Itraconazole Inhibits OXPHOS in AML, Targets Therapy-Resistant Leukemic Stem Cells

Acute myeloid leukemia (AML) continues to pose a significant clinical challenge, largely due to treatment resistance and subsequent relapse [1]. While targeted therapies against signaling cascades like the PI3K/AKT/mTOR and RAS/RAF/MAPK pathways are established strategies [2, 3], attention is increasingly turning to the unique metabolic dependencies of cancer cells. Specifically, their reliance on mitochondrial oxidative phosphorylation (OXPHOS) for energy production represents a potential therapeutic vulnerability [4]. The high cost and long timelines of novel drug development have spurred interest in drug repurposing, a strategy that identifies new uses for existing, approved medications with well-documented safety and pharmacokinetic profiles [5, 6]. A recent study investigates this approach, seeking to exploit the metabolic machinery of AML cells with a readily available drug.