An autologous dual-target CAR T-cell therapy engineered to express chimeric antigen receptors against BCMA and CD19; patient T cells are collected, modified ex vivo, and reinfused after lymphodepletion to eliminate BCMA+/CD19+ clonal plasma and B cells in relapsed/refractory systemic AL amyloidosis.
Autologous T cells are engineered ex vivo to express dual chimeric antigen receptors targeting BCMA and CD19. After lymphodepletion, the cells are reinfused to recognize and kill BCMA+ plasma cells and CD19+ B-lineage cells via CAR-mediated activation, degranulation (perforin/granzyme), and cytokine release, aiming to eliminate clonal cells that produce amyloidogenic light chains in systemic AL amyloidosis.
BCMA-targeted CAR T cells recognize BCMA on tumor cells and kill them via CAR-mediated activation with degranulation (perforin/granzyme) and apoptosis pathways (e.g., Fas/FasL).
An autologous dual-target CAR T-cell therapy engineered to express chimeric antigen receptors against BCMA and CD19; patient T cells are collected, modified ex vivo, and reinfused after lymphodepletion to eliminate BCMA+/CD19+ clonal plasma and B cells in relapsed/refractory systemic AL amyloidosis.
Autologous T cells are engineered ex vivo to express dual chimeric antigen receptors targeting BCMA and CD19. After lymphodepletion, the cells are reinfused to recognize and kill BCMA+ plasma cells and CD19+ B-lineage cells via CAR-mediated activation, degranulation (perforin/granzyme), and cytokine release, aiming to eliminate clonal cells that produce amyloidogenic light chains in systemic AL amyloidosis.
CAR T cells recognize CD19 on target cells, form an immunologic synapse, and kill via degranulation (perforin/granzyme–mediated apoptosis), with possible Fas/FasL signaling.
Intravenous anti‑CD20×anti‑CD3 bispecific antibody (T‑cell–redirecting IgG) that links CD3 on T cells to CD20 on B cells, activating cytotoxic T cells and inducing lysis of CD20+ malignant B cells.
Bispecific monoclonal antibody that binds CD3 on T cells and CD20 on B cells, physically linking them to activate and redirect cytotoxic T cells to lyse CD20-positive malignant B cells via immune synapse formation, degranulation, and cytokine release.
Bispecific antibody bridges CD3+ T cells to CD20+ cells, forming an immune synapse that activates T cells to release perforin/granzymes and cytotoxic cytokines, resulting in lysis of CD20-expressing B cells.
Anti‑CD20 chimeric monoclonal antibody that depletes B cells via antibody‑dependent cellular cytotoxicity (ADCC), complement‑dependent cytotoxicity (CDC), and apoptosis.
Anti-CD20 chimeric monoclonal antibody that binds CD20 on B cells and depletes CD20-positive cells via antibody-dependent cellular cytotoxicity, complement-dependent cytotoxicity, and induction of apoptosis.
Rituximab binds CD20 on B cells and induces killing via Fc-mediated ADCC by NK/macrophages, complement-dependent cytotoxicity, and direct apoptosis of CD20+ cells.
Kymriah; an autologous, genetically modified CD19-directed CAR T-cell therapy in which a patient’s T cells are lentivirally transduced to express an anti-CD19 chimeric antigen receptor with 4-1BB costimulatory and CD3zeta signaling domains. Upon binding CD19 on B cells, the CAR T cells activate, proliferate, secrete cytokines, and kill targets via perforin/granzyme-mediated cytotoxicity, eliminating CD19-positive malignant B cells in B-ALL, DLBCL, and FL.
Autologous T cells are lentivirally transduced to express an anti‑CD19 chimeric antigen receptor with 4‑1BB costimulatory and CD3ζ signaling domains. Upon binding CD19 on B cells, the CAR T cells activate, proliferate, secrete cytokines, and kill CD19‑positive malignant B cells via perforin/granzyme‑mediated cytotoxicity.
CD19-directed CAR T cells bind CD19, activate, and kill target cells via perforin/granzyme-mediated cytolysis.