Off-the-shelf allogeneic CAR T-cell therapy engineered to express a CAR targeting CLL-1 (CLEC12A) to activate T-cell cytotoxicity against AML blasts and leukemic stem cells.
Off-the-shelf allogeneic T cells engineered with a chimeric antigen receptor targeting CLL-1 (CLEC12A) recognize AML blasts and leukemic stem cells; antigen binding activates the CAR signaling domain to drive T-cell activation and cytotoxic killing of target cells via perforin/granzyme release and cytokines.
CAR T cells recognize CLL-1 on target cells; CAR signaling activates T-cell cytotoxicity, killing targets via perforin/granzyme-mediated apoptosis (and associated immune effector mechanisms).
Off-the-shelf allogeneic CAR T-cell therapy engineered to express a CAR targeting CD33 to induce antigen-specific T-cell activation and lysis of AML cells.
Allogeneic off-the-shelf T cells are engineered to express a chimeric antigen receptor targeting CD33; upon binding CD33 on AML cells, the CAR activates T-cell signaling (CD3ζ with costimulatory domains) to induce cytokine release and perforin/granzyme-mediated lysis of the malignant cells.
CD33-specific CAR T cells recognize CD33 and, upon CAR activation, directly kill target cells via perforin/granzyme-mediated cytolysis and apoptosis.
Autologous cellular immunotherapy consisting of patient-derived, tumor-specific T cells (TIL-like) expanded ex vivo via antigen presentation and infused intravenously to recognize leukemia neoantigens/associated antigens via TCR and mediate cytotoxic killing of malignant blasts.
Autologous tumor‑reactive T cells are enriched and expanded ex vivo via antigen presentation and then infused intravenously; they use their endogenous TCRs to recognize leukemia neoantigens/leukemia‑associated antigens in an HLA‑restricted manner and mediate cytotoxic killing of malignant blasts via perforin/granzyme pathways.
Adoptively transferred T cells recognize HLA-presented leukemia-associated peptides via their endogenous TCRs and directly kill target cells through perforin/granzyme-mediated cytotoxicity.
Off-the-shelf allogeneic CAR T-cell therapy engineered to express a CAR targeting CD38 to promote T-cell mediated cytotoxicity against AML cells expressing CD38.
Allogeneic off-the-shelf T cells engineered with a CD38-specific chimeric antigen receptor bind CD38 on AML cells, triggering CAR signaling and T-cell activation to mediate cytotoxic killing (perforin/granzyme) of CD38-expressing leukemic cells.
CD38-targeted CAR T cells bind CD38 on target cells; CAR signaling activates T-cell cytotoxicity, killing CD38+ cells via perforin/granzyme-mediated apoptosis (and related death pathways).
Off-the-shelf allogeneic CAR T-cell therapy engineered to express a CAR targeting CD123 (IL-3Rα) to drive antigen-specific T-cell killing of AML blasts and leukemic stem cells.
Allogeneic (off-the-shelf) T cells engineered to express a chimeric antigen receptor targeting CD123 (IL-3Rα). CAR engagement of CD123 on AML blasts and leukemic stem cells triggers T-cell activation, proliferation, cytokine release, and perforin/granzyme-mediated cytotoxic killing of target cells.
CAR T cells recognize CD123 on target cells, form an immunologic synapse, and induce apoptosis via perforin/granzyme release (and possibly Fas/FasL).