumor cells. IL-15RF enhances the cytotoxic effect of the NK cells and the activated anti-tumor T-cells. When used in combination with monoclonal antibodies, the hnCD16 Fc receptor of FT596 binds to the Fc portion of tumor cell-bound monoclonal antibodies, leading to NK cell activation, cytokine secretion and enhanced antibody-dependent cellular cytotoxicity (ADCC). CD19 antigen is a B-cell specific cell surface antigen expressed in all B-cell lineage malignancies. CD16, also known as Fc-gamma receptor III, is normally expressed on the surface of NK cells, neutrophils, monocytes and macrophages, and plays a key role in initiating ADCC. It is often downregulated in certain cancers, thereby inhibiting the anti-tumor immune response.
  • Ipsc-derived cd16-expressing natural killer cells ft516 - An allogeneic, off-the-shelf, natural killer (NK) cell product derived from a clonal master induced pluripotent stem cell (iPSC) line, and engineered to express a high-affinity, non-cleavable CD16 (hnCD16) Fc receptor, with potential antineoplastic and immunostimulatory activities. Upon administration, iPSC-derived CD16-expressing NK cells FT516 bind to the Fc portion of tumor cell-bound monoclonal antibodies and activate NK cell activation, cytokine secretion and antibody-dependent cellular cytotoxicity (ADCC). CD16, also known as Fc-gamma receptor III, is normally expressed on the surface of NK cells, neutrophils, monocytes and macrophages, and plays a key role in initiating ADCC. It is often downregulated in certain cancers, thereby inhibiting the anti-tumor immune response. FT516 NK cells' hnCD16 Fc receptor prevents downregulation and optimizes binding to tumor-targeting antibodies for enhanced ADCC.
  • Ipsc-derived natural killer cells ft500 - A preparation of off-the-shelf, natural killer (NK) cells derived from a clonal master induced pluripotent stem cell (iPSC) line, with potential antineoplastic and immunostimulatory activities. Upon administration, iPSC-derived natural killer cells FT500 bind to stress-induced ligands on tumor cells, leading to tumor cell lysis and release of tumor neoantigens. Additionally, iPSC-NK cells secrete inflammatory cytokines and chemokines including interferon-gamma (IFN-gamma), tumor necrosis factor-alpha (TNF-alpha), C-C motif chemokines 3, 4, and 22 (CCL3, CCL4, and CCL22), and C-X-C motif chemokine 10 (CXCL10), thereby enhancing T-cell activity and recruitment to the tumor site.
  • Iratumumab - A fully human monoclonal antibody with potential antineoplastic activity. MDX-060 is a fully humanized antibody that targets CD30, a member of the tumor necrosis factor receptor superfamily found on activated lymphocytes. CD30 is over-expressed in various lymphoproliferative disorders, Hodgkin disease and other lymphomas, and other cancers.
  • Iridium ir 192 - A radioactive isotope of iridium. Iridium-192 emits gamma rays and has a half-life of 74 days. A high dose rate of this radioisotope can be used in brachytherapy to treat tumors by selectively delivering a cytotoxic dose of radiation to the tumor site.
  • Irinotecan - A semisynthetic derivative of camptothecin, a cytotoxic, quinoline-based alkaloid extracted from the Asian tree Camptotheca acuminata. Irinotecan, a prodrug, is converted to a biologically active metabolite 7-ethyl-10-hydroxy-camptothecin (SN-38) by a carboxylesterase-converting enzyme. One thousand-fold more potent than its parent compound irinotecan, SN-38 inhibits topoisomerase I activity by stabilizing the cleavable complex between topoisomerase I and DNA, resulting in DNA breaks that inhibit DNA replication and trigger apoptotic cell death. Because ongoing DNA synthesis is necessary for irinotecan to exert its cytotoxic effects, it is classified as an S-phase-specific agent.
  • Irinotecan hydrochloride - The hydrochloride salt of a semisynthetic derivative of camptothecin, a cytotoxic, quinoline-based alkaloid extracted from the Asian tree Camptotheca acuminata. Irinotecan, a prodrug, is converted to a biologically active metabolite 7-ethyl-10-hydroxy-camptothecin (SN-38) by a carboxylesterase-converting enzyme. One thousand-fold more potent than its parent compound irinotecan, SN-38 inhibits topoisomerase I activity by stabilizing the cleavable complex between topoisomerase I and DNA, resulting in DNA breaks that inhibit DNA replication and trigger apoptotic cell death. Because ongoing DNA synthesis is necessary for irinotecan to exert its cytotoxic effects, it is classified as an S-phase-specific agent.
