Anti‑CD20 monoclonal antibody that depletes B cells via antibody-dependent cellular cytotoxicity, complement-dependent cytotoxicity, and induction of apoptosis.
Anti-CD20 monoclonal antibody that binds CD20 on B cells and depletes CD20-positive cells via antibody-dependent cellular cytotoxicity, complement-dependent cytotoxicity, and induction of apoptosis.
YES
DIRECT
Rituximab binds CD20 on B cells and recruits immune effectors via its Fc to mediate ADCC; it also activates complement (CDC/MAC) and can trigger apoptosis upon cross-linking, killing CD20+ cells.
Intravenous humanized anti-HER2 monoclonal antibody that binds the HER2 extracellular domain to inhibit signaling and mediates antibody-dependent cellular cytotoxicity via Fcγ receptor–bearing immune cells.
Humanized anti-HER2 (ERBB2) monoclonal IgG1 that binds the HER2 extracellular domain, blocking HER2 signaling and receptor dimerization, and engaging Fc-gamma receptor-bearing immune cells to mediate antibody-dependent cellular cytotoxicity against HER2-overexpressing tumor cells.
NO
INDIRECT
Trastuzumab binds HER2 on tumor cells; its Fc engages CD16a (FcγRIIIa) on NK cells to trigger ADCC that kills HER2-overexpressing cells, not the CD16a-expressing effector cells.
An antibody–drug conjugate (HER3-DXd; U3-1402) consisting of a fully human anti-HER3 (ERBB3) IgG1 monoclonal antibody linked via a cleavable linker to DXd, a membrane-permeable topoisomerase I inhibitor. It binds HER3 on tumor cells, is internalized, and releases DXd intracellularly to inhibit topoisomerase I, causing DNA damage and cell death with a potential bystander effect.
Patritumab deruxtecan is a HER3-targeted antibody–drug conjugate. The patritumab antibody binds HER3 (ERBB3) on tumor cells, is internalized, and a cleavable linker releases the DXd payload intracellularly. DXd inhibits topoisomerase I by stabilizing the Topo I–DNA complex and preventing religation of DNA breaks, leading to DNA damage and apoptotic cell death. The membrane-permeable payload can exert a bystander effect on neighboring tumor cells.
YES
DIRECT
An anti-HER3 antibody–drug conjugate binds HER3, is internalized, and releases the DXd payload that inhibits topoisomerase I, causing DNA damage and apoptotic death of HER3+ cells (with potential bystander effect).
An antibody–drug conjugate (HER3-DXd; U3-1402) consisting of a fully human anti-HER3 (ERBB3) IgG1 monoclonal antibody linked via a cleavable linker to DXd, a membrane-permeable topoisomerase I inhibitor. It binds HER3 on tumor cells, is internalized, and releases DXd intracellularly to inhibit topoisomerase I, causing DNA damage and cell death with a potential bystander effect.
Patritumab deruxtecan is a HER3-targeted antibody–drug conjugate. The patritumab antibody binds HER3 (ERBB3) on tumor cells, is internalized, and a cleavable linker releases the DXd payload intracellularly. DXd inhibits topoisomerase I by stabilizing the Topo I–DNA complex and preventing religation of DNA breaks, leading to DNA damage and apoptotic cell death. The membrane-permeable payload can exert a bystander effect on neighboring tumor cells.
NO
INDIRECT
The ADC binds HER3 on tumor cells, is internalized, and releases DXd, which inhibits topoisomerase I to induce DNA damage and apoptosis; topoisomerase I expression alone does not mediate targeting or direct killing.
Chimeric IgG1 anti-CD20 monoclonal antibody (brands: MabThera, Truxima, Ruxience, Rixathon) that binds CD20 on pre-B and mature B lymphocytes, depleting these cells via antibody-dependent cellular cytotoxicity, complement-dependent cytotoxicity, and apoptosis; spares CD20− plasma cells and hematopoietic stem cells.
Chimeric IgG1 monoclonal antibody targeting CD20 on pre-B and mature B lymphocytes; depletes CD20+ B cells via antibody-dependent cellular cytotoxicity, complement-dependent cytotoxicity, and apoptosis, while sparing CD20− plasma cells and hematopoietic stem cells.
YES
DIRECT
Binding to CD20 triggers Fc-mediated ADCC and complement-dependent cytotoxicity, and can induce apoptosis of CD20+ B cells.