eligibility_summary
Adults 18–70 with R/R AML or R/R CMML-2, ECOG 0–2, LILRB4+ marrow, adequate hepatic/renal/cardiac (LVEF≥50%)/pulmonary (SpO2>92%), contraception and consent. Exclude recent CAR-T/gene therapy or other trials, major CV/cerebrovascular disease, serious arrhythmias, uncontrolled HTN, active HBV/HCV/syphilis, autoimmune/immunodeficiency, other active cancers, CNS disease/leukemia, recent transplant or GVHD, recent immunosuppression/chemo/targeted, psych/drug abuse, pregnant, investigator unfit.
trial_source
clinical_trials.gov from Dec 2, 2025
annotation_status
ai
ai_summary
Intervention: Autologous LILRB4 STAR‑T cells (gene‑modified cellular immunotherapy) given after lymphodepletion with fludarabine (purine analog antimetabolite) and cyclophosphamide (DNA‑alkylating agent). Mechanism of action: STAR‑T is a synthetic antigen receptor in which antibody variable domains are grafted onto TCR constant chains to assemble with the CD3 complex, enabling antigen recognition to signal through the native TCR/CD3 pathway. The receptor targets LILRB4 (ILT3/CD85k), an inhibitory receptor overexpressed on monocytic leukemias. Cells/pathways targeted: LILRB4‑positive myeloid/monocytic leukemia blasts (AML with monocytic features, CMML), activation of TCR/CD3 signaling in engineered T cells leading to perforin/granzyme‑mediated cytotoxicity, lymphodepletion reduces host lymphocytes to promote STAR‑T expansion and persistence.