Anti-CD52 monoclonal antibody that induces broad depletion of T and B lymphocytes for conditioning before hematopoietic cell transplantation.
Humanized IgG1 anti-CD52 monoclonal antibody that binds CD52 on T and B lymphocytes (and other CD52+ leukocytes), inducing antibody-dependent cellular cytotoxicity, complement-dependent cytotoxicity, and apoptosis to deplete lymphocytes and provide immunosuppression for transplant conditioning.
Alemtuzumab binds CD52 on lymphocytes and induces killing via Fc-mediated ADCC, complement-dependent cytotoxicity (CDC), and direct apoptosis of CD52+ cells.
FLT3-directed CAR-T cell therapy consisting of autologous T cells genetically engineered to express a chimeric antigen receptor targeting FLT3 (CD135) on leukemia cells, triggering T-cell activation, cytokine release, and cytotoxic killing of FLT3-positive AML blasts.
Autologous T cells engineered to express an anti-FLT3 (CD135) chimeric antigen receptor bind FLT3 on leukemia cells; CAR engagement activates T-cell effector functions (cytokine release and perforin/granzyme-mediated cytotoxicity) that selectively kill FLT3-positive AML blasts.
Anti-FLT3 CAR-T cells bind FLT3 on target cells and kill them via CTL effector functions, primarily perforin/granzyme-mediated apoptosis (with cytokine-driven cytotoxicity).
Autologous patient T cells genetically engineered to express a chimeric antigen receptor targeting the EX02 antigen on AML blasts; upon binding, CAR signaling (CD3ζ/costimulatory domains) activates T cells to release cytokines and mediate perforin/granzyme-dependent cytotoxicity, with in vivo expansion and persistence.
Autologous T cells are genetically engineered to express a chimeric antigen receptor that binds the EX02 antigen on AML blasts. CAR engagement triggers CD3ζ and costimulatory signaling to activate the T cells, leading to cytokine release, proliferation/expansion, and perforin/granzyme-mediated cytotoxic killing of EX02-positive leukemia cells, with persistence in vivo.
CAR engagement of EX02 activates T cells to form an immune synapse and kill EX02-positive cells via perforin/granzyme-mediated cytolysis (and death receptor pathways).
Autologous chimeric antigen receptor T-cell therapy administered after lymphodepletion; targets the patient’s malignancy (e.g., CD19 in B-cell NHL/ALL, BCMA in multiple myeloma) to mediate cytotoxicity and achieve expansion/persistence.
Autologous T cells are engineered ex vivo to express a chimeric antigen receptor (e.g., targeting CD19 or BCMA) that recognizes tumor antigens independently of MHC. After lymphodepletion, the CAR T cells are reinfused; antigen engagement triggers CD3ζ and costimulatory (e.g., CD28 or 4-1BB) signaling, driving T‑cell activation, proliferation, cytokine release, and cytotoxic killing of target cells via perforin/granzyme pathways, with in vivo expansion and persistence mediating antitumor effects.
CAR T cells bind CD19 on target cells, activate CD3zeta and costimulatory signaling, and kill the CD19+ cells via perforin/granzyme-mediated cytolysis and death-receptor pathways.
Autologous chimeric antigen receptor T-cell therapy administered after lymphodepletion; targets the patient’s malignancy (e.g., CD19 in B-cell NHL/ALL, BCMA in multiple myeloma) to mediate cytotoxicity and achieve expansion/persistence.
Autologous T cells are engineered ex vivo to express a chimeric antigen receptor (e.g., targeting CD19 or BCMA) that recognizes tumor antigens independently of MHC. After lymphodepletion, the CAR T cells are reinfused; antigen engagement triggers CD3ζ and costimulatory (e.g., CD28 or 4-1BB) signaling, driving T‑cell activation, proliferation, cytokine release, and cytotoxic killing of target cells via perforin/granzyme pathways, with in vivo expansion and persistence mediating antitumor effects.
BCMA-specific CAR T cells bind BCMA on target cells; CAR signaling activates the T cells to kill via perforin/granzyme release and death-receptor pathways.