An antibody–drug conjugate (ADC) comprising a humanized anti–TROP-2 IgG1 monoclonal antibody linked to SN-38 (the active metabolite of irinotecan). It targets TROP-2–expressing tumor cells, is internalized, releases SN-38 intracellularly, inhibits topoisomerase I, induces DNA damage and apoptosis, and can cause bystander killing due to membrane-permeable SN-38.
Humanized anti–TROP-2 IgG1 antibody–drug conjugate that delivers SN-38. After binding TROP-2 on tumor cells and internalization, linker cleavage releases SN-38 intracellularly, inhibiting topoisomerase I and stabilizing topo I–DNA complexes to induce DNA damage, S-phase arrest, and apoptosis; membrane-permeable SN-38 can cause bystander killing.
YES
DIRECT
The ADC binds TROP-2, is internalized, and releases SN-38, which inhibits topoisomerase I to cause DNA damage and apoptosis; membrane-permeable SN-38 can also produce bystander killing.
An antibody–drug conjugate (ADC) comprising a humanized anti–TROP-2 IgG1 monoclonal antibody linked to SN-38 (the active metabolite of irinotecan). It targets TROP-2–expressing tumor cells, is internalized, releases SN-38 intracellularly, inhibits topoisomerase I, induces DNA damage and apoptosis, and can cause bystander killing due to membrane-permeable SN-38.
Humanized anti–TROP-2 IgG1 antibody–drug conjugate that delivers SN-38. After binding TROP-2 on tumor cells and internalization, linker cleavage releases SN-38 intracellularly, inhibiting topoisomerase I and stabilizing topo I–DNA complexes to induce DNA damage, S-phase arrest, and apoptosis; membrane-permeable SN-38 can cause bystander killing.
NO
INDIRECT
The ADC targets TROP-2 on tumor cells; after internalization, SN-38 is released and inhibits topoisomerase I to induce DNA damage and apoptosis. Killing is directed by TROP-2 binding, not by topoisomerase I expression itself (with potential bystander effect).
Investigational antibody–drug conjugate carrying a topoisomerase I inhibitor payload; binds a tumor-associated antigen to deliver the cytotoxin intracellularly, causing DNA single-strand breaks/replication stress and tumor-cell apoptosis (possible bystander effect).
Nectin-4–targeted IgG1 antibody–drug conjugate with a cleavable linker delivering a topoisomerase I inhibitor payload; upon antigen binding and internalization, the payload is released to inhibit topoisomerase I, causing DNA single-strand breaks/replication stress, cell-cycle arrest, and apoptosis in nectin-4–expressing tumor cells (with potential bystander effect).
YES
DIRECT
The ADC binds Nectin-4 on target cells, is internalized, and the cleavable linker releases a topoisomerase I inhibitor that causes DNA damage/replication stress, leading to cell-cycle arrest and apoptosis (with potential bystander effect).
Investigational antibody–drug conjugate carrying a topoisomerase I inhibitor payload; binds a tumor-associated antigen to deliver the cytotoxin intracellularly, causing DNA single-strand breaks/replication stress and tumor-cell apoptosis (possible bystander effect).
Nectin-4–targeted IgG1 antibody–drug conjugate with a cleavable linker delivering a topoisomerase I inhibitor payload; upon antigen binding and internalization, the payload is released to inhibit topoisomerase I, causing DNA single-strand breaks/replication stress, cell-cycle arrest, and apoptosis in nectin-4–expressing tumor cells (with potential bystander effect).
NO
INDIRECT
SHR-A2102 targets Nectin-4 on the cell surface, is internalized, and releases a topoisomerase I inhibitor that causes DNA damage and apoptosis. Topoisomerase I is the intracellular enzyme inhibited after delivery, not the antigen that determines cell targeting.