Autologous T cells genetically engineered to express a CAR with an FMC63 anti-CD19 scFv, CD28 hinge/transmembrane, and intracellular CD3ε, CD28, and CD3ζ signaling domains; given as a single IV infusion to eliminate CD19+ B cells and reset humoral immunity.
Autologous T cells are engineered with an FMC63 anti‑CD19 scFv linked to CD28 hinge/transmembrane and intracellular CD3ε, CD28, and CD3ζ signaling domains. Upon binding CD19 on B cells, the CAR delivers activation and costimulatory signals that drive T‑cell cytotoxicity (perforin/granzyme) and cytokine release, depleting CD19+ B‑cell populations to ablate autoreactive clones and reset humoral immunity.
Anti-CD19 CAR-T cells bind CD19 and, via CD28/CD3zeta signaling, activate T-cell cytotoxicity to kill target cells by perforin/granzyme-mediated lysis and Fas–FasL/cytokine-induced apoptosis.
An antibody–drug conjugate (Enhertu) comprising a humanized anti‑HER2 IgG1 (trastuzumab) linked via a cleavable linker to the topoisomerase I inhibitor payload deruxtecan (DXd); targets HER2‑expressing tumor cells and delivers cytotoxic DXd intracellularly while also blocking HER2 signaling and mediating ADCC.
Humanized anti‑HER2 monoclonal antibody (trastuzumab) linked via a cleavable linker to the topoisomerase I inhibitor deruxtecan (DXd). After binding HER2 and internalization, DXd is released to inhibit topoisomerase I, causing DNA damage, cell-cycle arrest, and apoptosis with a bystander effect; the antibody also blocks HER2 signaling and mediates Fc‑dependent ADCC.
The anti-HER2 antibody binds HER2, is internalized, and releases the DXd topoisomerase I inhibitor, causing DNA damage, cell-cycle arrest, and apoptosis; Fc can also mediate ADCC, with a bystander effect from released payload.
Autologous dual-target CD19/BCMA CAR-T cell therapy designed to deplete CD19+ B cells and BCMA+ plasmablasts/plasma cells to reduce pathogenic autoantibodies in generalized myasthenia gravis.
Autologous T cells engineered with dual chimeric antigen receptors targeting CD19 and BCMA recognize and kill CD19+ B cells and BCMA+ plasmablasts/plasma cells, depleting antibody-producing lineages and reducing pathogenic autoantibodies.
CD19-targeted CAR-T cells bind CD19 on B cells and kill them via immune synapse–mediated cytotoxicity, primarily perforin/granzyme-induced apoptosis (and death receptor pathways).
Autologous dual-target CD19/BCMA CAR-T cell therapy designed to deplete CD19+ B cells and BCMA+ plasmablasts/plasma cells to reduce pathogenic autoantibodies in generalized myasthenia gravis.
Autologous T cells engineered with dual chimeric antigen receptors targeting CD19 and BCMA recognize and kill CD19+ B cells and BCMA+ plasmablasts/plasma cells, depleting antibody-producing lineages and reducing pathogenic autoantibodies.
GC012F CAR-T cells bind BCMA on target cells, triggering T-cell activation and immune synapse formation, leading to perforin/granzyme-mediated lysis and apoptotic death.
Autologous, second-generation bispecific CAR T-cell therapy targeting CD19 and CD20; utilizes CD3 zeta signaling and 4-1BB costimulation to enhance T-cell activation, expansion, and persistence; administered as a single IV infusion after lymphodepletion for relapsed/refractory large B-cell lymphoma.
Autologous T cells engineered with a second-generation bispecific CAR that recognizes CD19 and CD20 on B-cell malignancies. Antigen binding activates CD3 zeta signaling to drive T-cell cytotoxicity, while the 4-1BB costimulatory domain enhances expansion and persistence, leading to depletion of malignant (and normal) B cells and helping prevent antigen-escape relapse.
Bispecific CAR T cells bind CD19 on B cells, triggering CD3ζ signaling with 4-1BB costimulation to activate T cells, which kill targets via perforin/granzyme-mediated cytolysis and apoptosis.