Autologous T cells engineered with a chimeric antigen receptor targeting CD19 to eliminate CD19-positive malignant B cells.
Autologous T cells genetically engineered to express a chimeric antigen receptor that binds CD19 on B cells, activating T-cell signaling (CD3ζ with co-stimulatory domains) to mediate perforin/granzyme-dependent cytotoxicity and eliminate CD19-positive malignant B cells.
CAR T cells bind CD19 on target cells and, upon activation, kill via perforin/granzyme-mediated cytotoxicity (and Fas–FasL), inducing apoptosis/lysis of CD19+ cells.
Autologous CD19-directed chimeric antigen receptor T-cell (CAR-T) therapy that targets and eliminates CD19+ B cells to reduce autoantibody production and humoral immune activation.
Autologous T cells engineered to express a CD19-specific chimeric antigen receptor bind CD19 on B cells and plasmablasts, activate cytotoxic effector functions, and deplete CD19+ B cells, thereby reducing autoantibody production and humoral immune activation.
CD19-directed CAR T cells bind CD19 on B cells and directly kill them via T-cell cytotoxic mechanisms (perforin/granzyme-mediated apoptosis and Fas/FasL).
A bispecific antibody (CD20×CD3) that binds CD20 on B cells and CD3 on T cells to redirect T-cell cytotoxicity against B-cell malignancies.
Glofitamab is a CD20×CD3 bispecific monoclonal antibody that simultaneously binds CD20 on malignant B cells and CD3 on T cells, forming an immunologic synapse that activates and redirects T-cell cytotoxicity (perforin/granzyme release and cytokine production) to kill CD20-positive B-cell tumors independent of MHC presentation.
Bispecific CD20×CD3 antibody bridges CD20+ cells to T cells, forming an immunologic synapse that activates T-cell cytotoxicity (perforin/granzyme-mediated lysis) to kill CD20-expressing cells.
An anti-CD20 monoclonal antibody that depletes CD20-positive B cells; used here as part of the iR2 regimen.
Chimeric anti‑CD20 monoclonal antibody that binds CD20 on B cells and depletes them via antibody‑dependent cellular cytotoxicity, complement‑dependent cytotoxicity, and direct apoptosis, leading to elimination of CD20‑positive malignant and normal B cells.
Rituximab binds CD20 on B cells and induces killing via Fc-mediated ADCC by NK cells/macrophages, complement-dependent cytotoxicity (CDC), and can trigger direct apoptotic signaling upon CD20 cross-linking.
Patient-derived T cells engineered to express a chimeric antigen receptor that targets disease-driving immune cells; CAR engagement triggers cytotoxic killing independent of the native TCR to reduce autoantibody-producing cells and restore platelet counts in ITP.
Autologous T cells engineered to express a chimeric antigen receptor that recognizes an antigen on disease-driving immune cells; CAR engagement activates T-cell cytotoxicity independent of the native TCR, depleting autoantibody-producing cells and modulating autoimmunity to restore platelet counts in ITP.
CAR engagement activates T-cell cytotoxicity, leading to perforin/granzyme release (and death receptor signaling) that kills antigen-expressing cells.