Anti-CD20 monoclonal antibody that depletes B cells via ADCC, complement activation, and apoptosis.
Chimeric anti-CD20 monoclonal IgG1 that binds CD20 on B lymphocytes and depletes them via antibody-dependent cellular cytotoxicity, complement-dependent cytotoxicity, and induction of apoptosis.
YES
DIRECT
Rituximab binds CD20 on B cells and induces killing via antibody-dependent cellular cytotoxicity (Fc-engaged NK cells/macrophages), complement-dependent cytotoxicity, and direct apoptosis.
HER2-targeted antibody–drug conjugate; anti-HER2 IgG1 linked to the topoisomerase I inhibitor deruxtecan. Binds HER2, internalizes, and releases a cytotoxic payload causing DNA damage with a bystander effect.
HER2-directed antibody–drug conjugate composed of trastuzumab linked to the topoisomerase I inhibitor deruxtecan (DXd). After binding HER2 on tumor cells and internalization, the payload is released to inhibit topoisomerase I, causing DNA damage, cell cycle arrest, and apoptosis, with a membrane-permeable bystander killing effect; the antibody component can also mediate ADCC.
YES
DIRECT
The ADC binds HER2, is internalized, and releases the deruxtecan payload that inhibits topoisomerase I, causing DNA damage and apoptosis; the IgG1 Fc can also mediate ADCC, with some bystander killing from the membrane-permeable payload.
HER2-targeted antibody–drug conjugate; anti-HER2 IgG1 linked to the topoisomerase I inhibitor deruxtecan. Binds HER2, internalizes, and releases a cytotoxic payload causing DNA damage with a bystander effect.
HER2-directed antibody–drug conjugate composed of trastuzumab linked to the topoisomerase I inhibitor deruxtecan (DXd). After binding HER2 on tumor cells and internalization, the payload is released to inhibit topoisomerase I, causing DNA damage, cell cycle arrest, and apoptosis, with a membrane-permeable bystander killing effect; the antibody component can also mediate ADCC.
NO
INDIRECT
The ADC targets HER2, not Top1. After HER2 binding and internalization, deruxtecan inhibits Top1 to cause DNA damage and apoptosis (with bystander killing and ADCC), but Top1 expression alone does not make cells targets of the drug.
Anti-CD20 monoclonal antibody that targets CD20-positive B cells in NHL and promotes NK cell–mediated ADCC.
Chimeric anti-CD20 monoclonal antibody that binds CD20 on pre-B and mature B cells and depletes them via NK cell antibody-dependent cellular cytotoxicity (through Fc gamma receptor IIIa/CD16), complement-dependent cytotoxicity, and induction of apoptosis.
YES
DIRECT
Rituximab binds CD20 on B cells and induces killing via NK cell–mediated ADCC (FcγRIIIa/CD16), complement-dependent cytotoxicity, and can also trigger apoptosis upon crosslinking.
Anti-HER2 antibody–drug conjugate (RC48) that binds HER2, internalizes, and releases MMAE to disrupt microtubules, causing G2/M arrest and apoptosis; may also mediate ADCC/bystander effects.
Anti-HER2 antibody–drug conjugate: disitamab binds HER2 on tumor cells, is internalized, and via a cleavable linker releases MMAE, which binds tubulin to inhibit microtubule polymerization, causing G2/M arrest and apoptosis; may also induce ADCC and bystander killing.
NO
INDIRECT
The ADC binds HER2 on tumor cells, is internalized, and releases MMAE, which binds the vinca site on tubulin to disrupt microtubules, causing G2/M arrest and apoptosis; tubulin is the intracellular payload target, not the cell-surface target determining killing.