Murine-derived, second-generation chimeric antigen receptor T cells targeting CD19 with 4-1BB costimulation for targeted killing and T-cell persistence.
Autologous T cells engineered to express a murine-derived anti-CD19 chimeric antigen receptor with 4-1BB costimulation and CD3z signaling; upon binding CD19 on B cells, the CAR triggers MHC-independent T-cell activation, proliferation, cytokine release, and cytolytic killing, with 4-1BB enhancing T-cell persistence.
CAR binding to CD19 activates the engineered T cell to kill target cells via perforin/granzyme-mediated cytolysis (and Fas–FasL), MHC-independently.
IgG-based bispecific T-cell–engaging monoclonal antibody (anti-CD20 × anti-CD3) that redirects cytotoxic T cells to deplete CD20+ B cells.
IgG-based bispecific antibody that binds CD20 on B cells and CD3 on T cells, bringing them into proximity to activate T cells and induce perforin/granzyme-mediated lysis of CD20+ malignant (and normal) B cells.
Bispecific antibody bridges CD3 on T cells to CD20 on target cells, activating T cells to deliver perforin/granzyme-mediated lysis of CD20+ cells.
Anti-CD20 chimeric monoclonal antibody that depletes B cells via ADCC, CDC, and apoptosis.
Chimeric anti-CD20 monoclonal antibody that binds CD20 on B lymphocytes and depletes them via antibody-dependent cellular cytotoxicity, complement-dependent cytotoxicity, and induction of apoptosis.
Rituximab binds CD20 on B cells and kills via Fc-mediated ADCC, complement-dependent cytotoxicity, and direct apoptosis signaling.
Autologous chimeric antigen receptor T-cell therapy engineered to target CD33 and CD123 on AML cells, inducing T-cell activation and cytotoxic killing with in vivo expansion/persistence.
Autologous T cells are genetically engineered to express chimeric antigen receptors that bind CD33 and CD123 on AML cells. Antigen engagement triggers T‑cell activation, cytokine release, proliferation, and perforin/granzyme‑mediated cytotoxic killing, with in vivo expansion and persistence enabling ongoing clearance of CD33/CD123‑positive leukemic cells.
CD33-specific CAR T cells bind CD33 on target cells, triggering T-cell activation and perforin/granzyme-mediated killing (with possible death receptor pathways), leading to apoptosis of CD33+ cells.
Autologous chimeric antigen receptor T-cell therapy engineered to target CD33 and CD123 on AML cells, inducing T-cell activation and cytotoxic killing with in vivo expansion/persistence.
Autologous T cells are genetically engineered to express chimeric antigen receptors that bind CD33 and CD123 on AML cells. Antigen engagement triggers T‑cell activation, cytokine release, proliferation, and perforin/granzyme‑mediated cytotoxic killing, with in vivo expansion and persistence enabling ongoing clearance of CD33/CD123‑positive leukemic cells.
CAR T cells bind CD123 on target cells and kill them via perforin/granzyme-mediated cytotoxicity (and death-receptor apoptosis).