Humanized T-cell–engaging bispecific antibody targeting Claudin-6 on tumor cells and engaging T cells to promote immune synapse formation, T-cell activation, and cytotoxic killing of CLDN6-positive solid tumors; administered weekly with a priming dose.
Fc-silenced humanized IgG1 bispecific antibody that binds Claudin-6 on tumor cells and CD3 on T cells, redirecting cytotoxic T cells to CLDN6-positive tumors to form immune synapses, activate T cells, and drive targeted lysis of CLDN6-expressing solid tumor cells.
CTIM-76 bridges CD3 on T cells to CLDN6 on tumor cells, forming an immune synapse and activating T cells to kill CLDN6+ cells via perforin/granzyme-mediated cytolysis.
Oral small-molecule BCL-2 (BH3-mimetic) inhibitor that induces mitochondrial apoptosis in leukemic blasts.
Selective BCL-2 BH3-mimetic that binds the hydrophobic groove of BCL-2, displacing pro-apoptotic BH3-only proteins and restoring mitochondrial apoptosis (MOMP and caspase activation) in BCL-2–dependent tumor cells; does not inhibit BCL-XL, reducing thrombocytopenia risk.
Venetoclax directly binds and inhibits BCL-2 as a BH3 mimetic, displacing pro-apoptotic BH3-only proteins to activate BAX/BAK, trigger mitochondrial outer membrane permeabilization, cytochrome c release, and caspase-mediated intrinsic apoptosis in BCL-2–dependent cells.
Autologous dual-target chimeric antigen receptor (CAR) T-cell therapy in which a patient’s T cells are genetically engineered to co-express CARs targeting BCMA and CD19, enabling direct antigen recognition and CAR-mediated activation and cytotoxic killing of malignant plasma cells and B-lineage cells; designed to reduce antigen escape in relapsed/refractory multiple myeloma.
Autologous T cells are genetically engineered to co-express chimeric antigen receptors targeting BCMA and CD19. Binding to these antigens on malignant plasma cells and B-lineage cells triggers CAR-mediated activation, proliferation, and cytotoxic killing, with dual targeting designed to reduce antigen escape in relapsed/refractory multiple myeloma.
CAR T cells bind BCMA on target cells, become activated, and kill via perforin/granzyme-mediated cytolysis (and Fas–FasL/apoptotic pathways).
Autologous dual-target chimeric antigen receptor (CAR) T-cell therapy in which a patient’s T cells are genetically engineered to co-express CARs targeting BCMA and CD19, enabling direct antigen recognition and CAR-mediated activation and cytotoxic killing of malignant plasma cells and B-lineage cells; designed to reduce antigen escape in relapsed/refractory multiple myeloma.
Autologous T cells are genetically engineered to co-express chimeric antigen receptors targeting BCMA and CD19. Binding to these antigens on malignant plasma cells and B-lineage cells triggers CAR-mediated activation, proliferation, and cytotoxic killing, with dual targeting designed to reduce antigen escape in relapsed/refractory multiple myeloma.
CAR T cells bind CD19 on target cells, triggering T-cell activation and killing via perforin/granzyme release and death-receptor signaling, leading to apoptosis/lysis of CD19+ cells.
HER2-targeted antibody-drug conjugate that binds ERBB2, is internalized, and releases a cytotoxic payload to kill HER2-expressing cells and suppress HER2-driven signaling.
HER2-targeted antibody–drug conjugate: the trastuzumab antibody binds HER2 (ERBB2) on tumor cells, is internalized, and a cleavable linker releases the camptothecin-derived payload (rezetecan), which inhibits topoisomerase I by stabilizing Topo I–DNA complexes, causing DNA strand breaks, replication arrest, and apoptosis; concurrently suppresses HER2-driven signaling.
The trastuzumab ADC binds HER2 on tumor cells, is internalized, and releases a camptothecin-derived payload (rezetecan) that inhibits Topoisomerase I, causing DNA damage, replication arrest, and apoptosis of HER2-expressing cells.