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.
YES
DIRECT
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.
YES
DIRECT
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.
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.
YES
DIRECT
NKG2D-CAR on NK-92 cells binds ULBP5 (an NKG2D ligand) on target cells, triggering NK activation and CAR signaling that induces perforin/granzyme-mediated cytotoxicity and tumor cell lysis/apoptosis.
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.
YES
DIRECT
NKG2D-CAR on NK-92 cells binds ULBP6 on target cells, activating NK degranulation and perforin/granzyme-mediated lysis (apoptosis).
Allogeneic induced-pluripotent-stem-cell–derived CD19-directed CAR-NK cell therapy; engineered NK cells recognize CD19 on malignant B cells and kill via NK cytotoxic pathways.
Allogeneic iPSC-derived NK cells engineered with an anti-CD19 CAR (FMC63 scFv with CD28/CD3ζ signaling) and IL-15 recognize CD19 on malignant B cells and kill them via NK cytotoxic pathways; IL-15 enhances NK survival/persistence. Cells include a truncated EGFR safety switch enabling elimination with cetuximab and gene edits to reduce rejection by host immune cells.
YES
DIRECT
Anti-CD19 CAR-NK cells bind CD19 on target cells and, upon CAR signaling, directly lyse them via NK degranulation (perforin/granzymes) and death-receptor apoptosis.