Autologous BCMA-directed chimeric antigen receptor (CAR) T-cell therapy in which a patient’s T cells are engineered to express a CAR targeting BCMA, enabling depletion of BCMA-positive plasmablasts/plasma cells to reduce autoantibody production in systemic lupus erythematosus.
Autologous CD8+ T cells are transiently engineered via mRNA to express a CAR targeting BCMA, enabling antigen-specific recognition and cytotoxic elimination of BCMA-positive plasmablasts/plasma cells, thereby depleting autoantibody-producing cells and reducing pathogenic humoral immunity in SLE.
CAR-engineered CD8+ T cells bind BCMA on target cells, form an immunologic synapse, and induce cytolysis primarily via perforin/granzyme-mediated apoptosis (and potentially Fas–FasL).
Anti-HER2 antibody–drug conjugate (RC48) that delivers MMAE; binds HER2, internalizes, and releases MMAE to disrupt microtubules and kill tumor cells.
Anti-HER2 monoclonal antibody–drug conjugate that binds HER2, is internalized, and releases the microtubule inhibitor MMAE via a cleavable linker, inhibiting tubulin polymerization to induce G2/M arrest and apoptosis in HER2-expressing tumor cells.
ADC binds HER2, is internalized, and releases MMAE intracellularly to inhibit tubulin polymerization, causing G2/M arrest and apoptosis of HER2-expressing cells.
An intravenous bispecific T‑cell–redirecting antibody (MUC16×CD3) that binds MUC16 on tumor cells and CD3 on T cells to recruit and activate cytotoxic T cells, inducing tumor cell lysis.
A bispecific MUC16×CD3 T‑cell–redirecting antibody that binds MUC16 on tumor cells and CD3 on T cells, crosslinking and activating cytotoxic T cells to drive targeted lysis of MUC16‑expressing cancer cells.
Bispecific MUC16×CD3 antibody crosslinks T cells to MUC16+ cells, activating T cells to deliver perforin/granzymes and lyse the target cells.
Autologous CAR T-cell gene therapy in which patient T cells are engineered to express two fully human CARs: anti-CD19 with CD28/CD3ζ signaling and anti-CD20 with 4-1BB/CD3ζ signaling to enhance activation and persistence and reduce antigen-loss escape.
Autologous T cells are genetically engineered to express two CARs: an anti‑CD19 CAR with CD28/CD3ζ signaling and an anti‑CD20 CAR with 4‑1BB/CD3ζ signaling. Upon binding CD19 or CD20 on B cells, the CARs activate T‑cell cytotoxicity and cytokine release to kill malignant B cells; CD28 promotes rapid activation/expansion and 4‑1BB enhances persistence. Dual antigen targeting is intended to reduce antigen‑loss escape and results in on‑target B‑cell aplasia.
CAR T cells recognize CD19 via the CAR, form an immunologic synapse, and kill CD19+ cells through perforin/granzyme-mediated lysis and death-receptor pathways.
Autologous CAR T-cell gene therapy in which patient T cells are engineered to express two fully human CARs: anti-CD19 with CD28/CD3ζ signaling and anti-CD20 with 4-1BB/CD3ζ signaling to enhance activation and persistence and reduce antigen-loss escape.
Autologous T cells are genetically engineered to express two CARs: an anti‑CD19 CAR with CD28/CD3ζ signaling and an anti‑CD20 CAR with 4‑1BB/CD3ζ signaling. Upon binding CD19 or CD20 on B cells, the CARs activate T‑cell cytotoxicity and cytokine release to kill malignant B cells; CD28 promotes rapid activation/expansion and 4‑1BB enhances persistence. Dual antigen targeting is intended to reduce antigen‑loss escape and results in on‑target B‑cell aplasia.
CAR T cells recognize CD20 via the anti‑CD20 CAR (4‑1BB/CD3ζ), become activated, and kill CD20+ cells through perforin/granzyme release and death‑receptor pathways (e.g., Fas/FasL).