Autologous T cells genetically engineered to express a chimeric antigen receptor (CAR) that recognizes tumor antigens independently of MHC, leading to T-cell activation, cytotoxic killing of malignant hematologic cells, and cytokine release.
Autologous T cells are genetically engineered to express a chimeric antigen receptor that binds tumor antigens independent of MHC, triggering T‑cell activation, expansion, and cytotoxic killing of malignant hematologic cells with associated cytokine release.
CAR T cells recognize CD19 on target cells via the engineered CAR, become activated, and kill the bound cells through perforin/granzyme-mediated cytolysis and apoptosis (and Fas–FasL pathways).
Autologous T cells genetically engineered to express a chimeric antigen receptor (CAR) that recognizes tumor antigens independently of MHC, leading to T-cell activation, cytotoxic killing of malignant hematologic cells, and cytokine release.
Autologous T cells are genetically engineered to express a chimeric antigen receptor that binds tumor antigens independent of MHC, triggering T‑cell activation, expansion, and cytotoxic killing of malignant hematologic cells with associated cytokine release.
BCMA-specific CAR T cells bind BCMA on target cells, become activated, form an immunologic synapse, and kill via perforin/granzyme release and Fas–FasL–mediated apoptosis.
Autologous CD19-directed chimeric antigen receptor T-cell therapy; patient T cells engineered to express an anti-CD19 CAR with CD3zeta and costimulatory domains that, upon antigen engagement, activate T-cell signaling, expansion, cytokine release, and cytotoxic killing of CD19+ B-lineage leukemia cells; expected on-target B-cell aplasia.
Autologous T cells engineered to express an anti‑CD19 chimeric antigen receptor with CD3ζ and costimulatory domains. CAR engagement of CD19 on B‑lineage leukemic cells triggers T‑cell activation, proliferation, cytokine release, and perforin/granzyme‑mediated cytotoxic killing, leading to clearance of CD19+ blasts and on‑target B‑cell aplasia.
Anti-CD19 CAR-T cells bind CD19 on target cells, form an immune synapse, and kill via perforin/granzyme-mediated apoptosis (and death receptor pathways).
Chimeric anti-CD20 monoclonal antibody that depletes CD20+ B cells via CDC, ADCC, and apoptosis, reducing pathogenic autoantibodies (e.g., anti-PLA2R) driving membranous nephropathy.
Chimeric anti-CD20 monoclonal antibody that binds CD20 on B cells and depletes them via complement-dependent cytotoxicity, antibody-dependent cellular cytotoxicity, and apoptosis, thereby reducing pathogenic autoantibodies (e.g., anti-PLA2R) and dampening immune-mediated injury.
Rituximab binds CD20 on B cells and triggers complement-dependent cytotoxicity and Fc-mediated ADCC, and can directly induce apoptosis, depleting CD20+ cells.
Antibody–drug conjugate targeting Trop-2; internalization releases SN-38 (topoisomerase I inhibitor) to induce DNA damage and tumor cell death, with a bystander effect.
Humanized anti–Trop-2 monoclonal antibody conjugated to SN-38. After binding Trop-2 on tumor cells and internalization, the linker is cleaved to release SN-38, which inhibits topoisomerase I, stabilizing Topo I–DNA complexes to cause DNA breaks and apoptosis, with a bystander effect.
ADC binds TROP-2, is internalized, linker is cleaved to release SN-38, which inhibits topoisomerase I causing DNA damage and apoptosis (with a bystander effect).