Subcutaneous bispecific T-cell–redirecting monoclonal antibody (anti-BCMA×CD3) that binds BCMA on malignant plasma cells and CD3 on T cells to activate and redirect T-cell cytotoxicity against myeloma cells.
Bispecific anti-BCMA×CD3 monoclonal antibody that binds BCMA on myeloma cells and CD3 on T cells, bringing them into proximity to activate and redirect T-cell cytotoxicity for targeted lysis of BCMA-expressing plasma cells.
NO
INDIRECT
Teclistamab binds CD3 on T cells to activate and redirect them to kill BCMA-expressing myeloma cells via perforin/granzyme cytotoxicity; CD3+ T cells themselves are not the lytic target.
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.
YES
DIRECT
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.
YES
DIRECT
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.
YES
DIRECT
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).
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.
NO
INDIRECT
The ADC targets TROP2 on tumor cells, is internalized, and releases tirumotecan, which inhibits DNA topoisomerase I to cause DNA damage and apoptosis. Topoisomerase I is the intracellular payload target, not the cytotoxic antigen; its expression alone does not trigger targeting or killing.