A HER2-targeted antibody–drug conjugate composed of a humanized anti-HER2 monoclonal antibody linked via a cleavable linker to deruxtecan (DXd), a membrane-permeable topoisomerase I inhibitor. Binds HER2, is internalized, and releases DXd to inhibit topoisomerase I, causing DNA damage and a bystander effect; dosed 5.4 mg/kg IV every 3 weeks.
Humanized anti-HER2 monoclonal antibody linked via a cleavable linker to deruxtecan (DXd), a membrane-permeable topoisomerase I inhibitor. After binding HER2 on tumor cells, the ADC is internalized and the linker is cleaved in lysosomes to release DXd, which inhibits topoisomerase I, inducing DNA damage and apoptosis; the membrane-permeable payload produces a bystander killing effect in adjacent cells.
ADC binds HER2, is internalized, and releases the DXd topoisomerase I inhibitor in lysosomes, causing DNA damage and apoptosis; the membrane‑permeable payload can also cause bystander killing.
Allogeneic, gene-edited T-cell therapy engineered with a reverse, universal CAR displaying an extracellular peptide epitope; given as a single IV infusion to enable dose-tunable engagement of CD123+ AML cells when bridged by R-TM123.
Allogeneic, gene-edited T cells expressing a reverse, universal CAR that displays an extracellular peptide epitope. Anti-leukemia activity is adapter-dependent: the bispecific protein R-TM123 binds both the RevCAR epitope and CD123 on tumor cells, bridging the engineered T cells to CD123+ blasts to trigger CAR signaling and cytotoxic killing with dose-tunable control.
R-TM123 bridges CD123 on target cells to the RevCAR on engineered T cells, activating CAR signaling and T cell–mediated killing (perforin/granzyme apoptosis) of CD123+ cells.
Recombinant antibody-derived bispecific adapter protein that binds the RevCAR epitope on Allo-RevCAR01-T and CD123 on AML cells, bridging tumor and T cell to trigger CAR signaling; administered as continuous IV infusion.
Recombinant antibody‑derived bispecific adapter that simultaneously binds the RevCAR epitope on Allo‑RevCAR01‑T cells and CD123 on AML cells, bridging T cells and tumor cells to trigger CAR signaling and T‑cell cytotoxicity; enables dose‑tunable, reversible engagement via continuous infusion.
R-TM123 bridges Allo-RevCAR01-T cells to CD123+ AML cells, activating CAR signaling and inducing T cell–mediated cytotoxicity (perforin/granzyme-mediated lysis) of CD123-expressing cells.
Intravenous bispecific monoclonal antibody (anti-BCMA × anti-CD3) that redirects T cells to kill BCMA-expressing malignant plasma cells; also known as REGN5458.
Linvoseltamab is an intravenous bispecific monoclonal antibody (anti-BCMA × anti-CD3) that simultaneously binds BCMA on malignant plasma cells and CD3 on T cells, forming an immunologic synapse that activates and redirects T cells to kill BCMA-expressing myeloma cells through cytotoxic granule release and cytokine-mediated mechanisms.
Anti-BCMA×anti-CD3 bispecific links T cells to BCMA+ cells, activating T-cell cytotoxicity (immunologic synapse, perforin/granzyme release and cytokine-mediated killing).
Intravenous monoclonal antibody targeting SLAMF7/CS1 that activates NK cells and mediates ADCC against myeloma cells.
Humanized monoclonal antibody that binds SLAMF7/CS1 on myeloma and NK cells, activating NK cells and promoting Fc-mediated antibody-dependent cellular cytotoxicity (ADCC) to kill SLAMF7-positive myeloma cells.
Elotuzumab binds SLAMF7 on myeloma cells; its Fc engages FcγRIIIa (CD16) on NK cells to trigger ADCC, and it also activates NK cells via SLAMF7, leading to lysis of SLAMF7-positive tumor cells.