Autologous T cells genetically modified to express a chimeric antigen receptor targeting mesothelin, enabling MHC-independent recognition and cytotoxic killing of mesothelin-positive tumor cells after reinfusion (typically 1–10×10^6 cells/kg IV; local delivery optional).
Autologous T cells are genetically engineered to express a chimeric antigen receptor specific for mesothelin, enabling MHC-independent recognition of mesothelin-positive tumor cells. CAR engagement triggers CD3ζ and costimulatory signaling, leading to T-cell activation, cytokine release, proliferation, and targeted cytotoxic killing of mesothelin-expressing cancer cells.
YES
DIRECT
CAR T cells bind mesothelin on target cells and induce killing via perforin/granzyme-mediated cytolysis and Fas–FasL apoptosis after CAR signaling.
Autologous CAR-T cells engineered to target HER2 (ERBB2), designed for MHC-independent recognition and killing of HER2-expressing tumors with activation via CD3ζ and costimulatory signaling domains.
Autologous T cells engineered to express a HER2-specific chimeric antigen receptor. Binding to HER2 triggers CD3zeta and costimulatory signaling, activating the T cells to proliferate, release cytokines, and kill HER2-expressing tumor cells via perforin/granzyme in an MHC-independent manner.
YES
DIRECT
HER2-directed CAR-T cells bind HER2 on target cells, activating CD3zeta/costimulatory signaling and inducing T-cell cytotoxicity via perforin/granzyme-mediated lysis (and death receptor pathways), MHC-independent.
Autologous CAR-T cells engineered to target the immune checkpoint ligand B7-H3 (CD276), promoting T-cell activation and cytotoxicity against B7-H3–positive solid tumors upon reinfusion.
Autologous T cells are engineered to express a chimeric antigen receptor that binds B7-H3 (CD276) on tumor cells. Antigen engagement triggers CD3 zeta and costimulatory signaling in an MHC-independent manner, driving T-cell activation, proliferation, cytokine release, and cytotoxic killing of B7-H3-positive solid tumor cells.
YES
DIRECT
CAR-T cells recognize B7-H3 on target cells and, upon CAR activation, kill them via perforin/granzyme-mediated cytolysis and apoptosis (Fas–FasL/cytokine effects).
Autologous CAR-T cells engineered to recognize CD19 on B-lineage malignancies, inducing T-cell activation and tumor cell lysis in an MHC-independent manner after reinfusion.
Autologous T cells are engineered to express a chimeric antigen receptor that binds CD19 on B-lineage tumor cells in an MHC-independent manner, triggering T-cell activation (CD3ζ with costimulatory signaling), cytokine release, proliferation, and cytotoxic killing of CD19-positive cells.
YES
DIRECT
CAR-T cells recognize CD19 and, upon engagement, directly kill target cells via perforin/granzyme-mediated cytolysis and death-receptor pathways (e.g., Fas–FasL).
Autologous CAR-T cells engineered to target BCMA (TNFRSF17) on plasma cells, enabling MHC-independent recognition and cytotoxic killing of BCMA-expressing hematologic malignancies.
Autologous T cells are engineered with a chimeric antigen receptor that binds BCMA (TNFRSF17) on plasma cells, enabling MHC-independent recognition. Antigen engagement triggers CAR signaling (CD3ζ with costimulatory domains such as CD28 or 4‑1BB), leading to T‑cell activation, proliferation, cytokine release, and perforin/granzyme‑mediated cytotoxic killing of BCMA‑expressing malignant plasma cells (e.g., multiple myeloma).
YES
DIRECT
BCMA-directed CAR-T cells bind BCMA on target cells, triggering T-cell activation and perforin/granzyme-mediated cytotoxic apoptosis (± Fas–FasL).