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December 8, 2025Blood

F1 subunit-specific ATP synthase inhibition disrupts AML mitochondrial metabolism distinctly from other electron transport chain inhibitors

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Authors

MVMatthew T. VillaumeSTStefano TizianiMSMichael R. Savona

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Overview

Preclinical evaluation shows distinct metabolic effects of ATP synthase versus other OXPHOS inhibitors in AML cells, indicating unique therapeutic potential.

Key Points

  • Cell cycle arrest was significantly induced by EB2023 in AML cells, demonstrating its potent effect on proliferation.
  • Mass spectrometry analysis revealed varied metabolic responses to oxygen consumption rate across OXPHOS inhibitors, particularly EB2023.
  • Inhibition of ATP synthase specifically by EB2023 maintained cellular ADP/ATP ratios better than complex I inhibition, suggesting a unique mechanism.
  • Mitochondrial ROS levels and metabolic adaptations differed greatly between inhibitors, highlighting EB2023's therapeutic promise.

Cite This Study

Villaume et al. (2025) studied this question.

synapsesocial.com/papers/69362f6c4fa91c937236df9ehttps://doi.org/10.1182/blood-2025-6103
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Also Consider

Synapse has enriched 5 closely related papers on similar clinical questions. Consider them for comparative context:

  1. 1EB2023 primes mitochondria for BCL2 dependence and induces pyroptotic cell death via AMPK signaling and the unfolded protein response2025
  2. 2Nonclinical evaluation of APL-4098, a novel GCN2 kinase inhibitor, reveals potent anti-leukemic effects through mitochondrial stress induction and synergy with venetoclax, targeting AML blasts and LSCs2025
  3. 3Investigating KAT2A protac therapy for targeting leukemic blast differentiation in acute myeloid leukaemia.2025
  4. 4COMPARATIVE STUDY OF SODIUM OXAMATE AND METFORMIN CYTOTOXICITY AGAINST LEWIS LUNG CARCINOMA CELLS UNDER ANCHORAGE-INDEPENDENT GROWTH2025
  5. 5Identifying novel 'druggable’ targets via Npm1A-turboid fusion and mass spectrometry to overcome genetic or adaptive resistance to menin inhibitors in mtNPM1 AML2025