eligibility_summary
Include: 18–70, R/R AML (non‑APL) with CLL1 and/or CD38 ≥20%, ECOG 0–1, survival ≥3 mo, Hb ≥80 g/L (no transfusion ≤7 d), adequate hepatic/renal/cardiac/respiratory function (LVEF ≥35%), AEs ≤G1, off steroids day −7 to +30, contraception, consent, follow‑up. Exclude: APL, recent investigational therapy, unknown‑lineage AML, active GVHD/infection/CNS disease, major cardiac disease, stroke/epilepsy ≤6 mo, HIV/HBV/HCV/TPPA+, pulmonary fibrosis, severe allergy, recent/planned major surgery, Cy/Flu contraindication, pregnancy/lactation/planned conception, other cancer (unless exempt), investigator judgment.
trial_source
clinical_trials.gov from Dec 2, 2025
annotation_status
ai
ai_summary
Intervention: CLL1 and CD38 dual‑target CAR‑T cell therapy (autologous, genetically engineered T cells). Mechanism: Engineered CARs recognize CLL1 (CLEC12A) and CD38 on AML cells, triggering antigen‑dependent T‑cell activation and cytotoxic killing (immune synapse formation, perforin/granzyme release, cytokine secretion) independent of the native TCR, dual targeting aims to broaden tumor coverage and reduce antigen escape. Targets: AML blasts and leukemic stem/progenitor cells expressing CLL1, broader AML populations expressing CD38 (a surface NADase/receptor also present on some normal hematopoietic/immune cells). Pathways: CAR signaling cascades within T cells upon CLL1/CD38 engagement, targeting of CLL1/CLEC12A and CD38 surface antigen pathways on myeloid leukemia cells. Population: r/r AML with ≥20% CLL1 and/or CD38 expression. Status: Early Phase 1, single‑arm, terminated (collaborator decision).