Gene-modified, allogeneic cord blood–derived natural killer (NK) cells engineered with a TROP2-specific chimeric antigen receptor and transduced to express IL-15; administered intraperitoneally to target TROP2-positive tumors and enhance NK survival and persistence.
Allogeneic cord blood-derived NK cells engineered with a TROP2-specific chimeric antigen receptor and IL-15 expression. CAR recognition of TROP2 on tumor cells triggers NK activation and cytolytic killing (perforin/granzyme), while IL-15 supports NK survival, proliferation, and persistence; delivered intraperitoneally to target TROP2-positive tumors.
CAR-NK cells recognize TROP2 on target cells, triggering NK activation and degranulation with perforin/granzyme–mediated cytolysis (and death-receptor signaling), killing TROP2-positive cells.
Autologous T cells genetically modified via lentiviral transduction to express fourth-generation chimeric antigen receptors targeting CD19 and BCMA, with an inducible caspase-9 safety switch, to deplete autoreactive B cells and antibody-producing plasma cells.
Autologous T cells are engineered via lentiviral transduction to express fourth-generation chimeric antigen receptors targeting CD19 (B cells) and BCMA (plasma cells). Antigen engagement activates T-cell cytotoxicity and cytokine release, depleting autoreactive B cells and antibody-producing plasma cells to reduce pathogenic autoantibodies. An inducible caspase-9 safety switch allows controlled elimination of the CAR T cells if needed.
CAR T cells bind CD19 via the CAR, form an immune synapse, and kill CD19+ cells through T-cell effector mechanisms (perforin/granzyme-mediated lysis and Fas–FasL apoptosis).
Autologous T cells genetically modified via lentiviral transduction to express fourth-generation chimeric antigen receptors targeting CD19 and BCMA, with an inducible caspase-9 safety switch, to deplete autoreactive B cells and antibody-producing plasma cells.
Autologous T cells are engineered via lentiviral transduction to express fourth-generation chimeric antigen receptors targeting CD19 (B cells) and BCMA (plasma cells). Antigen engagement activates T-cell cytotoxicity and cytokine release, depleting autoreactive B cells and antibody-producing plasma cells to reduce pathogenic autoantibodies. An inducible caspase-9 safety switch allows controlled elimination of the CAR T cells if needed.
BCMA-specific CAR T cells recognize BCMA on target cells and directly kill them via perforin/granzyme-mediated cytolysis and apoptosis (and Fas–FasL signaling).
Human IgG1 monoclonal antibody immune checkpoint inhibitor targeting PD-L1; blocks PD-L1 from binding PD-1 and B7.1 (CD80) to restore antitumor T-cell activity, and its IgG1 Fc can mediate ADCC via Fcγ receptors on NK cells and macrophages.
Human IgG1 monoclonal antibody immune checkpoint inhibitor that binds PD-L1 and blocks its interaction with PD-1 and B7.1 (CD80), restoring antitumor T-cell activity; its Fc region can engage Fc-gamma receptors to mediate ADCC against PD-L1–expressing cells.
Avelumab binds PD-L1 on target cells and, via its IgG1 Fc, engages Fc-gamma receptors (e.g., CD16) on NK cells to trigger ADCC (and phagocytosis), directly killing PD-L1–expressing cells; it also blocks PD-1/PD-L1 to restore T-cell cytotoxicity.
Autologous anti-CD19 chimeric antigen receptor (CAR) T-cell therapy administered as a single intravenous infusion to deplete CD19+ B-lineage cells and reduce pathogenic autoantibodies in generalized myasthenia gravis.
Autologous T cells are genetically modified to express an anti-CD19 chimeric antigen receptor with 4-1BB costimulation. After infusion, these CAR-T cells recognize CD19 on B-lineage cells and mediate cytotoxic killing, depleting B cells and plasmablasts to reduce pathogenic autoantibody production in generalized myasthenia gravis.
Anti-CD19 CAR-T cells recognize CD19 on B-lineage cells and directly kill them via T-cell cytotoxic mechanisms (perforin/granzyme release and death-receptor–mediated apoptosis).