  • Irinotecan sucrosofate - A liposomal formulation of the semisynthetic camptothecin analogue irinotecan with potential antineoplastic activity. During the S phase of the cell cycle, irinotecan selectively stabilizes topoisomerase I-DNA covalent complexes, inhibiting religation of topoisomerase I-mediated single-strand DNA breaks and producing lethal double-strand DNA breaks when complexes are encountered by the DNA replication machinery. Liposome encapsulation of this agent promotes efficient drug delivery into the cytosol from the endosome compartment of the cell.
  • Irinotecan/p-glycoprotein inhibitor hm30181ak combination tablet - An orally bioavailable combination tablet containing the semisynthetic camptothecin derivative irinotecan and the multidrug resistance (MDR) efflux pump P-glycoprotein (P-gp) inhibitor HM30181AK, with potential antineoplastic activity. HM30181A binds to P-gp and prevents the P-gp-mediated efflux of irinotecan from tumor cells, which may result in greater intracellular concentrations of irinotecan and enhanced cytotoxicity. Retained intracellularly, the prodrug irinotecan is converted, by a carboxylesterase-converting enzyme, to the biologically active metabolite 7-ethyl-10-hydroxy-camptothecin (SN-38). SN-38 inhibits topoisomerase I activity by stabilizing the cleavable complex between topoisomerase I and DNA, resulting in DNA breaks that inhibit DNA replication and trigger apoptotic cell death. P-gp, encoded by the MDR-1 gene, is a member of the ATP-binding cassette (ABC) superfamily of transmembrane transporters and is overexpressed by some MDR tumors, preventing the intracellular accumulation of various cytotoxic agents.
  • Irinotecan-eluting beads - Microporous hydrospheres of polyvinylalcohol (PVA) impregnated with irinotecan with potential antineoplastic activity. In transarterial chemoembolization (TACE), irinotecan-eluting beads are administered into blood vessels that feed the tumor, occluding tumor blood vessels and inducing ischemic tumor necrosis while simultaneously delivering high-dose chemotherapy locally. Irinotecan, a semisynthetic derivative of camptothecin, inhibits topoisomerase I activity by stabilizing the cleavable complex between topoisomerase I and DNA, resulting in DNA breaks that inhibit DNA replication and trigger apoptotic cell death.
  • Irofulven - A semisynthetic sesquiterpene derivative of illudin S, a natural toxin isolated from the fungus Omphalotus illudens. Irofulven alkylates DNA and protein macromolecules, forms adducts, and arrests cells in the S-phase of the cell cycle. This agent requires NADPH-dependent metabolism by alkenal/one oxidoreductase for activity. Irofulven is more active in vitro against tumor cells of epithelial origin and is more resistant to deactivation by p53 loss and MDR1 than other alkylating agents.
  • Iroplact - A recombinant form of the endogenous chemokine platelet factor 4 with potential antiangiogenesis and antineoplastic activities. As a heparin-binding tetramer, iroplact inhibits growth factor-stimulated endothelial cell proliferation, migration, and angiogenesis; it has been shown that this agent inhibits fibroblast growth factor 2 (FGF2) angiogenic activity downstream from the FGF2 receptor. Its activity is antagonized by heparin. Recombinant platelet factor 4 may also directly inhibit the proliferation of some tumor cell types.
  • Irosustat - Steroid sulfatase inhibitor BN 83495 selectively binds to and inhibits steroid sulfatase (STS), which may inhibit the production of locally active estrogens and so inhibit estrogen-dependent cell growth in tumor cells, such as those of the breast, ovary, and endometrium. STS is a cytoplasmic enzyme responsible for the conversion of circulating inactive estrone sulfate and estradiol sulfate to biologically active unconjugated estrone and estradiol, respectively.
