Autologous gene-modified T cells engineered with an EGFRvIII synNotch receptor that induces expression of a CAR targeting EphA2 and IL-13Rα2; administered IV as cellular immunotherapy for EGFRvIII+ glioblastoma.
Autologous T cells engineered with an EGFRvIII-directed synNotch receptor that, upon binding EGFRvIII on tumor cells, induces expression of a CAR targeting EphA2 and IL-13Ralpha2. This logic-gated activation confines CAR expression to EGFRvIII+ tumors, enabling targeted T-cell cytotoxicity and cytokine release against EphA2- and IL-13Ralpha2-expressing glioblastoma cells.
Upon EGFRvIII-triggered synNotch activation, the T cells express an anti‑EphA2 CAR; CAR engagement with EphA2 on tumor cells drives T‑cell cytotoxicity via perforin/granzyme release and apoptosis-inducing pathways.
Autologous gene-modified T cells engineered with an EGFRvIII synNotch receptor that induces expression of a CAR targeting EphA2 and IL-13Rα2; administered IV as cellular immunotherapy for EGFRvIII+ glioblastoma.
Autologous T cells engineered with an EGFRvIII-directed synNotch receptor that, upon binding EGFRvIII on tumor cells, induces expression of a CAR targeting EphA2 and IL-13Ralpha2. This logic-gated activation confines CAR expression to EGFRvIII+ tumors, enabling targeted T-cell cytotoxicity and cytokine release against EphA2- and IL-13Ralpha2-expressing glioblastoma cells.
After synNotch activation by EGFRvIII, the T cells express a CAR that binds IL-13Ralpha2; CAR engagement triggers T-cell killing via immune synapse formation with perforin/granzyme release and Fas–FasL-mediated apoptosis of IL-13Ralpha2+ cells.
Chimeric anti-CD20 monoclonal antibody (Ruxience) that depletes pre-B and mature B cells via complement-dependent cytotoxicity and antibody-dependent cellular cytotoxicity, reducing autoreactive B cells, antigen presentation, and autoantibody production.
Chimeric anti-CD20 monoclonal antibody that binds CD20 on pre-B and mature B cells and depletes them via complement-dependent cytotoxicity and antibody-dependent cellular cytotoxicity, reducing autoreactive B cells, antigen presentation, and autoantibody production.
Anti-CD20 antibody binds CD20 on B cells and induces complement-dependent cytotoxicity and Fc-mediated ADCC (and phagocytosis), leading to depletion of CD20+ cells.
Off-the-shelf, allogeneic T cells genetically modified to express a 4SCAR chimeric antigen receptor targeting BCMA (TNFRSF17), providing CD3ζ signaling with co-stimulation to mediate targeted cytotoxicity and cytokine release against multiple myeloma cells.
Off-the-shelf allogeneic T cells engineered to express a 4SCAR chimeric antigen receptor that binds BCMA (TNFRSF17). Antigen engagement delivers CD3ζ activation with co-stimulation, driving T-cell activation, proliferation, cytokine release, and cytolytic killing of BCMA-positive multiple myeloma cells.
Anti-BCMA CAR T cells bind BCMA on target cells, become activated, and kill via T-cell cytolytic pathways (perforin/granzyme and Fas–FasL-mediated apoptosis).
Off-the-shelf, allogeneic CAR T-cell product using a 4SCAR design directed at CD138 (syndecan-1) to recognize malignant plasma cells and activate T-cell effector functions for myeloma cell killing.
Off-the-shelf allogeneic T cells engineered with a 4SCAR chimeric antigen receptor specific for CD138 (syndecan-1). CAR engagement activates CD3zeta and co-stimulatory signaling, inducing T-cell cytotoxicity and cytokine release to eliminate CD138-positive myeloma/plasma cells.
Anti-CD138 CAR T cells recognize CD138 on target cells, activate, form an immunologic synapse, and kill via perforin/granzyme-mediated apoptosis (and Fas–FasL), with cytokine release.