" /> Anti-CD137/PD-L1 Bispecific Antibody AP203 - CISMeF





Preferred Label : Anti-CD137/PD-L1 Bispecific Antibody AP203;

NCIt synonyms : Anti-4-1BB/PD-L1 Bispecific Antibody AP203; Anti-PD-L1/Anti-CD137 Bispecific Antibody AP203; PD-L1 x CD137 Bispecific Antibody AP203;

NCIt definition : A bispecific antibody targeting both the human programmed death-ligand 1 (PD-L1) and CD137 (4-1BB; tumor necrosis factor receptor superfamily member 9; TNFRSF9), with potential checkpoint inhibitory, immunostimulating and antineoplastic activities. Upon administration, anti-CD137/PD-L1 bispecific antibody AP203 simultaneously targets and binds to CD137, which is expressed on a variety of leukocyte subsets including activated T-lymphocytes, and PD-L1 expressed on tumor cells, thereby crosslinking PD-L1-expressing tumor cells and T-lymphocytes. Crosslinking of PD-L1-expressing tumor cells and activated T-lymphocytes may enhance T-lymphocyte-mediated lysis of PD-L1-expressing tumor cells. Through CD137 binding, AP203 acts as a conditional CD137 agonist, resulting in T-cell co-stimulation and enhanced anti-tumor activity. At the same time, AP203 prevents PD-L1 from binding to and activating its receptor, programmed cell death 1 (PD-1; PDCD1; CD279; programmed death-1). This abrogates T-cell inhibition, activates antigen-specific T-lymphocytes and enhances cytotoxic T-cell-mediated tumor cell lysis, which may lead to a reduction in tumor growth. PD-L1 binding to PD-1 on activated T-cells inhibits the expansion and survival of CD8-positive T-cells, suppresses the immune system and results in immune evasion. CD137, a surface glycoprotein of the tumor necrosis factor receptor superfamily, is an inducible costimulatory receptor that plays a key role in T-cell proliferation, survival and cytolytic activity.;

Molecule name : AP-203; AP 203;

NCI Metathesaurus CUI : CL1798556;

Details


You can consult :


Nous contacter.
12/05/2024


[Home] [Top]

© Rouen University Hospital. Any partial or total use of this material must mention the source.