  • Irradiated allogeneic human lung cancer cells expressing ox40l-ig vaccine hs-130 - An allogeneic irradiated human lung cancer cell vaccine expressing a fusion protein composed of the OX40 ligand (OX40L) linked to an immunoglobulin (Ig) (OX40L-Ig), with potential immunomodulating and antineoplastic activities. Upon intradermal administration of irradiated allogeneic human lung cancer cells expressing OX40L-Ig vaccine HS-130, the irradiated lung cancer cells continuously express OX40L-Ig. OX40L may then target, bind to and activate its cognate receptor, tumor necrosis factor receptor superfamily member 4 (TNFRSF4; OX40; CD134), which is expressed on activated T-cells. OX40L/OX40 binding promotes increased cytokine production, and induces the proliferation and activation of memory and effector T-lymphocytes against the human lung cancer cells. In turn, this promotes a CTL-mediated immune response against the endogenous lung cancer cells. OX40L, a cell surface glycoprotein and member of the tumor necrosis factor (TNF) ligand family, provides a co-stimulatory signal for the proliferation and survival of activated T-cells.
  • Isatuximab - A humanized IgG1 monoclonal antibody directed against the cell surface glycoprotein CD-38 with potential antineoplastic activity. Isatuximab specifically binds to CD38 on CD38-positive tumor cells. This may trigger antitumoral antibody-dependent cellular cytotoxicity (ADCC), complement-dependent cytotoxicity (CDC) and apoptosis eventually leading to cell lysis in CD38-expressing tumor cells. CD38, a type II transmembrane glycoprotein, is present on various immune cells and hematologic malignancies, and its expression has been correlated with poor prognosis.
  • Isobrucein b - A quassinoid phytochemical isolated from the tropical plant Cedronia granatensis with potential antineoplastic and chemopreventive activities.
  • Isocoumarin nm-3 - An orally bioavailable antiangiogenic isocoumarin with potential antineoplastic activity. NM-3 inhibits vascular endothelial growth factor (VEGF), a pro-angiogenic growth factor, thereby inhibiting endothelial cell proliferation. This agent also induces apoptosis by a mechanism involving reactive oxygen species.
  • Iso-fludelone - A third-generation epothilone B analogue with potential anti-mitotic and antineoplastic activites. Iso-fludelone 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 other generations of epothilones, iso-fludelone exhibits increased stability, water solubility, potency, duration of action, tumor penetration as well as reduced toxicity. In addition, this agent is a not a substrate of the P-glycoprotein (P-gp), a multidrug resistance pump often overexpressed in cancer cells.
  • Isotretinoin - A naturally-occurring retinoic acid with potential antineoplastic activity. Isotretinoin binds to and activates nuclear retinoic acid receptors (RARs); activated RARs serve as transcription factors that promote cell differentiation and apoptosis. This agent also exhibits immunomodulatory and anti-inflammatory responses and inhibits ornithine decarboxylase, thereby decreasing polyamine synthesis and keratinization.
  • Ispinesib - A synthetic small molecule, derived from quinazolinone, with antineoplastic properties. Ispinesib selectively inhibits the mitotic motor protein, kinesin spindle protein (KSP), resulting in inhibition of mitotic spindle assembly, induction of cell cycle arrest during the mitotic phase, and cell death in tumor cells that are actively dividing. Because KSP is not involved in nonmitotic processes, such as neuronal transport, ispinesib may be less likely to cause the peripheral neuropathy often associated with the tubulin-targeting agents.
  • Ispinesib mesylate - The mesylate salt form of ispinesib, a synthetic small molecule, derived from quinazolinone, and kinesin spindle protein (KSP) inhibitor, with antineoplastic activity. Ispinesib selectively inhibits KSP and prevents its binding to microtubules, resulting in inhibition of mitotic spindle assembly, induction of cell cycle arrest during the M-phase, and cell death in tumor cells that are actively dividing.
  • Iss 1018 cpg oligodeoxynucleotide - A short, synthetic, unmethylated CpG motif-based oligodeoxynucleotide (CpG ODN) with immunostimulatory activity. As an immunostimulatory sequence (ISS) that signals through Toll-like receptor 9 (TLR9), ISS 1018 CpG ODN induces the production of immunoglobulin by B cells and interferon (IFN) -alpha, IFN-beta, interleukin (IL) -12, and tumor necrosis factor (TNF) -alpha by plasmacytoid dendritic cells (pDC). pDC, through cell-cell contact, and IFN-alpha and -beta, in turn, induce natural killer (NK) cell proliferation, NK cell production of IFN-gamma, and NK cell-mediated cytotoxicity; secreted IFNs also stimulate bystander T cell activation and differentiation of naive CD4+ T cells into T-helper 1 cells on specific antigen challenge. In addition, ISS 1018 CpG ODN promotes antigen presentation and co-stimulatory molecule expression.
