" /> Anti-4-1BB/PD-L1 Bispecific Antibody BH3120 - CISMeF





Preferred Label : Anti-4-1BB/PD-L1 Bispecific Antibody BH3120;

NCIt synonyms : 4-1BB x PD-L1 Bispecific Antibody BH3120; PD-L1/4-1BB BsAb BH3120; Anti-PD-L1/4-1BB Bispecific Antibody BH3120; Anti-4-1BB/Anti-PD-L1 Monoclonal Antibody BH3120;

NCIt definition : A heterodimeric immunoglobulin (IgG)-like bispecific antibody, with biased binding affinities, targeting human programmed death-ligand 1 (PD-L1; cluster of differentiation 274; CD274) and 4-1BB (CD137; tumor necrosis factor receptor superfamily member 9; TNFRSF9), with potential checkpoint inhibitory, immunostimulating and antineoplastic activities. Upon administration, anti-4-1BB/PD-L1 bispecific antibody BH3120 simultaneously targets and binds with its anti-4-1BB arm and with moderate affinity to 4-1BB, which is expressed on a variety of leukocyte subsets including activated T-lymphocytes, and, with its anti-PD-L1 arm with high affinity to PD-L1, which is expressed on tumor cells. Upon PD-L1 binding and PD-L1-mediated cross-linking, the 4-1BB activation signal is induced and BH3120 acts as a conditional 4-1BB agonist in the tumor microenvironment (TME), resulting in T-cell co-stimulation and enhances T-lymphocyte-mediated anti-tumor activity. At the same time, BH3120 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. 4-1BB, 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 : BH 3120; BH-3120;

NCI Metathesaurus CUI : CL1927047;

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08/05/2025


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