Autologous genetically engineered T cells expressing a chimeric antigen receptor targeting CD19 on B-lineage cells; induce cytotoxic depletion of CD19+ naive and memory B cells and plasmablasts to reduce pathogenic autoantibody production in refractory SLE.
Autologous T cells are genetically engineered to express a CD19-specific chimeric antigen receptor. Upon binding CD19 on B-lineage cells, they activate and kill targets via T-cell cytotoxic mechanisms (perforin/granzyme), depleting CD19+ naive and memory B cells and plasmablasts to reduce pathogenic autoantibody production and B cell–driven autoimmunity.
CAR-T cells recognize CD19 on B-lineage cells and directly kill them via T-cell cytotoxic mechanisms, primarily perforin/granzyme-mediated apoptosis (and death-receptor signaling).
Autologous T cells genetically engineered to express a chimeric antigen receptor targeting carcinoembryonic antigen (CEA) on tumor cells, leading to T-cell activation and cytotoxic killing; administered IV or IP after lymphodepletion to promote expansion and persistence.
Autologous T cells are genetically engineered to express a chimeric antigen receptor that binds carcinoembryonic antigen (CEA) on tumor cells, leading to antigen-specific T‑cell activation, proliferation, cytokine release, and cytotoxic killing of CEA-expressing cancer cells; lymphodepleting chemotherapy is used to enhance CAR-T expansion and persistence.
CAR-T cells bind CEA on target cells via the CAR, become activated, and kill the CEA-expressing cells primarily through perforin/granzyme release and Fas–FasL–mediated apoptosis, with supportive cytokine-mediated cytotoxicity.
Anti-BCMA antibody–drug conjugate that binds BCMA on malignant plasma cells, internalizes, and releases the microtubule inhibitor MMAF to induce apoptosis; also mediates ADCC/ADCP.
Afucosylated anti-BCMA monoclonal antibody conjugated to the microtubule inhibitor MMAF. Binds BCMA on malignant plasma cells, internalizes, and releases MMAF to inhibit tubulin polymerization causing G2/M arrest and apoptosis; also mediates ADCC/ADCP.
The ADC binds BCMA on target cells, is internalized, and releases MMAF to inhibit tubulin polymerization, causing G2/M arrest and apoptosis; its Fc also mediates ADCC/ADCP against BCMA-expressing cells.
Gene-modified autologous T cells expressing a chimeric antigen receptor targeting CD19; infused IV to deplete CD19+ B-lineage cells and reduce autoantibody-driven inflammation.
Autologous T cells engineered with a CD19-directed chimeric antigen receptor recognize and eliminate CD19+ B-lineage cells (including B cells and plasmablasts), reducing autoantibody production, antigen presentation, and B–T cell costimulation, thereby dampening inflammatory pathways.
Anti-CD19 CAR-T cells recognize CD19 on target cells, become activated, and kill them via T-cell cytotoxic pathways (perforin/granzyme release and death-receptor–mediated apoptosis).
Autologous T cells engineered to express a chimeric antigen receptor targeting CD19 to recognize and kill CD19-positive B-cell lymphoma cells; part of a dual-target CAR T product.
Autologous T cells are genetically engineered to express a chimeric antigen receptor that binds CD19 on B cells. CAR engagement activates the T cells via CD3ζ/co-stimulatory signaling, driving proliferation, cytokine release, and perforin/granzyme-mediated cytotoxic killing, resulting in depletion of CD19-positive malignant B cells (and normal B cells).
CAR T cells bind CD19 on target cells, become activated via CD3ζ/co-stimulatory signaling, and kill through immunologic synapse formation with perforin/granzyme release (and death-receptor pathways), leading to apoptosis of CD19+ cells.