eligibility_summary
Include: Adults 18–70 with advanced, NKG2DL‑positive solid tumors after failure/intolerance/no standard therapy, ECOG 0–1, ≥3‑mo survival, measurable disease, fit for apheresis with adequate PBMC, adequate marrow/organ/coagulation/pulmonary/cardiac function. Exclude: prior gene/T‑cell therapy, uncontrolled or viral infection (HIV/HBV/HCV), autoimmune disease/transplant/immunosuppression, cardiopulmonary/CNS disease, recent therapy (<4 wks), pregnancy/lactation, investigator judgment.
trial_source
clinical_trials.gov from Dec 2, 2025
annotation_status
ai
ai_summary
Intervention: KD-025, an autologous NKG2D-based CAR-T cell therapy (gene-engineered T-cell product) administered after lymphodepleting chemotherapy in a phase 1, single-arm trial for advanced NKG2DL-positive solid tumors. Mechanism: Patient T cells are modified to express a CAR using the NKG2D receptor ectodomain fused to intracellular activation/costimulatory domains (e.g., CD3ζ), enabling binding to stress-induced NKG2D ligands (MICA, MICB, ULBP1–6) broadly expressed on tumors. Engagement activates T cells, leading to cytotoxicity (perforin/granzyme) and cytokine release. Targets/pathways: tumor cells expressing NKG2DL, NKG2D–NKG2DL stress-ligand axis and downstream T-cell activation signaling. Tumors include ovarian, cholangiocarcinoma, colorectal, etc.