Bispecific antibody-drug conjugate targeting EGFR and HER3; after internalization, releases a topoisomerase I inhibitor payload (brengitecan) to induce DNA damage and tumor cell death.
Bispecific ADC that binds EGFR and HER3 on tumor cells, is internalized, and releases the topoisomerase I inhibitor payload brengitecan to induce DNA damage and tumor cell death.
The ADC binds HER3 (and EGFR) on tumor cells, is internalized, and releases the topoisomerase I inhibitor brengitecan, causing DNA damage and tumor cell death.
A CD20×CD3 T-cell–engaging bispecific humanized monoclonal antibody that binds CD20 on B cells and CD3 on T cells, redirecting and activating T cells to kill CD20+ lymphoma cells via perforin/granzyme-mediated cytotoxicity.
CD20×CD3 bispecific humanized monoclonal antibody that binds CD20 on B cells and CD3 on T cells, crosslinking them to redirect and activate T cells to kill CD20+ B‑cell malignancies via perforin/granzyme-mediated cytotoxicity.
Glofitamab crosslinks CD20 on target cells with CD3 on T cells, activating T cells to kill CD20+ cells via perforin/granzyme-mediated cytolysis.
A humanized, glycoengineered type II anti-CD20 monoclonal antibody that induces direct B‑cell death and enhances antibody-dependent cellular cytotoxicity and phagocytosis.
Humanized, glycoengineered type II anti‑CD20 IgG1 that binds CD20 on B cells and drives B‑cell depletion via direct caspase‑independent cell death and enhanced Fc‑mediated effector functions (ADCC and phagocytosis) through increased FcγRIIIa binding.
Obinutuzumab binds CD20 on B cells, triggering direct caspase-independent cell death and engaging Fc-gamma RIIIa on effector cells to mediate ADCC and phagocytosis, leading to target-cell killing.
Chimeric anti-CD20 monoclonal antibody that depletes CD20+ B cells via complement-dependent cytotoxicity (CDC), antibody-dependent cellular cytotoxicity (ADCC), and apoptosis.
Anti-CD20 chimeric monoclonal antibody that binds CD20 on pre-B and mature B cells and depletes them via complement-dependent cytotoxicity, antibody-dependent cellular cytotoxicity, and induction of apoptosis.
Rituximab binds CD20 on B cells and depletes them via complement-dependent cytotoxicity (CDC), Fc-mediated antibody-dependent cellular cytotoxicity (ADCC) by NK cells/macrophages, and direct induction of apoptosis.
A chimeric IgG1 anti-GD2 monoclonal antibody immunotherapy (brand: Qarziba) used as maintenance after response in relapsed/refractory high‑grade osteosarcoma. It binds the disialoganglioside GD2 on tumor cells and triggers immune effector killing via Fc-mediated ADCC and phagocytosis, and complement‑dependent cytotoxicity (CDC). Dosed as continuous IV 14 mg/m2/day on days 1–5 every 28 days for 5 cycles.
Chimeric IgG1 anti-GD2 monoclonal antibody that binds GD2 on tumor cells and elicits immune effector killing via Fcγ receptor–mediated ADCC and phagocytosis, and complement-dependent cytotoxicity (CDC).
Anti-GD2 IgG1 binds GD2 on target cells and recruits immune effectors to kill via FcγR-mediated ADCC and phagocytosis, and complement-dependent cytotoxicity (CDC).