Chimeric IgG1 anti-EGFR monoclonal antibody that blocks EGFR ligand binding and downstream signaling; can mediate ADCC.
Chimeric IgG1 anti-EGFR monoclonal antibody that binds the extracellular domain of EGFR, blocking ligand binding and receptor dimerization to inhibit downstream signaling and tumor cell proliferation; Fc region can mediate NK cell–mediated ADCC.
YES
DIRECT
Cetuximab binds EGFR on target cells and engages NK cells via its Fc to trigger ADCC, killing EGFR+ cells; EGFR blockade may also promote apoptosis.
Rabbit polyclonal antilymphocyte globulin used for in vivo T-cell depletion to reduce graft-versus-host disease risk.
Rabbit polyclonal IgG against multiple human T‑cell surface antigens (e.g., CD2, CD3, CD4, CD8, HLA) that depletes T lymphocytes via complement-dependent cytotoxicity, Fc-mediated ADCC/phagocytosis, and apoptosis, producing in vivo T‑cell immunosuppression to reduce GVHD risk.
YES
DIRECT
rATG binds CD8α on T cells and triggers complement-dependent lysis and Fc-mediated ADCC/phagocytosis, leading to apoptosis/depletion of CD8+ cells.
An antibody–drug conjugate consisting of an anti-HER2 monoclonal antibody linked to the topoisomerase I inhibitor deruxtecan (DXd). It binds HER2-expressing tumor cells, is internalized, and releases DXd to induce DNA damage and apoptosis, with potential bystander effect.
Anti-HER2 monoclonal antibody linked to the topoisomerase I inhibitor deruxtecan (DXd). Binds HER2 on tumor cells, is internalized, and releases DXd to inhibit Top1, causing DNA damage, cell-cycle arrest, and apoptosis; also mediates ADCC and has a membrane-permeable payload enabling a bystander killing effect.
YES
DIRECT
Binds HER2, is internalized, and releases the topoisomerase I inhibitor deruxtecan (DXd), causing Top1 inhibition, DNA damage, cell-cycle arrest, and apoptosis; Fc can also mediate ADCC. Membrane-permeable payload allows bystander killing.
An antibody–drug conjugate consisting of an anti-HER2 monoclonal antibody linked to the topoisomerase I inhibitor deruxtecan (DXd). It binds HER2-expressing tumor cells, is internalized, and releases DXd to induce DNA damage and apoptosis, with potential bystander effect.
Anti-HER2 monoclonal antibody linked to the topoisomerase I inhibitor deruxtecan (DXd). Binds HER2 on tumor cells, is internalized, and releases DXd to inhibit Top1, causing DNA damage, cell-cycle arrest, and apoptosis; also mediates ADCC and has a membrane-permeable payload enabling a bystander killing effect.
NO
INDIRECT
The ADC targets HER2 for delivery; after HER2-mediated internalization, DXd is released and inhibits Top1 to cause DNA damage and apoptosis. Top1 expression alone does not direct targeting or killing (bystander effects may occur but are not Top1-target–driven).
An antibody–drug conjugate comprising an anti-TROP2 monoclonal antibody linked to SN-38 (the active metabolite of irinotecan). After binding TROP2 on tumor cells and internalization, it releases SN-38 to inhibit topoisomerase I, causing DNA damage and apoptosis, with possible bystander effect.
Anti-TROP2 monoclonal antibody linked to the topoisomerase I inhibitor SN-38. After binding TROP2 on tumor cells and internalization, the linker is cleaved to release SN-38, which inhibits topoisomerase I, causing DNA damage and apoptosis; the membrane-permeable payload can also produce a bystander effect.
YES
DIRECT
The anti-TROP2 ADC binds TROP2, is internalized, and releases SN-38, which inhibits topoisomerase I, causing DNA damage and apoptosis (with possible bystander effect).