Anti-CD2 monoclonal antibody biologic that binds CD2 on T cells and NK cells, blocks CD2–CD58 costimulatory signaling, and preferentially depletes/modulates memory T cells to reduce alloimmune and autoimmune activity after liver transplant.
Humanized IgG1 monoclonal antibody against CD2 that binds T and NK cells, blocks CD2–CD58 costimulatory signaling, and depletes/modulates CD2+ (especially memory) T cells via immune effector mechanisms (e.g., ADCC/CDC), suppressing alloimmune and autoimmune activity.
Anti-CD2 IgG1 binds CD2 on T/NK cells and its Fc engages effector pathways (ADCC via FcγR-bearing cells and complement-dependent cytotoxicity), leading to lysis/depletion of CD2+ cells.
Bispecific antibody-drug conjugate (izalontamab brengitecan; BMS-986507) targeting EGFR and HER3; after binding and internalization, releases a topoisomerase I inhibitor payload (brengitecan) that induces DNA damage and tumor cell death.
Bispecific ADC targeting EGFR and HER3; after receptor binding and internalization, the linker is cleaved to release the topoisomerase I inhibitor brengitecan, inducing DNA damage and apoptosis in EGFR/HER3-expressing tumor cells.
The ADC binds EGFR on tumor cells, is internalized, and releases the topoisomerase I inhibitor brengitecan, causing DNA damage and apoptosis.
Bispecific antibody-drug conjugate (izalontamab brengitecan; BMS-986507) targeting EGFR and HER3; after binding and internalization, releases a topoisomerase I inhibitor payload (brengitecan) that induces DNA damage and tumor cell death.
Bispecific ADC targeting EGFR and HER3; after receptor binding and internalization, the linker is cleaved to release the topoisomerase I inhibitor brengitecan, inducing DNA damage and apoptosis in EGFR/HER3-expressing tumor cells.
The bispecific ADC binds HER3 on tumor cells, is internalized, and releases the topoisomerase I inhibitor brengitecan, causing DNA damage and apoptosis of the HER3-expressing cells.
Human afucosylated IgG1 monoclonal antibody (AMG 451; KHK4083) administered subcutaneously that targets OX40 (TNFRSF4) on activated T cells, blocking OX40–OX40L co-stimulatory signaling and mediating ADCC to deplete OX40+ T cells, thereby reducing T-cell activation, survival, and memory and attenuating type 2 inflammation.
Human afucosylated IgG1 monoclonal antibody targeting OX40 (TNFRSF4) on activated T cells; blocks OX40–OX40L co-stimulatory signaling and leverages enhanced ADCC to deplete OX40+ effector/memory T cells, reducing T-cell activation, survival, and type 2 inflammatory responses.
Afucosylated IgG1 binding to OX40 recruits FcγRIIIa-expressing effectors (e.g., NK cells) to mediate ADCC, with possible ADCP, depleting OX40+ T cells.
Glycoengineered, humanized type II anti-CD20 IgG1 monoclonal antibody that depletes CD20+ B cells via direct cell death and enhanced antibody-dependent cellular cytotoxicity and phagocytosis.
Glycoengineered humanized type II anti-CD20 IgG1 that binds CD20 on B cells and depletes them via enhanced Fc gamma receptor III–mediated antibody-dependent cellular cytotoxicity and phagocytosis, plus direct cell death/apoptosis driven by its type II binding properties and afucosylated Fc.
Obinutuzumab binds CD20 on B cells; its afucosylated Fc engages FcγRIII (on NK cells/macrophages) to drive ADCC and phagocytosis, and its type II binding also induces direct, caspase‑independent cell death/apoptosis.