eligibility_summary
Adults 18–75 with AML in morphologic remission (<5% BM blasts) pre‑allogeneic HCT and very high relapse risk: MRD by MFC pre‑HCT with RIC/NMA, MRD at day +30, or monosomal karyotype/TP53 disease. Need hematologic recovery (ANC ≥1×10^9/L, platelets ≥50×10^9/L), ECOG 0–2, adequate renal/hepatic function, negative pregnancy test, and negative DSA for mismatched grafts. Exclude active disease, GVHD needing IST, uncontrolled infection, HIV/HBV/HCV, major cardiac disease, or recent non‑exempt cancers.
trial_source
clinical_trials.gov from Dec 2, 2025
annotation_status
ai
ai_summary
Interventions: venetoclax (oral small-molecule BCL-2 inhibitor) plus azacitidine (hypomethylating nucleoside analog, DNMT inhibitor) in 28-day cycles post-allogeneic HCT, with optional donor lymphocyte infusion (DLI, biological CD3+ T-cell therapy) for persistent MRD, venetoclax monotherapy may follow. Mechanisms/targets: Venetoclax blocks the anti-apoptotic BCL-2 pathway to trigger mitochondrial apoptosis in AML blasts. Azacitidine incorporates into DNA/RNA to inhibit DNA methyltransferase, leading to hypomethylation, re-expression of tumor suppressor genes, cytotoxicity, and apoptosis priming that sensitizes AML cells to venetoclax. DLI enhances graft-versus-leukemia via donor T-cell–mediated cytotoxicity. Cells/pathways targeted: AML blasts, BCL-2 survival signaling, DNA methylation/epigenetic regulation, and allogeneic T-cell immune responses against MRD.