Gene-modified, off-the-shelf allogeneic NK-92 cell therapy expressing an NKG2D chimeric antigen receptor that binds stress-induced ligands (e.g., MICA/MICB) on tumor cells to trigger NK-cell cytotoxicity (perforin/granzyme release and cytokine secretion).
Allogeneic NK-92 cells engineered to express an NKG2D-based chimeric antigen receptor that binds stress-induced NKG2D ligands (e.g., MICA/MICB/ULBPs) on tumor cells, triggering NK-cell activation and CAR signaling to drive perforin/granzyme-mediated cytotoxicity and cytokine secretion, resulting in tumor cell lysis.
NKG2D-CAR NK-92 cells bind MICB on target cells, activating NK/CAR signaling and degranulation to release perforin and granzymes, causing apoptosis/lysis of the target cells.
Gene-modified, off-the-shelf allogeneic NK-92 cell therapy expressing an NKG2D chimeric antigen receptor that binds stress-induced ligands (e.g., MICA/MICB) on tumor cells to trigger NK-cell cytotoxicity (perforin/granzyme release and cytokine secretion).
Allogeneic NK-92 cells engineered to express an NKG2D-based chimeric antigen receptor that binds stress-induced NKG2D ligands (e.g., MICA/MICB/ULBPs) on tumor cells, triggering NK-cell activation and CAR signaling to drive perforin/granzyme-mediated cytotoxicity and cytokine secretion, resulting in tumor cell lysis.
NKG2D-CAR on NK-92 binds ULBP1 on target cells, activating NK degranulation with perforin/granzymes to induce apoptosis/lysis.
Gene-modified, off-the-shelf allogeneic NK-92 cell therapy expressing an NKG2D chimeric antigen receptor that binds stress-induced ligands (e.g., MICA/MICB) on tumor cells to trigger NK-cell cytotoxicity (perforin/granzyme release and cytokine secretion).
Allogeneic NK-92 cells engineered to express an NKG2D-based chimeric antigen receptor that binds stress-induced NKG2D ligands (e.g., MICA/MICB/ULBPs) on tumor cells, triggering NK-cell activation and CAR signaling to drive perforin/granzyme-mediated cytotoxicity and cytokine secretion, resulting in tumor cell lysis.
NKG2D-CAR NK-92 cells recognize ULBP2 on target cells via the NKG2D CAR, triggering NK activation and cytotoxic degranulation (perforin/granzymes) leading to target cell apoptosis/lysis.
Gene-modified, off-the-shelf allogeneic NK-92 cell therapy expressing an NKG2D chimeric antigen receptor that binds stress-induced ligands (e.g., MICA/MICB) on tumor cells to trigger NK-cell cytotoxicity (perforin/granzyme release and cytokine secretion).
Allogeneic NK-92 cells engineered to express an NKG2D-based chimeric antigen receptor that binds stress-induced NKG2D ligands (e.g., MICA/MICB/ULBPs) on tumor cells, triggering NK-cell activation and CAR signaling to drive perforin/granzyme-mediated cytotoxicity and cytokine secretion, resulting in tumor cell lysis.
NKG2D-CAR on NK-92 binds ULBP3 on target cells, triggering NK activation and degranulation with perforin/granzyme release to induce apoptosis/lysis (with possible FasL/TRAIL contributions).
Gene-modified, off-the-shelf allogeneic NK-92 cell therapy expressing an NKG2D chimeric antigen receptor that binds stress-induced ligands (e.g., MICA/MICB) on tumor cells to trigger NK-cell cytotoxicity (perforin/granzyme release and cytokine secretion).
Allogeneic NK-92 cells engineered to express an NKG2D-based chimeric antigen receptor that binds stress-induced NKG2D ligands (e.g., MICA/MICB/ULBPs) on tumor cells, triggering NK-cell activation and CAR signaling to drive perforin/granzyme-mediated cytotoxicity and cytokine secretion, resulting in tumor cell lysis.
NKG2D-CAR on NK-92 cells binds ULBP4 (an NKG2D ligand) on target cells, activating the CAR/NK cell to form an immune synapse and kill via perforin/granzyme-mediated cytotoxicity.