Type II, glycoengineered anti-CD20 monoclonal antibody that depletes CD20+ B cells via enhanced ADCC and direct cell death.
Type II, glycoengineered anti-CD20 IgG1 monoclonal antibody that binds CD20 on B cells and, via enhanced FcγRIIIa engagement (afucosylated Fc), drives potent antibody-dependent cellular cytotoxicity (ADCC) and direct, caspase-independent cell death, leading to depletion of CD20+ B cells.
NO
INDIRECT
Obinutuzumab binds CD20 on B cells; its afucosylated Fc engages CD16a on NK cells to trigger ADCC, killing CD20+ B cells. CD16a-expressing cells are effectors, not targets, and are not killed by the drug.
TROP2-directed antibody–drug conjugate targeting TACSTD2 on epithelial tumor cells; internalization and payload release lead to cytotoxicity in TROP2-expressing cells.
TROP2 (TACSTD2)-directed IgG1 antibody–drug conjugate linked via a cleavable linker to SHR9265 (an exatecan-derived topoisomerase I inhibitor). After binding TROP2 on tumor cells and internalization, linker cleavage releases the payload, inhibiting topoisomerase I, blocking DNA replication and inducing cell cycle arrest and apoptosis in TROP2-expressing cells.
YES
DIRECT
ADC binds TROP2 on target cells, is internalized, and releases an exatecan-derived topoisomerase I inhibitor, causing DNA damage/replication block leading to cell cycle arrest and apoptosis in TROP2-expressing cells.
Type I anti-CD20 monoclonal antibody that depletes CD20+ B cells via complement-dependent cytotoxicity (CDC) and ADCC.
Type I anti-CD20 chimeric monoclonal antibody that binds CD20 on B cells and depletes them via complement-dependent cytotoxicity (CDC), antibody-dependent cellular cytotoxicity (ADCC), and phagocytosis.
YES
DIRECT
Rituximab binds CD20 on B cells and induces killing via complement-dependent cytotoxicity (CDC), Fc-mediated antibody-dependent cellular cytotoxicity (ADCC) by NK cells, and antibody-dependent phagocytosis by macrophages.
A bispecific T‑cell engager (BiTE) antibody that binds CD19 on B‑lymphoblasts and CD3 on T cells to create an immune synapse, activate TCR/CD3 signaling, and induce perforin/granzyme‑mediated cytotoxic killing of CD19+ leukemia cells.
Bispecific single‑chain antibody that binds CD19 on B‑lymphoblasts and CD3 on T cells, bringing them into proximity to form an immune synapse, activate TCR/CD3 signaling, and induce perforin/granzyme‑mediated cytotoxic killing of CD19+ leukemia cells.
YES
DIRECT
Blinatumomab links CD3 on T cells to CD19 on target cells, forming an immune synapse and activating T cells to release perforin and granzymes that induce apoptosis of CD19+ cells.
A bispecific T‑cell engager (BiTE) antibody that binds CD19 on B‑lymphoblasts and CD3 on T cells to create an immune synapse, activate TCR/CD3 signaling, and induce perforin/granzyme‑mediated cytotoxic killing of CD19+ leukemia cells.
Bispecific single‑chain antibody that binds CD19 on B‑lymphoblasts and CD3 on T cells, bringing them into proximity to form an immune synapse, activate TCR/CD3 signaling, and induce perforin/granzyme‑mediated cytotoxic killing of CD19+ leukemia cells.
NO
INDIRECT
Blinatumomab binds CD3 on T cells to activate and redirect them to kill CD19+ target cells via perforin/granzyme; CD3+ T cells are not the cells killed.