Autologous, lentiviral-transduced dual STAR-T cell therapy targeting BCMA and LILRB4; synthetic antigen receptors engage BCMA and LILRB4 to signal via native TCR/CD3, activating T-cell cytotoxicity. Dose: 1E6–1E7 cells/kg IV; repeat dosing allowed.
Autologous T cells are lentivirally engineered to express dual synthetic antigen receptors that bind BCMA and LILRB4 and signal through the native TCR/CD3 complex. Target engagement activates T-cell cytotoxicity and cytokine release against BCMA+ myeloma cells and LILRB4+ cells in the tumor milieu, aiming to enhance efficacy and reduce antigen escape/immunosuppression.
Engineered STAR-T cells bind BCMA and signal via TCR/CD3 to form an immunologic synapse, releasing perforin/granzymes (and Fas/FasL, cytokines) to kill BCMA+ cells.
Autologous, lentiviral-transduced dual STAR-T cell therapy targeting BCMA and LILRB4; synthetic antigen receptors engage BCMA and LILRB4 to signal via native TCR/CD3, activating T-cell cytotoxicity. Dose: 1E6–1E7 cells/kg IV; repeat dosing allowed.
Autologous T cells are lentivirally engineered to express dual synthetic antigen receptors that bind BCMA and LILRB4 and signal through the native TCR/CD3 complex. Target engagement activates T-cell cytotoxicity and cytokine release against BCMA+ myeloma cells and LILRB4+ cells in the tumor milieu, aiming to enhance efficacy and reduce antigen escape/immunosuppression.
Engineered STAR-T cells bind LILRB4 via synthetic receptors and signal through native TCR/CD3 to trigger T-cell cytotoxicity (perforin/granzyme and death-receptor pathways) killing LILRB4+ cells.
Allogeneic, gene-edited CD19-directed CAR T-cell therapy that retains endogenous TCR and knocks out SPPL3 (Power3) to reduce alloreactivity and improve persistence; mediates CD19-specific cytotoxicity against malignant B cells.
Allogeneic, gene-edited CD19-directed CAR T cells that recognize CD19 on malignant B cells to induce T-cell activation and cytotoxic killing. The product retains the endogenous TCR to support signaling and persistence, while SPPL3 (Power3) knockout reduces alloreactivity and host-mediated rejection, enhancing expansion and durability of the donor CAR T cells.
CAR T cells bind CD19 on target B cells, become activated, and kill via perforin/granzyme release and death receptor pathways (e.g., Fas-FasL).
HER2-targeted monoclonal antibody that blocks ERBB2 signaling and mediates ADCC.
Humanized IgG1 monoclonal antibody that binds the extracellular domain of HER2 (ERBB2), blocks receptor signaling and dimerization, and triggers antibody-dependent cellular cytotoxicity via Fcγ receptor–bearing immune cells, inhibiting growth of HER2-overexpressing tumor cells.
Binds HER2 on target cells and engages Fcγ receptor–bearing immune cells (e.g., NK cells) to mediate antibody‑dependent cellular cytotoxicity, leading to lysis of HER2+ cells.
Autologous chimeric antigen receptor T-cell therapy engineered to recognize a B-lineage surface antigen and kill antigen-positive cells, depleting autoreactive B-lineage cells to reduce autoantibody production in SLE.
Autologous T cells engineered with a chimeric antigen receptor that recognizes a B-lineage surface antigen; upon antigen binding, CAR T cells become activated and cytotoxically eliminate antigen-positive B-lineage cells (e.g., autoreactive B cells/plasmablasts), thereby depleting autoantibody-producing cells and reducing pathogenic autoimmunity in SLE.
CAR T cells bind the target B-lineage antigen and directly kill antigen-positive cells via perforin/granzyme-mediated cytolysis and death-receptor apoptosis.