{"meta":{"totalResults":1,"from":0},"results":[{"aliases":[{"type":"CodeName","name":"AK112"},{"type":"CodeName","name":"AK-112"},{"type":"CodeName","name":"AK 112"},{"type":"CodeName","name":"SMT112"},{"type":"CodeName","name":"SMT 112"},{"type":"CodeName","name":"SMT-112"},{"type":"Synonym","name":"anti-PD-1/anti-VEGF bispecific antibody AK112"},{"type":"Synonym","name":"PD-1/VEGF bispecific antibody AK112"},{"type":"Synonym","name":"anti-PD-1/VEGF bispecific antibody AK112"}],"definition":{"html":"A bispecific antibody directed against the negative immunoregulatory human cell receptor programmed cell death protein 1 (PD-1; PDCD1; CD279) and the human vascular endothelial growth factor (VEGF), with potential immune checkpoint inhibitory, anti-angiogenic and antineoplastic activities. Upon administration, ivonescimab simultaneously targets and binds to both PD-1 expressed on certain T cells and VEGF expressed on tumor cells. The binding of ivonescimab to PD-1 prevents the activation of PD-1 by its ligands, programmed cell death-1 ligand 1 (PD-L1; CD274) and/or 2 (PD-L2; CD273). This abrogates T-cell inhibition, activates antigen-specific T-lymphocytes and enhances cytotoxic T-lymphocyte (CTL)-mediated tumor cell lysis, which may lead to a reduction in tumor growth. The binding of ivonescimab to VEGF prevents binding of VEGF to its receptor VEGFR, abrogates VEGF/VEGFR-mediated signaling and may lead to the inhibition of vascular endothelial cell proliferation. The inhibition of tumor angiogenesis may further decrease tumor cell proliferation and prevent metastasis. PD-1, a transmembrane protein in the immunoglobulin superfamily (IgSF) expressed on T cells, functions as an immune checkpoint that negatively regulates T-cell activation and effector function when activated by its ligands PD-L1 and/or PD-L2; it plays an important role in tumor evasion from host immunity. VEGF is overexpressed in a variety of cancers and is associated with increased invasiveness and decreased survival.","text":"A bispecific antibody directed against the negative immunoregulatory human cell receptor programmed cell death protein 1 (PD-1; PDCD1; CD279) and the human vascular endothelial growth factor (VEGF), with potential immune checkpoint inhibitory, anti-angiogenic and antineoplastic activities. Upon administration, ivonescimab simultaneously targets and binds to both PD-1 expressed on certain T cells and VEGF expressed on tumor cells. The binding of ivonescimab to PD-1 prevents the activation of PD-1 by its ligands, programmed cell death-1 ligand 1 (PD-L1; CD274) and/or 2 (PD-L2; CD273). This abrogates T-cell inhibition, activates antigen-specific T-lymphocytes and enhances cytotoxic T-lymphocyte (CTL)-mediated tumor cell lysis, which may lead to a reduction in tumor growth. The binding of ivonescimab to VEGF prevents binding of VEGF to its receptor VEGFR, abrogates VEGF/VEGFR-mediated signaling and may lead to the inhibition of vascular endothelial cell proliferation. The inhibition of tumor angiogenesis may further decrease tumor cell proliferation and prevent metastasis. PD-1, a transmembrane protein in the immunoglobulin superfamily (IgSF) expressed on T cells, functions as an immune checkpoint that negatively regulates T-cell activation and effector function when activated by its ligands PD-L1 and/or PD-L2; it plays an important role in tumor evasion from host immunity. VEGF is overexpressed in a variety of cancers and is associated with increased invasiveness and decreased survival."},"drugInfoSummaryLink":null,"nciConceptId":"C184865","nciConceptName":"Ivonescimab","termId":800843,"name":"ivonescimab","firstLetter":"i","type":"DrugTerm","termNameType":"PreferredName","prettyUrlName":"ivonescimab"}],"links":null}