Allogeneic, gene-engineered CAR T-cell therapy targeting BCMA (TNFRSF17) and CD19 to deplete B-lineage cells and plasma cells, intended to reduce AQP4-IgG in refractory AQP4-IgG+ NMOSD; dosed at 1.0–4.0 x 10^6 CD3+CAR+ cells/kg.
Allogeneic gene-engineered CAR T cells co-targeting BCMA (TNFRSF17) and CD19; upon antigen engagement they mediate cytotoxic killing of CD19+ B cells and BCMA+ plasmablasts/plasma cells, broadly depleting B-lineage cells and reducing pathogenic AQP4-IgG.
BCMA CAR engagement activates CAR T cells, which kill BCMA+ plasmablasts/plasma cells via perforin/granzyme-mediated cytolysis (and death-receptor pathways).
Allogeneic, gene-engineered CAR T-cell therapy targeting BCMA (TNFRSF17) and CD19 to deplete B-lineage cells and plasma cells, intended to reduce AQP4-IgG in refractory AQP4-IgG+ NMOSD; dosed at 1.0–4.0 x 10^6 CD3+CAR+ cells/kg.
Allogeneic gene-engineered CAR T cells co-targeting BCMA (TNFRSF17) and CD19; upon antigen engagement they mediate cytotoxic killing of CD19+ B cells and BCMA+ plasmablasts/plasma cells, broadly depleting B-lineage cells and reducing pathogenic AQP4-IgG.
Anti-CD19 CAR T cells bind CD19 on target B cells and kill them via T-cell cytotoxic mechanisms (perforin/granzyme release and death-receptor pathways).
Autologous T cells genetically modified to express a chimeric antigen receptor targeting CD19 on B cells to mediate cytotoxic killing.
Autologous T cells are genetically engineered to express a chimeric antigen receptor that binds CD19 on B cells, enabling MHC-independent recognition and activation of cytotoxic functions (perforin/granzyme release and cytokine secretion) to eliminate CD19-positive malignant and normal B cells, with in vivo expansion/persistence supporting antitumor activity.
CAR-T cells bind CD19 on target B cells via the CAR, triggering T-cell effector functions (perforin/granzyme-mediated apoptosis, with possible Fas/FasL and cytokine effects) that lyse CD19+ cells.
Defucosylated humanized IgG1 monoclonal antibody targeting CCR4 on malignant skin-homing T cells and regulatory T cells; enhances NK cell–mediated ADCC and reduces CCR4-dependent trafficking.
Defucosylated humanized IgG1 monoclonal antibody targeting CCR4 that blocks CCR4-mediated chemokine signaling and trafficking while inducing enhanced NK cell–mediated ADCC to deplete CCR4+ malignant T cells and regulatory T cells.
Antibody binds CCR4 on target cells; its defucosylated IgG1 Fc engages FcγRIIIa on NK cells to trigger antibody-dependent cellular cytotoxicity (ADCC), leading to lysis/apoptosis of CCR4+ cells.
Allogeneic (off-the-shelf) bispecific CAR-modified natural killer (NK) cell therapy targeting BCMA and GPRC5D for multiple myeloma; single infusion after lymphodepletion to mediate cytotoxicity against malignant plasma cells.
Allogeneic bispecific CAR-engineered NK cells recognizing BCMA and GPRC5D on myeloma cells; CAR engagement activates NK cytotoxicity (perforin/granzyme, cytokines) to induce apoptosis of malignant plasma cells and mitigate antigen escape.
Bispecific CAR-NK cells bind GPRC5D on target cells, triggering NK degranulation (perforin/granzymes) and death ligand pathways to induce apoptosis/lysis.