drug_type
RELEVANT_DRUG
intervention_type
Cellular therapy (CAR T cells)
drug_description
An autologous NKG2D-based CAR T-cell therapy in which patient T cells are gene-engineered to express a chimeric antigen receptor using the NKG2D receptor ectodomain fused to intracellular activation/costimulatory domains (e.g., CD3ζ). The cells target stress-induced NKG2D ligands (MICA, MICB, ULBP1–6) on tumor cells to mediate cytotoxicity and cytokine release.
nci_thesaurus_concept_id
C179622
nci_thesaurus_definition
A preparation of autologous T-lymphocytes that have been genetically modified to express a chimeric antigen receptor (CAR) encoding human natural-killer group 2, member D receptor protein (NKG2D or KLRK1) coupled to the co-immunostimulatory signaling domain 4-1BB, normally expressed on T-cells, and linked to the intracellular CD3 zeta domain (CD3z), which is needed for TCR signaling, with potential immunostimulating and antineoplastic activities. Upon infusion back into the patient, autologous NKG2D CAR T cells KD-025 specifically recognize and bind to tumor cells expressing NKG2D ligands (NKG2DLs), resulting in cytokine secretion and lysis of NKG2D ligand-expressing tumor cells. NKG2DLs, such as MICA, MICB, and members of the UL16-binding proteins (ULBP)/retinoic acid early transcript 1 (RAET1) family, are overexpressed on a variety of cancer cell types, but are not expressed on most normal, healthy cells.
drug_mesh_term
Chimeric Antigen Receptor T-Cell Therapy
drug_category
CAR T
drug_class
Cellular Therapy
drug_delivery_route
Intravenous
drug_mechanism_of_action
Autologous T cells are engineered to express an NKG2D-based CAR (NKG2D ectodomain fused to 4-1BB and CD3ζ signaling domains) that recognizes stress-induced NKG2D ligands (MICA, MICB, ULBP1–6) on tumors, activating T cells to release cytokines and mediate perforin/granzyme-dependent cytotoxicity against NKG2DL-positive cancer cells.
drug_name
KD-025
nct_id_drug_ref
NCT06509490