Antibody–drug conjugate targeting Nectin‑4; after binding and internalization it releases the MMAE microtubule inhibitor to disrupt tubulin polymerization and induce apoptosis (with possible bystander and ADCC effects).
Humanized anti–Nectin-4 monoclonal antibody conjugated to the microtubule inhibitor MMAE. After binding Nectin-4 on tumor cells and internalization, the linker is cleaved to release MMAE, which inhibits tubulin polymerization, causing G2/M arrest and apoptosis; potential bystander killing and ADCC may contribute.
NO
INDIRECT
9MW2821 targets Nectin-4 on the cell surface; after internalization it releases MMAE, which binds beta-tubulin (vinca domain) to block microtubule polymerization and cause G2/M arrest and apoptosis. Cells expressing beta-tubulin alone are not specifically targeted; any effect would be bystander from Nectin-4–positive cells.
Gene-modified cellular therapy consisting of 0.5–3×10^9 CAR-positive natural killer (NK) cells designed to redirect NK cytotoxicity and immune modulation toward pathogenic immune cells; administered after lymphodepletion.
Gene‑modified natural killer cells engineered with a chimeric antigen receptor (CAR) to redirect NK recognition and cytotoxicity toward disease-driving immune cells. Upon CAR engagement of the target antigen (not disclosed), the NK cells mediate killing via perforin/granzyme pathways and cytokine-driven immune modulation, aiming to deplete pathogenic autoreactive lymphocytes. Lymphodepletion is used to enhance CAR‑NK engraftment and persistence.
YES
DIRECT
CAR-engineered NK cells bind the antigen and kill target cells via NK degranulation with perforin/granzyme–mediated apoptosis (and ancillary cytokine-mediated cytotoxicity).
Autologous CD19-directed CAR T-cell therapy; genetically modified T cells expressing a CAR with CD3ζ and a costimulatory domain to target and kill CD19+ malignant B cells.
Autologous T cells are genetically engineered to express a CD19-specific chimeric antigen receptor with CD3ζ signaling and a costimulatory domain. Upon binding CD19 on B cells, the CAR activates T-cell cytotoxicity, cytokine release, and proliferation, resulting in targeted killing and depletion of CD19+ malignant (and normal) B cells.
YES
DIRECT
CAR T cells bind CD19 and directly kill CD19+ cells via perforin/granzyme-mediated cytolysis and death-receptor (e.g., Fas) apoptosis, with cytokine release enhancing cytotoxicity.
Also known as DuoBody CD3xCD30; a subcutaneous bispecific IgG T-cell–redirecting antibody that co-binds CD3 on T cells and CD30 on tumor cells to form an immune synapse, activate TCR/CD3 signaling, and induce cytotoxicity and cytokine release in CD30+ malignancies.
Fc-silenced bispecific IgG1 that co-binds CD3 on T cells and CD30 on tumor cells, forming an immune synapse to activate TCR/CD3 signaling and redirect cytotoxic T lymphocytes to kill CD30+ tumor cells with associated cytokine release.
YES
DIRECT
Bispecific T-cell engager binds CD30 on target cells and CD3 on T cells, forming an immune synapse that activates TCR/CD3 signaling; redirected CTLs kill CD30+ cells via perforin/granzyme-mediated cytolysis.
Also known as DuoBody CD3xCD30; a subcutaneous bispecific IgG T-cell–redirecting antibody that co-binds CD3 on T cells and CD30 on tumor cells to form an immune synapse, activate TCR/CD3 signaling, and induce cytotoxicity and cytokine release in CD30+ malignancies.
Fc-silenced bispecific IgG1 that co-binds CD3 on T cells and CD30 on tumor cells, forming an immune synapse to activate TCR/CD3 signaling and redirect cytotoxic T lymphocytes to kill CD30+ tumor cells with associated cytokine release.
NO
INDIRECT
The drug binds CD3 on T cells to activate and redirect them to kill CD30+ tumor cells via immune synapse and TCR/CD3 signaling; CD3+ T cells are effectors, not targets.