ArticleScience advances2025
Mechanism and cellular actions of the potent AMPK inhibitor BAY-3827.
Article in Science advances, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 papers, 1 of them a synthesis that pooled it.
What it found
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The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
4 citing papers in PubMed, 1 synthesis or guideline pooled it.
- The role and mechanisms of AMPK in neurovascular unit injury in Parkinson's disease.Frontiers in aging neuroscience · 2026Pooled it
- Activation of AMPK as a therapeutic strategy for FBXL4-related mitochondrial DNA depletion syndrome.EMBO molecular medicine · 2026Article
- AMPK promotes TFEB transcriptional activity through dephosphorylation at both MTORC1-dependent and -independent sites.Autophagy · 2026Article
- Amoeboid cancer cells at a glance.Journal of cell science · 2026Review
Corrections and comments
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Authors and funding
13 authors.
Funding
Abstract
Inhibition of adenosine 5'-monophosphate (AMP)-activated protein kinase (AMPK) is under increasing investigation for its therapeutic potential in many diseases. Existing AMPK inhibitors are however limited, with poor selectivity and substantial off-target effects. Here, we provide mechanistic insights and describe the cellular selectivity of the recently identified AMPK inhibitor BAY-3827. A 2.5-Å cocrystal structure of the AMPK kinase domain with BAY-3827 revealed distinct features including a disulfide bridge between the αD helix Cys
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the Socratic graph.