Autologous tumor-infiltrating lymphocyte (TIL) cell therapy in which a patient’s tumor-infiltrating T cells are expanded ex vivo and reinfused to recognize tumor neoantigens via TCR–MHC and mediate cytotoxic CD8+ activity against cancer cells.
Autologous tumor-infiltrating T cells are isolated from the patient’s tumor, expanded ex vivo, and reinfused to recognize tumor neoantigens via native TCR–MHC interactions, leading to cytotoxic CD8+ T-cell–mediated killing of cancer cells and cytokine-driven antitumor activity.
Autologous TILs recognize the peptide–HLA complex via native TCRs and directly kill target cells by perforin/granzyme-mediated lysis and Fas–FasL apoptosis.
Genetically engineered natural killer (NK) cells expressing a chimeric antigen receptor that targets CD123 (IL-3 receptor alpha) on tumor cells to trigger NK-mediated cytotoxicity against CD123-positive malignancies (e.g., AML, BPDCN). Administered as intravenous infusions with dose-escalation by CAR+ cells/kg.
Genetically engineered natural killer cells expressing a CD123-specific chimeric antigen receptor bind IL-3Rα (CD123) on tumor cells, activating NK effector signaling to induce targeted cytotoxicity via perforin/granzyme release, death-receptor pathways, and cytokine-mediated killing of CD123-positive malignant cells (e.g., AML, BPDCN).
CAR-engineered NK cells bind CD123 on target cells and directly kill them via perforin/granzyme degranulation and death-receptor–mediated apoptosis (e.g., FasL/TRAIL).
An antibody–drug conjugate targeting Trop-2 that delivers the cytotoxic payload SN-38 to Trop-2–expressing tumor cells, leading to topoisomerase I inhibition, DNA damage, cell-cycle arrest, and apoptosis; can exert a bystander effect.
Humanized anti–Trop-2 monoclonal antibody delivers the topoisomerase I inhibitor SN-38 to Trop-2–expressing tumor cells. After binding and internalization, linker cleavage releases SN-38, stabilizing Topo I–DNA complexes to cause DNA breaks, leading to cell-cycle arrest and apoptosis; membrane-permeable payload can produce a bystander effect.
ADC binds Trop-2, is internalized, and releases SN-38, which inhibits topoisomerase I, causing DNA damage, cell-cycle arrest, and apoptosis in Trop-2–expressing cells; membrane-permeable SN-38 can also cause a bystander effect.
Autologous dual-target CAR-T cell therapy in which a patient’s T cells are engineered to express chimeric antigen receptors recognizing CD19 and CD20 on B cells, triggering CD3ζ-based signaling with costimulation to induce cytokine release and cytotoxic killing; dual targeting aims to limit antigen escape in B‑cell malignancies.
Autologous T cells are genetically engineered to express dual CARs recognizing CD19 and CD20 on B cells. Antigen engagement triggers CD3ζ signaling with costimulation, activating and expanding the T cells to secrete cytokines and mediate cytotoxic killing of malignant B cells; dual targeting is intended to limit antigen escape.
CAR-T cells engineered to recognize CD19 are activated via CD3ζ/costimulatory signaling and directly kill CD19+ cells through perforin–granzyme cytolysis and death-receptor pathways.
Autologous dual-target CAR-T cell therapy in which a patient’s T cells are engineered to express chimeric antigen receptors recognizing CD19 and CD20 on B cells, triggering CD3ζ-based signaling with costimulation to induce cytokine release and cytotoxic killing; dual targeting aims to limit antigen escape in B‑cell malignancies.
Autologous T cells are genetically engineered to express dual CARs recognizing CD19 and CD20 on B cells. Antigen engagement triggers CD3ζ signaling with costimulation, activating and expanding the T cells to secrete cytokines and mediate cytotoxic killing of malignant B cells; dual targeting is intended to limit antigen escape.
CAR-T cells recognize CD20 via the CAR, triggering CD3zeta/costimulatory signaling and T-cell effector functions (perforin/granzyme release and Fas–FasL interactions) to kill the target cell.