Autologous, fully human anti-CD19 chimeric antigen receptor T-cell (CAR-T) therapy engineered to target and deplete CD19+ B cells to reduce pathogenic autoantibodies; administered after lymphodepletion.
Autologous T cells engineered to express an anti-CD19 CAR (human scFv with CD8alpha hinge/transmembrane, CD28 costimulatory and CD3zeta signaling domains) that recognize CD19 and kill B-lineage cells, depleting pathogenic CD19+ B cells/plasmablasts and reducing autoantibody production.
Anti-CD19 CAR-T cells bind CD19 on target cells and directly induce cytolysis via T-cell effector mechanisms (perforin/granzyme release and death receptor–mediated apoptosis).
Autologous gene-modified T cells engineered to express an anti-CD7 chimeric antigen receptor with costimulatory and CD3ζ signaling domains; administered as a single infusion to redirect T-cell cytotoxicity against CD7+ malignant T cells in r/r T-ALL/T-LBL.
Autologous T cells genetically engineered to express a CD7-specific chimeric antigen receptor with costimulatory and CD3z signaling domains. CAR engagement of CD7 on malignant T cells activates the engineered T cells to proliferate, secrete cytokines, and kill CD7+ targets via perforin/granzyme-mediated cytotoxicity in r/r T-ALL/T-LBL.
Anti-CD7 CAR T cells recognize CD7 on target cells and kill them via immune-synapse–mediated perforin/granzyme cytotoxicity leading to apoptosis.
Autologous, lentivirally transduced chimeric antigen receptor (CAR) T-cell therapy engineered to express a CAR targeting glycoprotein non-metastatic B (GPNMB) on tumor cells, leading to CAR-mediated T-cell activation and cytotoxic killing of GPNMB-expressing cells.
Autologous T cells are lentivirally transduced to express a chimeric antigen receptor targeting GPNMB on tumor cells; CAR engagement activates the T cells and induces cytotoxic killing of GPNMB-expressing cells.
CAR T cells bind GPNMB on target cells, become activated, and kill via perforin/granzyme-mediated cytolysis (and Fas–FasL apoptosis).
Autologous T cells engineered ex vivo to express an HPV-specific T-cell receptor and reinfused as monotherapy to target HPV antigen–expressing tumors via TCR–MHC engagement and cytotoxic T-cell effector functions.
Autologous T cells are genetically engineered to express an HPV-specific T-cell receptor that recognizes HPV-derived peptides presented by HLA/MHC on tumor cells; TCR–MHC engagement activates cytotoxic T-cell signaling, leading to perforin/granzyme-mediated lysis and cytokine-driven killing of HPV antigen–expressing cancer cells.
Engineered TCR-T cells recognize HPV E6/E7 peptide–HLA I complexes on tumor cells and kill them via cytotoxic T-cell effector functions (perforin/granzyme release and Fas–FasL–mediated apoptosis).
Fc-enhanced anti–CTLA-4 monoclonal antibody that enhances T-cell priming and can deplete intratumoral Tregs via Fc-mediated cytotoxicity.
Fc-engineered IgG1 anti-CTLA-4 monoclonal antibody that blocks CTLA-4 to enhance T-cell priming/activation and, via enhanced Fc effector functions, depletes intratumoral regulatory T cells (ADCC/ADCP), promoting cytotoxic T-lymphocyte–mediated antitumor immunity.
The anti-CTLA-4 IgG1 binds CTLA-4 on Tregs and, via its Fc engaging Fc receptors on NK cells/macrophages, induces ADCC/ADCP to deplete CTLA-4–expressing cells.