eligibility_summary
Eligible adults 18–70 with confirmed PML‑RARα APL, relapse‑resistant to arsenic (ATO) after prior remission and not reinducible, ECOG 0–2, expected survival >3 months, and consent. Exclude drug allergy, significant exam/ECG/lab/vital abnormalities, severe hepatic/renal disease, infections, uncontrolled diabetes, major cardiac/QT issues, autoimmune disease, pregnancy/lactation, epilepsy/CNS disorder, active HBV/HAV or HIV, other trials, or any condition deemed unsafe.
trial_source
clinical_trials.gov from Dec 2, 2025
annotation_status
ai
ai_summary
Single-arm study in arsenic-resistant relapsed APL (PML-RARα+): run-in with arsenic trioxide (ATO) plus venetoclax, then interferon α-2b + ATO + venetoclax. Interventions and mechanisms: • Interferon α-2b (biologic cytokine immunotherapy) activates JAK-STAT, exerts antiproliferative and pro-differentiation effects, and boosts immune clearance (enhanced NK/T-cell activity, antigen presentation). • Arsenic trioxide (inorganic differentiating/anti-leukemic agent) promotes SUMOylation/ubiquitin-proteasome degradation of the PML-RARα fusion, restores PML nuclear bodies, induces apoptosis and partial differentiation. • Venetoclax (oral small-molecule BH3-mimetic) selectively inhibits BCL-2 to trigger mitochondrial apoptosis. Targets: malignant promyelocytes and leukemic stem/progenitor cells, PML-RARα oncoprotein, BCL-2–dependent mitochondrial survival pathway, interferon-responsive/immune pathways. Primary aim: efficacy (ORR) and safety.