Autologous CAR T-cell therapy engineered to target CD19 on B cells with a CD34 truncation tag for selection, metabolically programmed toward a Th1/Th17-like phenotype to enhance cytotoxicity, persistence, and fitness.
Autologous T cells are engineered to express a chimeric antigen receptor that recognizes CD19 on B cells. A CD34 truncation tag enables selection/purification of CAR+ cells, and metabolic programming biases the product toward a Th1/Th17 phenotype to enhance cytotoxicity, persistence, and fitness. Upon infusion, CAR engagement of CD19 activates the T cells to release cytokines and lyse CD19+ malignant B cells.
CD19-specific CAR T cells bind CD19 on target cells, form an immunologic synapse, and kill via perforin/granzyme release and death-receptor signaling.
Autologous T lymphocytes genetically engineered to express a chimeric antigen receptor targeting CEA (CEACAM5) and infused intravenously to mediate antigen-specific tumor cell killing.
Autologous T cells engineered to express a chimeric antigen receptor specific for CEA (CEACAM5). CAR binding to CEA activates the T cells to release cytotoxic effector molecules and cytokines, mediating MHC-independent tumor cell killing.
CEA-targeted CAR-T cells bind CEACAM5 on target cells and, upon activation, kill them via perforin/granzyme-mediated cytolysis (and Fas–FasL apoptosis), MHC-independently.
Autologous anti-mesothelin CAR T-cell therapy; patient T cells are engineered to express a CAR targeting mesothelin (MSLN) to induce T-cell activation and cytotoxic killing of MSLN-positive tumor cells.
Autologous T cells are engineered to express a chimeric antigen receptor that binds mesothelin (MSLN) on tumor cells; CAR engagement triggers T‑cell activation and effector functions (e.g., perforin/granzyme release and cytokine production) resulting in selective killing of MSLN‑positive tumor cells.
Anti-mesothelin CAR T cells bind MSLN on target cells, activate, and kill via perforin/granzyme-mediated cytolysis and death receptor pathways.
Humanized anti-CD19 monoclonal antibody that depletes B-lineage cells (late memory B cells, plasmablasts, some plasma cells) to reduce pathogenic antibody production in NMOSD.
Humanized, afucosylated anti‑CD19 IgG1 monoclonal antibody that binds CD19 on B‑lineage cells and induces Fc‑mediated antibody‑dependent cellular cytotoxicity (and complement/phagocytosis) to deplete B cells, reducing plasmablast/early plasma cell pools and pathogenic autoantibody production (e.g., AQP4‑IgG in NMOSD).
Inebilizumab binds CD19 on B-lineage cells and, via its afucosylated IgG1 Fc, recruits effector mechanisms to kill the bound cell—NK cell ADCC, macrophage phagocytosis (ADCP), and complement-dependent cytotoxicity (CDC)—depleting CD19+ cells.
Chimeric anti-CD20 monoclonal antibody that depletes CD20+ B cells via ADCC/CDC and modulates immune responses, used to attenuate humoral autoimmunity.
Chimeric anti-CD20 monoclonal antibody that binds CD20 on pre-B and mature B cells and depletes them primarily via antibody-dependent cellular cytotoxicity and complement-dependent cytotoxicity, reducing pathogenic humoral immune responses.
Rituximab binds CD20 on B cells and triggers antibody-dependent cellular cytotoxicity via FcγR-bearing effector cells and complement-dependent cytotoxicity, with possible direct apoptosis upon crosslinking.