" /> Favezelimab/Pembrolizumab Formulation - CISMeF





Preferred Label : Favezelimab/Pembrolizumab Formulation;

NCIt synonyms : Coformulated Favezelimab Plus Pembrolizumab; Coformulated Favezelimab/Pembrolizumab; Favezelimab/Pembrolizumab Formulation MK-4280A; Coformulated MK-4280 Plus MK-3475;

NCIt definition : A coformulation containing favezelimab, a humanized, immunoglobulin G4 (IgG4) monoclonal antibody (MAb) directed against the inhibitory receptor lymphocyte activation gene-3 protein (LAG3), and pembrolizumab, a humanized monoclonal IgG4 antibody directed against human cell surface receptor PD-1 (programmed death-1 or programmed cell death-1), with potential immune checkpoint inhibitory and antineoplastic activities. Upon administration of the favezelimab/pembrolizumab formulation, favezelimab binds to LAG3 expressed on tumor-infiltrating lymphocytes (TILs) and blocks its binding with major histocompatibility complex (MHC) class II molecules expressed on tumor cells. This activates antigen-specific T-lymphocytes and enhances cytotoxic T-cell-mediated tumor cell lysis, which leads to a reduction in tumor growth. Pembrolizumab binds to PD-1, an inhibitory signaling receptor expressed on the surface of activated T-cells, and blocks the binding to and activation of PD-1 by its ligands, which results in the activation of T-cell-mediated immune responses against tumor cells LAG3, a member of the immunoglobulin superfamily (IgSF) expressed on various immune cells, negatively regulates both proliferation and activation of T-cells. Its expression on TILs is associated with tumor-mediated immune suppression. The ligands for PD-1 include programmed cell death ligand 1 (PD-L1), overexpressed on certain cancer cells, and programmed cell death ligand 2 (PD-L2), which is primarily expressed on antigen presenting cells (APCs). Activated PD-1 negatively regulates T-cell activation and plays a key role in in tumor evasion from host immunity.;

Molecule name : MK 4280A; MK-4280A;

NCI Metathesaurus CUI : CL1799312;

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15/05/2024


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