B7-H3 (CD276)–targeting antibody-drug conjugate that delivers a topoisomerase I inhibitor payload to tumor cells, causing DNA damage and tumor cell death.
Monoclonal antibody targeting B7-H3 (CD276) delivers a topoisomerase I inhibitor via a tumor protease–cleavable linker; upon binding and internalization in B7-H3–expressing tumor cells, the released payload inhibits topoisomerase I, causing DNA damage, replication blockade, cell cycle arrest, and apoptosis.
YES
DIRECT
ADC binds B7-H3 on target cells, is internalized, and releases a topoisomerase I inhibitor via protease-cleavable linker, causing DNA damage, replication blockade, cell cycle arrest, and apoptosis.
B7-H3 (CD276)–targeting antibody-drug conjugate that delivers a topoisomerase I inhibitor payload to tumor cells, causing DNA damage and tumor cell death.
Monoclonal antibody targeting B7-H3 (CD276) delivers a topoisomerase I inhibitor via a tumor protease–cleavable linker; upon binding and internalization in B7-H3–expressing tumor cells, the released payload inhibits topoisomerase I, causing DNA damage, replication blockade, cell cycle arrest, and apoptosis.
NO
INDIRECT
The ADC targets B7-H3 on tumor cells, is internalized, and releases a topoisomerase I inhibitor that causes DNA damage and apoptosis in B7-H3–positive cells; DNA topoisomerase I is the intracellular payload target, not the antigen targeted by the drug.
Subcutaneous bispecific T‑cell–engaging antibody that binds CD3 on T cells and CD20 on B cells to form an immune synapse, activate TCR/CD3 signaling, and induce T‑cell–mediated cytotoxicity; used here with step‑up dosing around CAR‑T.
Subcutaneous bispecific antibody that binds CD3 on T cells and CD20 on B cells, bringing them into proximity to form an immune synapse, activate TCR/CD3 signaling, and trigger T‑cell–mediated cytotoxicity (perforin/granzyme) against CD20+ B‑cell malignancies.
NO
INDIRECT
Epcoritamab binds CD3 on T cells to recruit/activate them against CD20+ B cells; activated T cells kill CD20-expressing cells via perforin/granzyme, not the CD3+ T cells.
Candidate rituximab biosimilar; chimeric IgG1 anti-CD20 monoclonal antibody that depletes CD20+ B cells via ADCC, CDC, and apoptosis, reducing autoantibody production and B–T cell interactions.
Chimeric IgG1 anti-CD20 monoclonal antibody that binds CD20 on B lymphocytes and depletes them via ADCC, complement-dependent cytotoxicity, and apoptosis, thereby reducing autoantibody production and B–T cell interactions (plasma cells largely spared).
YES
DIRECT
Anti-CD20 IgG1 binds CD20 on B cells and induces killing via Fc-mediated ADCC by effector cells, complement-dependent cytotoxicity (CDC), and apoptosis upon crosslinking.
Candidate rituximab biosimilar; chimeric IgG1 anti-CD20 monoclonal antibody that depletes CD20+ B cells via ADCC, CDC, and apoptosis, reducing autoantibody production and B–T cell interactions.
Chimeric IgG1 anti-CD20 monoclonal antibody that binds CD20 on B lymphocytes and depletes them via ADCC, complement-dependent cytotoxicity, and apoptosis, thereby reducing autoantibody production and B–T cell interactions (plasma cells largely spared).
NO
INDIRECT
The antibody binds CD20 on B cells; its Fc engages CD16a on NK cells to trigger ADCC (and complement activation), killing CD20+ B cells. CD16a-expressing cells act as effectors, not targets.