Intravenous bispecific T‑cell–engaging monoclonal antibody that binds BCMA on plasma cells and CD3 on T cells to redirect T‑cell cytotoxicity against BCMA‑positive cells; evaluated to prevent progression of high‑risk smoldering multiple myeloma.
Bispecific monoclonal antibody that binds BCMA on plasma cells and CD3 on T cells, forming an immune synapse to activate TCR/CD3 signaling and redirect T‑cell cytotoxicity (perforin/granzyme) against BCMA‑positive cells, depleting malignant and normal BCMA+ plasma cells.
The bispecific antibody links CD3 on T cells to BCMA on target cells, forming an immune synapse and activating TCR/CD3 signaling; engaged T cells kill BCMA+ cells via perforin/granzyme-mediated cytotoxicity.
Autologous, lentiviral-transduced T cells expressing an anti-CD19 chimeric antigen receptor (CAR) with CD3ζ and co-stimulatory domains; designed to recognize CD19 on B-lineage cells and mediate targeted cytotoxicity in B-cell malignancies.
Autologous lentiviral-transduced T cells engineered to express an anti-CD19 chimeric antigen receptor (CD3ζ plus co-stimulatory domains). Upon binding CD19 on B-lineage cells, the CAR activates T-cell effector functions—proliferation, cytokine release, and cytotoxicity—leading to selective elimination of CD19-positive malignant B cells and B-cell depletion.
Anti-CD19 CAR T cells bind CD19 on target B cells, activate, and kill via perforin/granzyme-mediated cytolysis and apoptotic pathways (e.g., Fas–FasL), leading to depletion of CD19+ cells.
Autologous, lentiviral-transduced T cells expressing an anti-CD20 chimeric antigen receptor (CAR) with CD3ζ and co-stimulatory domains; targets CD20 on B-lineage cells to enable T-cell activation and tumor cell killing.
Autologous T cells are lentivirally engineered to express an anti-CD20 chimeric antigen receptor with CD3zeta and co-stimulatory domains. Upon binding CD20 on B-lineage cells, CAR signaling activates the T cells, driving proliferation, cytokine release, and targeted cytotoxic killing of CD20-positive tumor cells, resulting in B-cell depletion.
Anti-CD20 CAR-T cells bind CD20 and directly kill target cells via T-cell effector functions (perforin/granzyme release and Fas–FasL–mediated apoptosis).
Autologous, lentiviral-transduced T cells engineered to express CARs targeting both CD19 and CD20 (dual-target CAR T) with CD3ζ and co-stimulatory domains, enabling recognition and elimination of CD19+ and/or CD20+ B-cell malignancies.
Autologous lentiviral-transduced T cells engineered with a dual CAR targeting CD19 and CD20. Binding to CD19/CD20 on B cells triggers CD3zeta signaling with co-stimulatory domains, inducing T-cell activation, expansion, cytokine release, and cytotoxic killing of malignant B cells; dual targeting is intended to mitigate antigen escape and relapse.
CAR T cells recognize CD19 via the CAR, triggering CD3ζ/co-stimulatory signaling and direct cytolysis of CD19+ cells (perforin/granzyme-mediated apoptosis).
Autologous, lentiviral-transduced T cells engineered to express CARs targeting both CD19 and CD20 (dual-target CAR T) with CD3ζ and co-stimulatory domains, enabling recognition and elimination of CD19+ and/or CD20+ B-cell malignancies.
Autologous lentiviral-transduced T cells engineered with a dual CAR targeting CD19 and CD20. Binding to CD19/CD20 on B cells triggers CD3zeta signaling with co-stimulatory domains, inducing T-cell activation, expansion, cytokine release, and cytotoxic killing of malignant B cells; dual targeting is intended to mitigate antigen escape and relapse.
CAR T cells recognize CD20 via the CAR, activating CD3zeta/co-stimulatory signaling and inducing T-cell effector functions (perforin/granzymes and Fas–FasL), resulting in lysis/apoptosis of CD20+ cells.