A humanized IgG4 bispecific T‑cell–engager monoclonal antibody that binds CD3 on T cells and BCMA on malignant plasma cells to trigger T‑cell cytotoxicity (brand: TECVAYLI).
Humanized IgG4 bispecific antibody that binds CD3 on T cells and BCMA on malignant plasma cells, crosslinking T cells to tumor cells to activate cytotoxic T-cell responses (perforin/granzyme release and cytokine-mediated killing) against BCMA-expressing myeloma cells.
YES
DIRECT
Teclistamab crosslinks CD3 on T cells to BCMA on target cells, activating T cells to kill BCMA+ cells via perforin/granzyme release and cytokine-mediated lysis.
A humanized IgG4 bispecific T‑cell–engager monoclonal antibody that binds CD3 on T cells and GPRC5D on myeloma cells to induce T‑cell killing (brand: TALVEY).
Humanized IgG4 bispecific antibody that binds CD3 on T cells and GPRC5D on myeloma cells, crosslinking them to activate cytotoxic T cells and kill GPRC5D-expressing tumor cells.
YES
DIRECT
Talquetamab bridges CD3 on T cells to GPRC5D on target cells, activating T cells to kill GPRC5D-expressing cells via perforin/granzyme-mediated cytotoxicity.
A humanized IgG4 bispecific T‑cell–engager monoclonal antibody that binds CD3 on T cells and GPRC5D on myeloma cells to induce T‑cell killing (brand: TALVEY).
Humanized IgG4 bispecific antibody that binds CD3 on T cells and GPRC5D on myeloma cells, crosslinking them to activate cytotoxic T cells and kill GPRC5D-expressing tumor cells.
NO
INDIRECT
Talquetamab bridges CD3 on T cells to GPRC5D on myeloma cells, activating T cells to kill GPRC5D+ tumor cells (perforin/granzyme). CD3+ T cells are not targeted for killing.
Anti-HER2 antibody–drug conjugate (T-DXd, DS-8201a) comprising trastuzumab linked to the topoisomerase I inhibitor deruxtecan (DXd); binds HER2, is internalized, and releases DXd to inhibit topo I and induce DNA damage, with a membrane-permeable payload enabling a bystander effect and potential ADCC via the Fc region.
Anti-HER2 monoclonal antibody (trastuzumab) conjugated to the topoisomerase I inhibitor deruxtecan (DXd). After binding HER2, the ADC is internalized and releases DXd, which inhibits topoisomerase I, causing DNA damage, replication arrest, and apoptosis; the membrane-permeable payload enables a bystander effect, and the Fc region can mediate ADCC.
NO
INDIRECT
The ADC binds HER2, is internalized, and releases DXd that inhibits topoisomerase I, causing DNA damage and apoptosis; topoisomerase I expression itself is not the targeting determinant (killing occurs in HER2-targeted cells, with possible bystander effect).
Investigational antibody-drug conjugate (humanized IgG1) targeting B7-H4 on tumor cells; after binding and internalization, a protease-cleavable linker releases a topoisomerase I inhibitor payload (DAR ~6) that causes DNA damage/replication stress and apoptosis.
Humanized IgG1 ADC that binds B7-H4 on tumor cells and is internalized; a protease-cleavable linker releases a topoisomerase I inhibitor payload that stabilizes TOP1–DNA cleavable complexes, preventing DNA re-ligation, inducing DNA damage/replication stress, cell-cycle arrest, and apoptosis in B7-H4–expressing cancer cells.
YES
DIRECT
ADC binds B7-H4 on tumor cells, is internalized, and a protease-cleavable linker releases a topoisomerase I inhibitor that stabilizes TOP1–DNA complexes, causing DNA damage, cell-cycle arrest, and apoptosis of B7-H4–expressing cells.