Humanized anti-HER2 IgG1 monoclonal antibody (trastuzumab-like) that binds the HER2 extracellular domain, inhibits HER2 signaling, and mediates Fc-dependent ADCC.
Humanized anti-HER2 (ErbB2) IgG1 monoclonal antibody that binds the HER2 extracellular domain, blocks HER2-mediated signaling/dimerization, inhibits proliferation of HER2-overexpressing tumor cells, and triggers Fc-dependent ADCC.
Inetetamab binds HER2 on tumor cells and its Fc engages Fcγ receptor–bearing effector cells (e.g., NK cells) to induce ADCC, leading to lysis of HER2-expressing cells.
Humanized anti-HER2 monoclonal antibody that binds the HER2 dimerization domain, blocking HER2/HER3 pairing and enhancing antibody-dependent cellular cytotoxicity (ADCC).
Humanized anti-HER2 monoclonal antibody that binds the HER2 dimerization domain (subdomain II), blocks HER2/HER3 dimerization and downstream PI3K/AKT and MAPK signaling, and mediates Fc-dependent ADCC against HER2-expressing tumor cells.
Pertuzumab binds HER2 on target cells and recruits FcγR-bearing immune cells to mediate ADCC; blockade of HER2 dimerization/signaling can also trigger apoptosis.
An antibody–drug conjugate (MK-2870/SKB264) targeting TROP2 that, after tumor cell internalization, releases the topoisomerase I inhibitor tirumotecan to induce DNA damage and cell death (potential bystander effect).
Humanized anti-TROP2 IgG1k antibody conjugated via a cleavable linker to the topoisomerase I inhibitor tirumotecan. After binding TROP2 on tumor cells and internalization, linker cleavage releases tirumotecan, inhibiting topoisomerase I, causing DNA damage, replication arrest, and apoptosis; membrane-permeable payload may produce a bystander effect.
An anti-TROP2 ADC binds TROP2 on tumor cells, is internalized, and releases the topoisomerase I inhibitor tirumotecan after linker cleavage, causing DNA damage, replication arrest, and apoptosis (with possible bystander killing).
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.
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.
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.