eligibility_summary
Adults ≥18, ECOG 0–1, measurable TROP2+ disease with peritoneal/retroperitoneal mets, adequate organs, WOCBP contraception, IP port/sampling. HGS ovarian/peritoneal/FT (≥2 lines or plat‑resistant, BRCA post‑PARPi), mesonephric‑like (≥1 platinum), pancreatic/ampullary (post FOLFIRINOX or gemcitabine). Exclude: pregnancy, recent Rx/radiation/live vaccine, active CNS mets, immunosuppression/autoimmune on Tx, serious infection, major CV/QTc>480, bleeding risk or major vessel invasion, not IP‑eligible.
trial_source
clinical_trials.gov from Dec 2, 2025
annotation_status
ai
ai_summary
Interventions: TROP2-CAR NK (KSR)—gene-modified, allogeneic cord blood–derived NK cells engineered with a TROP2-specific chimeric antigen receptor and transduced to express IL-15—delivered intraperitoneally after lymphodepleting chemotherapy (cyclophosphamide, an alkylating agent, fludarabine, a purine analog). Mechanism: CAR binding to TROP2 (TACSTD2) activates NK cytotoxicity, IL-15 provides autocrine support to enhance NK survival, proliferation, and persistence. Targets: TROP2-positive tumor cells in ovarian cancer, mesonephric-like adenocarcinoma, and pancreatic cancer, pathways include NK activation (perforin/granzyme) and IL-15/JAK-STAT, lymphodepletion reduces host lymphocytes to aid CAR-NK engraftment.