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.
YES
DIRECT
rATG contains polyclonal IgG that binds CD4 on T cells, triggering complement-dependent lysis and Fc-mediated ADCC/phagocytosis (and apoptosis), resulting in direct depletion of CD4+ 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.
YES
DIRECT
NKG2D-CAR NK-92 cells bind MICA on target cells, triggering NK activation and immune synapse formation, leading to perforin/granzyme-mediated lysis of the MICA-expressing 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.
YES
DIRECT
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.
YES
DIRECT
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.
YES
DIRECT
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.