Autologous T cells engineered to express a chimeric antigen receptor targeting CD30 for MHC-independent activation and killing of CD30-positive Hodgkin and T-cell lymphomas.
Autologous T cells are engineered to express a chimeric antigen receptor specific for CD30, enabling MHC-independent recognition of CD30-positive tumor cells. Upon binding CD30, CAR signaling activates the T cells, inducing proliferation, cytokine release, and cytotoxic killing via perforin/granzyme-mediated lysis of CD30-expressing Hodgkin and T-cell lymphoma cells.
Anti-CD30 CAR T cells bind CD30 on target cells, triggering T-cell activation and direct killing via perforin/granzyme-mediated cytolysis (and Fas/FasL apoptosis).
Autologous CAR T-cell product designed to recognize both CD20 and CD30 antigens to mediate MHC-independent cytotoxicity against CD20-positive or CD20/CD30 double-positive lymphomas, including post–CD19 CAR T relapse.
Autologous T cells engineered with a bispecific chimeric antigen receptor that binds CD20 and CD30 on malignant cells, triggering MHC-independent T-cell activation, cytokine release, and cytotoxic killing of CD20+ or CD20/CD30+ lymphomas, helping prevent antigen escape after CD19-directed therapy.
CAR T cells bind CD20 via the CAR, triggering MHC-independent activation and perforin/granzyme-mediated cytolysis (and Fas/FasL apoptosis) of CD20+ cells.
Rabbit polyclonal anti-thymocyte globulin that depletes T cells to prevent rejection and GVHD.
Rabbit polyclonal anti-thymocyte IgG that binds multiple T-cell surface antigens and depletes T cells via complement-dependent cytotoxicity, antibody-dependent cellular cytotoxicity, and apoptosis, producing immunosuppression to prevent rejection and GVHD.
Thymoglobulin binds CD3ε on T cells and induces complement-dependent lysis and Fc-mediated ADCC; crosslinking can also trigger apoptosis, depleting CD3+ cells.
Autologous CAR T-cell product designed to recognize both CD20 and CD30 antigens to mediate MHC-independent cytotoxicity against CD20-positive or CD20/CD30 double-positive lymphomas, including post–CD19 CAR T relapse.
Autologous T cells engineered with a bispecific chimeric antigen receptor that binds CD20 and CD30 on malignant cells, triggering MHC-independent T-cell activation, cytokine release, and cytotoxic killing of CD20+ or CD20/CD30+ lymphomas, helping prevent antigen escape after CD19-directed therapy.
CAR T cells bind CD30 on target cells, triggering MHC‑independent T‑cell activation and cytolysis via perforin/granzyme (and Fas/FasL) pathways.
Autologous T cells engineered to express a chimeric antigen receptor targeting B7-H3 (CD276) and incorporating an inducible caspase-9 (iC9) safety switch; administered intraperitoneally to mediate T-cell cytotoxicity against B7-H3–positive ovarian cancer.
Autologous T cells are gene-modified to express a chimeric antigen receptor that binds B7-H3 (CD276) on tumor cells, triggering T-cell activation and cytotoxic killing via perforin/granzyme and cytokine release. The product includes an inducible caspase-9 (iC9) safety switch that can be activated (e.g., by rimiducid) to ablate the CAR-T cells in case of severe toxicity; administered intraperitoneally for B7-H3–positive ovarian cancer.
CAR-T cells bind B7-H3 on target cells, form an immunologic synapse, and kill via perforin/granzyme-mediated apoptosis (and cytokine-dependent cytotoxicity).