Investigational HER2-directed biologic for HER2-positive tumors; specific type/mechanism not specified in the registry.
HER2-targeted trastuzumab-based monoclonal antibody site-specifically conjugated via a cleavable linker to the microtubule inhibitor MMAE. After binding HER2 on tumor cells and internalization, linker cleavage releases MMAE, which binds tubulin and inhibits microtubule polymerization, causing G2/M arrest and apoptosis in HER2-expressing cells; the antibody may also retain HER2 signaling blockade and ADCC activity.
NO
INDIRECT
The ADC targets HER2 on tumor cells, is internalized, and releases MMAE; the payload binds beta-tubulin to disrupt microtubules and induce G2/M arrest and apoptosis. Killing depends on HER2 targeting, not on beta-tubulin expression alone.
Anti-HER2 monoclonal antibody that blocks ERBB2 signaling and mediates antibody-dependent cellular cytotoxicity (ADCC).
Humanized monoclonal antibody targeting HER2/ERBB2 that blocks receptor signaling and dimerization, downregulates HER2, and induces Fc-mediated antibody-dependent cellular cytotoxicity against HER2-overexpressing tumor cells.
YES
DIRECT
Trastuzumab binds HER2 and its Fc engages Fcγ receptor–bearing effector cells (e.g., NK cells), triggering antibody-dependent cellular cytotoxicity and lysis of HER2+ cells; signaling blockade also inhibits growth.
An antibody–drug conjugate (Trodelvy) consisting of a humanized anti–TROP-2 monoclonal antibody (sacituzumab) linked to SN-38 (govitecan), a topoisomerase I inhibitor. It binds TROP-2 on tumor cells, is internalized, and releases SN-38 intracellularly, causing Topo I inhibition, DNA damage, and tumor cell death.
Humanized anti-TROP-2 monoclonal antibody linked to SN-38 (topoisomerase I inhibitor). After binding TROP-2 on tumor cells and internalization, linker cleavage releases SN-38, which stabilizes topoisomerase I-DNA complexes, causing DNA breaks, replication arrest, and apoptosis.
YES
DIRECT
The ADC binds TROP-2 on target cells, is internalized, and releases SN-38, a topoisomerase I inhibitor, causing DNA damage and apoptosis.
An antibody–drug conjugate (Trodelvy) consisting of a humanized anti–TROP-2 monoclonal antibody (sacituzumab) linked to SN-38 (govitecan), a topoisomerase I inhibitor. It binds TROP-2 on tumor cells, is internalized, and releases SN-38 intracellularly, causing Topo I inhibition, DNA damage, and tumor cell death.
Humanized anti-TROP-2 monoclonal antibody linked to SN-38 (topoisomerase I inhibitor). After binding TROP-2 on tumor cells and internalization, linker cleavage releases SN-38, which stabilizes topoisomerase I-DNA complexes, causing DNA breaks, replication arrest, and apoptosis.
NO
INDIRECT
The ADC binds TROP-2 on tumor cells, is internalized, and releases SN-38, which inhibits DNA topoisomerase I to cause DNA damage and apoptosis. Topoisomerase I is the intracellular enzyme target of the payload, not the cell-surface antigen used for selective killing; cells expressing only topoisomerase I are not specifically targeted.
A HER2-targeted antibody–drug conjugate that binds HER2 on tumor cells, is internalized, and releases a cytotoxic payload to induce tumor cell death, with potential bystander and immunogenic effects.
Trastuzumab-based HER2-targeted antibody-drug conjugate (trastuzumab rezetecan). After binding HER2 on tumor cells and internalization, a cleavable linker releases a camptothecin-derived topoisomerase I inhibitor (rezetecan), which stabilizes topo I–DNA complexes, causing DNA strand breaks, replication arrest, and apoptosis; may produce bystander killing and immunogenic effects.
YES
DIRECT
The ADC binds HER2 on target cells, is internalized, and releases a camptothecin-derived topoisomerase I inhibitor that stabilizes topo I-DNA complexes, causing DNA breaks, replication arrest, and apoptosis (with potential bystander effect).