Autologous CD19-directed chimeric antigen receptor (CAR) T-cell therapy. Patient T cells are genetically engineered to express a CD19-specific CAR with CD3ζ and a costimulatory domain, then infused intravenously to kill CD19+ B-lymphoblasts in relapsed/refractory B-ALL (including Ph+ after TKI failure), inducing cytotoxicity and B-cell aplasia.
Autologous T cells are genetically engineered to express a CD19-specific chimeric antigen receptor containing CD3ζ and a costimulatory domain. Upon binding CD19 on malignant and normal B cells, the CAR triggers T-cell activation, proliferation, and cytotoxic effector functions (perforin/granzyme release and cytokine-mediated killing), leading to apoptosis of CD19+ B-lymphoblasts and on-target B-cell aplasia.
CD19-directed CAR T cells bind CD19 on B cells, activate via CD3ζ/costimulatory signaling, and kill targets through perforin/granzyme-mediated cytolysis (and cytokine/death-receptor pathways), causing apoptosis of CD19+ cells.
Engineered natural killer T cells expressing a chimeric antigen receptor targeting CD70; designed to recognize and kill CD70-positive tumor cells via perforin/granzyme-mediated cytotoxicity and cytokine-driven immune activation, with potential tumor microenvironment remodeling.
Engineered natural killer T (NKT) cells expressing a CD70-targeted chimeric antigen receptor bind CD70 on tumor cells, triggering CAR-mediated activation that induces perforin/granzyme-dependent cytotoxic killing and cytokine-driven immune activation, with potential remodeling of the tumor microenvironment.
CD70-specific CAR-NKT cells recognize CD70 on target cells and directly kill them via CAR-triggered cytolytic degranulation (perforin/granzyme-mediated apoptosis).
Autologous, gene-modified CD19-directed CAR T-cell therapy in which a patient’s T cells are retrovirally engineered to express a CD19-specific CAR with CD28 costimulatory and CD3ζ signaling domains; upon CD19 binding the CAR T cells activate, expand, release cytokines, and kill CD19+ targets via perforin/granzyme-mediated cytolysis to eradicate residual B-ALL cells.
Autologous T cells are retrovirally engineered to express a CD19-specific CAR with CD28 costimulatory and CD3ζ signaling domains. Upon binding CD19 on B-lineage cells, the CAR T cells activate, proliferate, release cytokines, and mediate perforin/granzyme-dependent cytotoxicity to eliminate CD19+ leukemic and normal B cells.
CD19-specific CAR T cells bind CD19, activate, and kill target cells via perforin/granzyme-mediated cytolysis.
Subcutaneous anti-CD38 IgG1 monoclonal antibody that targets CD38 on malignant plasma cells and induces ADCC, CDC, ADCP, and apoptosis.
Human IgG1k anti‑CD38 monoclonal antibody that binds CD38 on malignant plasma cells, triggering immune effector–mediated killing (ADCC, ADCP, CDC) and direct apoptosis, while depleting CD38+ immunosuppressive cells (Tregs, Bregs, MDSCs).
Anti-CD38 IgG1 binds CD38 on target cells and induces NK cell–mediated ADCC, macrophage ADCP, complement-dependent cytotoxicity, and can trigger direct apoptosis.
Allogeneic CD19-directed CAR-γδ T-cell therapy; engineered gamma delta T cells expressing an anti-CD19 chimeric antigen receptor to mediate MHC-independent cytotoxic killing of malignant B cells in relapsed/refractory B-ALL.
Allogeneic gamma delta T cells engineered to express an anti-CD19 chimeric antigen receptor bind CD19 on malignant B cells and induce MHC-independent activation and cytotoxic killing (perforin/granzyme), aiming to eliminate relapsed/refractory B-ALL with reduced GVHD risk.
Anti-CD19 CAR-engineered γδ T cells recognize CD19 on target cells and induce MHC-independent killing via perforin/granzyme-mediated cytotoxicity.