  • Istiratumab - A bispecific monoclonal antibody directed against the human epidermal growth factor receptor ErbB3 (Her3) and the human insulin-like growth factor-1 receptor (IGF-1R), with potential antineoplastic activity. The anti-IGF-1R targeting arm of Istiratumab binds to IGF-1R on tumor cells thereby preventing the binding of the natural ligands IGF-1, 2 and heregulin (HRG) to IGF-1R; the anti-ErbB3 therapeutic arm prevents the binding of neuregulin (NRG) to ErbB3. This prevents the activation of the PI3K/AKT signal transduction pathway and may result in both the induction of apoptosis and a decrease in cellular proliferation in IGF-1R and ErbB3-overexpressing tumor cells. IGF-1R, a receptor tyrosine kinase of the insulin receptor superfamily, and ErB3, a member of the epidermal growth factor receptor (EGFR) family of receptor tyrosine kinases, are frequently overexpressed in solid tumors.
  • Itacitinib - An orally bioavailable inhibitor of Janus-associated kinase 1 (JAK1) with potential antineoplastic and immunomodulating activities. Upon oral administration, itacitinib selectively inhibits JAK-1, thereby inhibiting the phosphorylation of signal transducer and activator of transcription (STAT) proteins and the production of proinflammatory factors induced by other cytokines, including interleukin-23 (IL-23) and interleukin-6 (IL-6). The JAK-STAT pathway plays a key role in the signaling of many cytokines and growth factors and is involved in cellular proliferation, growth, hematopoiesis, and the immune response; JAK kinases may be upregulated in inflammatory diseases, myeloproliferative disorders, and various malignancies.
  • Itacitinib adipate - The adipate salt form of itacitinib, an orally bioavailable inhibitor of Janus-associated kinase 1 (JAK1) with potential antineoplastic and immunomodulating activities. Upon oral administration, itacitinib selectively inhibits JAK-1, thereby inhibiting the phosphorylation of signal transducer and activator of transcription (STAT) proteins and the production of proinflammatory factors induced by other cytokines, including interleukin-23 (IL-23) and interleukin-6 (IL-6). The JAK-STAT pathway plays a key role in the signaling of many cytokines and growth factors and is involved in cellular proliferation, growth, hematopoiesis, and the immune response; JAK kinases may be upregulated in inflammatory diseases, myeloproliferative disorders, and various malignancies.
  • Itk inhibitor cpi-818 - An orally available, small-molecule, irreversible inhibitor of interleukin-2 inducible T-cell kinase (ITK) with potential immunomodulatory and antineoplastic activities. Upon oral administration, ITK inhibitor CPI-818 selectively and covalently binds to the cysteine residue at position 442 (CYS-442) of ITK, thereby disrupting ITK-mediated signal transduction, while sparing tyrosine-protein kinase TXK (resting lymphocyte kinase, RLK) activity. This may abrogate T-cell receptor (TCR) signaling through ITK and inhibit TCR-induced proliferation of malignant T-cells. Additionally, inhibiting ITK activation may prevent the upregulation of GATA-3, a transcription factor that drives T-helper 2 (Th2) cell differentiation and is overexpressed in certain T-cell lymphomas. Thus, selective inhibition of ITK may inhibit Th2 responses without affecting T-helper 1 (Th1)-dependent immunity. ITK, a member of the Tec family of non-receptor protein tyrosine kinases plays a significant role in the T-cell development, differentiation and production of pro-inflammatory cytokines.
  • Itraconazole dispersion in polymer matrix - A proprietary oral formulation composed of the poorly soluble, synthetic triazole agent, itraconazole, dispersed in a polymer matrix, with antifungal and potential anti-angiogenic activities. Upon oral administration, itraconazole inhibits the enzyme cytochrome P450 lanosterol 14 alpha-demethylase, resulting in a decrease in fungal ergosterol synthesis. Although the exact mechanism through which itraconazole inhibits angiogenesis has yet to be fully elucidated, this agent appears to inhibit the Hedgehog (Hh) signaling pathway, cholesterol synthesis and mammalian target of rapamycin (mTOR) signaling in endothelial cells. This agent may also prevent the activation of and signaling by various angiogenic growth factors. By decreasing the tumor vasculature and nutrient supply, itraconazole ultimately inhibits tumor cell growth. The solid dispersion of itraconazole in the polymer matrix enhances dissolution of itraconazole in the gastrointestinal tract and increases its bioavailability; this allows for the administration of a much lower dose compared to itraconazole alone.
