Autologous, gene-modified CAR T-cell therapy engineered to express a CAR that binds NKG2D ligands; administered as a single IV infusion after lymphodepleting chemotherapy.
Autologous T cells are genetically modified to express a chimeric antigen receptor that recognizes NKG2D ligands (e.g., MICA, MICB, ULBP/RAET1) on tumor cells; CAR engagement activates the T cells to kill NKG2DL-positive cells and release effector cytokines. Administered after lymphodepleting chemotherapy.
LEU011 CAR T cells recognize MICA (an NKG2D ligand) on target cells, become activated, and kill the bound cells via perforin/granzyme-mediated cytolysis (and Fas-FasL apoptosis), with cytokine release.
Autologous, gene-modified CAR T-cell therapy engineered to express a CAR that binds NKG2D ligands; administered as a single IV infusion after lymphodepleting chemotherapy.
Autologous T cells are genetically modified to express a chimeric antigen receptor that recognizes NKG2D ligands (e.g., MICA, MICB, ULBP/RAET1) on tumor cells; CAR engagement activates the T cells to kill NKG2DL-positive cells and release effector cytokines. Administered after lymphodepleting chemotherapy.
NKG2D-based CAR T cells bind MICB on target cells, become activated, and kill them via T-cell cytotoxic pathways (perforin/granzyme and death-receptor signaling), with cytokine release.
Autologous, gene-modified CAR T-cell therapy engineered to express a CAR that binds NKG2D ligands; administered as a single IV infusion after lymphodepleting chemotherapy.
Autologous T cells are genetically modified to express a chimeric antigen receptor that recognizes NKG2D ligands (e.g., MICA, MICB, ULBP/RAET1) on tumor cells; CAR engagement activates the T cells to kill NKG2DL-positive cells and release effector cytokines. Administered after lymphodepleting chemotherapy.
CAR T cells engineered in LEU011 bind ULBP1 (an NKG2D ligand) on target cells, activating T-cell cytotoxicity with perforin/granzyme-mediated lysis and apoptosis.
Autologous, gene-modified CAR T-cell therapy engineered to express a CAR that binds NKG2D ligands; administered as a single IV infusion after lymphodepleting chemotherapy.
Autologous T cells are genetically modified to express a chimeric antigen receptor that recognizes NKG2D ligands (e.g., MICA, MICB, ULBP/RAET1) on tumor cells; CAR engagement activates the T cells to kill NKG2DL-positive cells and release effector cytokines. Administered after lymphodepleting chemotherapy.
LEU011 CAR T cells bind ULBP2 (an NKG2D ligand) on target cells and kill them via T‑cell effector mechanisms, primarily perforin/granzyme cytolysis and death‑receptor signaling, with accompanying cytokine release.
Autologous, gene-modified CAR T-cell therapy engineered to express a CAR that binds NKG2D ligands; administered as a single IV infusion after lymphodepleting chemotherapy.
Autologous T cells are genetically modified to express a chimeric antigen receptor that recognizes NKG2D ligands (e.g., MICA, MICB, ULBP/RAET1) on tumor cells; CAR engagement activates the T cells to kill NKG2DL-positive cells and release effector cytokines. Administered after lymphodepleting chemotherapy.
LEU011 CAR T cells recognize NKG2D ligands such as ULBP3 on target cells; CAR engagement activates the T cells to kill ULBP3-positive cells via perforin/granzyme-mediated cytolysis and death-receptor signaling.