An anti-HER2 antibody–drug conjugate that delivers the microtubule inhibitor MMAE to HER2-expressing tumor cells, causing mitotic arrest and apoptosis, and mediating ADCC.
Disitamab vedotin is an anti-HER2 antibody–drug conjugate that binds HER2 on tumor cells, is internalized, and releases the cytotoxic payload MMAE via a cleavable linker. MMAE inhibits tubulin polymerization, causing mitotic arrest and apoptosis. The antibody component can also mediate ADCC.
The anti-HER2 ADC binds HER2, is internalized, and releases MMAE to inhibit tubulin polymerization, causing mitotic arrest and apoptosis; Fc-mediated ADCC can also contribute.
Autologous gene-modified CAR T-cell therapy co-transduced to express dual chimeric antigen receptors targeting CD19 and BCMA; upon antigen binding, activates T-cell cytotoxicity and cytokine release to kill malignant B cells and plasmablastic/plasma-cell–like components.
Autologous T cells co-transduced to express dual CARs targeting CD19 and BCMA. Antigen binding triggers CAR signaling (CD3zeta with costimulation), activating T-cell cytotoxicity and cytokine release to kill CD19+/BCMA+ malignant B cells and plasmablastic/plasma-cell–like components, with dual targeting designed to reduce antigen escape.
CD19 on target cells is bound by the CD19 CAR on ARI0003 T cells, triggering CAR signaling (CD3ζ with costimulation) and T‑cell effector functions, leading to target-cell killing via perforin/granzyme-mediated lysis and apoptosis (and Fas/FasL), with cytokine release.
Autologous gene-modified CAR T-cell therapy co-transduced to express dual chimeric antigen receptors targeting CD19 and BCMA; upon antigen binding, activates T-cell cytotoxicity and cytokine release to kill malignant B cells and plasmablastic/plasma-cell–like components.
Autologous T cells co-transduced to express dual CARs targeting CD19 and BCMA. Antigen binding triggers CAR signaling (CD3zeta with costimulation), activating T-cell cytotoxicity and cytokine release to kill CD19+/BCMA+ malignant B cells and plasmablastic/plasma-cell–like components, with dual targeting designed to reduce antigen escape.
BCMA-specific CAR T cells bind BCMA, become activated via CD3ζ/costimulation, and kill BCMA+ cells through perforin/granzyme cytolysis and death-receptor–mediated apoptosis.
Autologous tumor-infiltrating lymphocyte (TIL) adoptive cell therapy administered intravenously after lymphodepleting chemotherapy to mediate TCR-dependent cytotoxicity against tumor cells.
Autologous TILs expanded ex vivo are reinfused after lymphodepleting chemotherapy. They recognize patient-specific tumor antigens via TCR-MHC and kill tumor cells through perforin/granzyme-mediated cytotoxicity and cytokine release, with IL-2 supporting T-cell activation, proliferation, and persistence.
TILs recognize the tumor neoantigen peptide–HLA-DR/DQ/DP complex via their TCRs and directly kill target cells through perforin/granzyme-mediated cytolysis (and Fas–FasL apoptosis).
A bispecific monoclonal antibody T-cell engager designed to bind CLDN6 on tumor cells and engage T cells to kill CLDN6-positive cancer cells; administered intravenously or subcutaneously.
Bispecific antibody that binds CLDN6 on tumor cells and CD3 on T cells, recruiting and activating cytotoxic T lymphocytes to kill CLDN6-positive tumor cells; bivalent CLDN6 and monovalent CD3 binding enhances selective targeting.
XmAb541 bridges CD3 on T cells to CLDN6 on tumor cells, forming an immune synapse and activating cytotoxic T cells to kill CLDN6-positive cells via perforin/granzyme-mediated lysis.