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 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.
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.
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.
Chimeric IgG1 anti-EGFR monoclonal antibody that blocks EGFR ligand binding and downstream signaling; can mediate ADCC.
Chimeric IgG1 anti-EGFR monoclonal antibody that binds the extracellular domain of EGFR, blocking ligand binding and receptor dimerization to inhibit downstream signaling and tumor cell proliferation; Fc region can mediate NK cell–mediated ADCC.
Cetuximab binds EGFR on target cells and engages NK cells via its Fc to trigger ADCC, killing EGFR+ cells; EGFR blockade may also promote apoptosis.
Rabbit polyclonal antilymphocyte globulin used for in vivo T-cell depletion to reduce graft-versus-host disease risk.
Rabbit polyclonal IgG against multiple human T‑cell surface antigens (e.g., CD2, CD3, CD4, CD8, HLA) that depletes T lymphocytes via complement-dependent cytotoxicity, Fc-mediated ADCC/phagocytosis, and apoptosis, producing in vivo T‑cell immunosuppression to reduce GVHD risk.
rATG binds CD8α on T cells and triggers complement-dependent lysis and Fc-mediated ADCC/phagocytosis, leading to apoptosis/depletion of CD8+ cells.