Chimeric anti-CD20 IgG1 monoclonal antibody that depletes CD20+ B cells via ADCC, CDC, and apoptosis to remodel the immunosuppressive tumor microenvironment.
Chimeric anti-CD20 IgG1 monoclonal antibody that binds CD20 on B cells and depletes CD20+ cells via antibody-dependent cellular cytotoxicity (ADCC), complement-dependent cytotoxicity (CDC), and apoptosis, thereby remodeling the immunosuppressive tumor microenvironment.
YES
DIRECT
Rituximab binds CD20 on B cells and triggers Fc-mediated ADCC by NK cells/macrophages, complement-dependent cytotoxicity (CDC), and can induce apoptosis upon crosslinking.
HER2-directed antibody–drug conjugate (ENHERTU, T-DXd) comprising trastuzumab linked via a cleavable linker to deruxtecan (DXd), a membrane-permeable topoisomerase I inhibitor; binds HER2, internalizes, releases DXd to cause DNA damage and apoptosis, while the trastuzumab component blocks HER2 signaling and mediates ADCC.
HER2-targeted antibody–drug conjugate: the trastuzumab antibody binds HER2 and is internalized; a cleavable linker releases the deruxtecan (DXd) payload, a membrane-permeable topoisomerase I inhibitor, causing DNA damage, cell-cycle arrest, and apoptosis, with a bystander killing effect. The antibody component also blocks HER2 signaling and mediates ADCC.
YES
DIRECT
The ADC binds HER2, is internalized, and releases deruxtecan (DXd), a topoisomerase I inhibitor, causing DNA damage and apoptosis; the Fc domain also mediates ADCC, with a membrane-permeable payload enabling bystander killing.
An antibody–drug conjugate (Trodelvy): a humanized anti–TROP‑2 monoclonal antibody linked to SN‑38 (active metabolite of irinotecan), a topoisomerase I inhibitor. After binding TROP‑2 on tumor cells, it is internalized and releases SN‑38 to induce DNA damage and apoptosis with a bystander effect.
Humanized anti–TROP-2 monoclonal antibody linked to SN-38 (topoisomerase I inhibitor). After binding TROP-2 on tumor cells, the ADC is internalized and cleaved to release SN-38, which stabilizes topo I–DNA complexes, causing DNA breaks, inhibition of DNA replication, and apoptosis, with a bystander killing effect.
YES
DIRECT
The anti–TROP-2 antibody–drug conjugate binds TROP-2, is internalized, and releases SN-38 (a topoisomerase I inhibitor) that causes DNA damage/replication arrest and apoptosis in target-expressing cells, with a bystander effect.
HER2-directed antibody–drug conjugate (ENHERTU, T-DXd) comprising trastuzumab linked via a cleavable linker to deruxtecan (DXd), a membrane-permeable topoisomerase I inhibitor; binds HER2, internalizes, releases DXd to cause DNA damage and apoptosis, while the trastuzumab component blocks HER2 signaling and mediates ADCC.
HER2-targeted antibody–drug conjugate: the trastuzumab antibody binds HER2 and is internalized; a cleavable linker releases the deruxtecan (DXd) payload, a membrane-permeable topoisomerase I inhibitor, causing DNA damage, cell-cycle arrest, and apoptosis, with a bystander killing effect. The antibody component also blocks HER2 signaling and mediates ADCC.
NO
INDIRECT
The ADC binds HER2 (not Top1), is internalized, and releases the DXd payload that inhibits Top1 inside exposed cells, causing DNA damage and apoptosis (with a bystander effect); killing is driven by HER2-mediated delivery rather than recognition of Top1.
Humanized anti-HER2 IgG1 monoclonal antibody that inhibits HER2/ERBB2 signaling and mediates antibody-dependent cellular cytotoxicity (ADCC).
Humanized IgG1 monoclonal antibody against HER2/ERBB2 that binds HER2 on tumor cells, inhibits HER2 signaling and receptor dimerization to suppress proliferation, and engages Fc receptors to mediate antibody-dependent cellular cytotoxicity (ADCC), with possible complement-dependent cytotoxicity, in HER2-overexpressing cancers.
YES
DIRECT
Trastuzumab binds HER2 on target cells and its Fc engages Fcγ receptor–bearing effector cells (e.g., NK cells) to mediate ADCC; it may also trigger complement-dependent cytotoxicity and can induce apoptosis via HER2 signaling blockade.