  • Ivac mutanome vaccine - An individualized, poly-neo-epitopic encoding, ribonucleic acid (RNA)-based cancer vaccine that targets a variety of patient-specific, immunogenic mutant epitopes, with potential immunostimulatory and antineoplastic activities. Upon intranodal administration, the RNA in the individualized mutanome vaccine is translated by antigen presenting cells (APCs) and the expressed protein is presented via major histocompatibility complex (MHC) molecules on the surface of the APCs. This leads to an induction of both cytotoxic T-lymphocyte (CTL) and memory T-cell immune responses against the patient-specific neoantigens.
  • Ivaltinostat - A histone deacetylase (HDAC) inhibitor with potential antineoplastic activity. Ivaltinosta tinhibits the catalytic activity of HDAC, resulting in an accumulation of highly acetylated chromatin histones, followed by the induction of chromatin remodeling and an altered pattern of gene expression. In particular, this agent enhances the histone acetylation of the tumor suppressor gene p53. This results in an accumulation of p53, p53-dependent transactivation and apoptosis in tumor cells. HDAC, an enzyme upregulated in many tumor types, deacetylates chromatin histone proteins.
  • Ivosidenib - An orally available inhibitor of isocitrate dehydrogenase type 1 (IDH1), with potential antineoplastic activity. Upon administration, AG-120 specifically inhibits a mutated form of IDH1 in the cytoplasm, which inhibits the formation of the oncometabolite, 2-hydroxyglutarate (2HG). This may lead to both an induction of cellular differentiation and an inhibition of cellular proliferation in IDH1-expressing tumor cells. IDH1, an enzyme in the citric acid cycle, is mutated in a variety of cancers; it initiates and drives cancer growth by both blocking cell differentiation and catalyzing the formation of 2HG.
  • Ivuxolimab - An agonistic antibody that recognizes the co-stimulatory receptor OX40 (CD134; TNFRSF4), with potential immunostimulatory activity. Upon administration, ivuxolimab selectively binds to and activates OX40; which induces proliferation of memory and effector T-lymphocytes. In the presence of tumor-associated antigens (TAAs), this may promote a T-cell-mediated immune response against TAA-expressing tumor cells. OX40, a cell surface glycoprotein and member of the tumor necrosis factor receptor superfamily (TNFRSF), is expressed on T-lymphocytes and plays an essential role in T-cell activation.
  • Ixabepilone - An orally bioavailable semisynthetic analogue of epothilone B with antineoplastic activity. Ixabepilone binds to tubulin and promotes tubulin polymerization and microtubule stabilization, thereby arresting cells in the G2-M phase of the cell cycle and inducing tumor cell apoptosis. This agent demonstrates antineoplastic activity against taxane-resistant cell lines.
  • Ixazomib - An active metabolite of MLN9708, a second generation, boron containing peptide proteasome inhibitor (PI) with potential antineoplastic activity. Ixazomib binds to and inhibits the 20S catalytic core of the proteasome, thereby blocking the targeted proteolysis normally performed by the proteasome, which results in an accumulation of unwanted or misfolded proteins; disruption of various cell signaling pathways may follow, resulting in the induction of apoptosis. Compared to first generation PIs, second generation PIs may have an improved pharmacokinetic profile with increased potency and less toxicity. Proteasomes are large protease complexes that degrade unneeded or damaged proteins that have been ubiquinated.
  • Ixazomib citrate - The citrate salt form of ixazomib, an orally bioavailable second generation proteasome inhibitor (PI) with potential antineoplastic activity. Ixazomib inhibits the activity of the proteasome, blocking the targeted proteolysis normally performed by the proteasome, which results in an accumulation of unwanted or misfolded proteins; disruption of various cell signaling pathways may follow, resulting in the induction of apoptosis. Compared to first generation PIs, second generation PIs may have an improved pharmacokinetic profile with increased potency and less toxicity. Proteasomes are large protease complexes that degrade unneeded or damaged proteins that have been ubiquinated.

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