Modulation of autophagy by the novel mitochondrial complex I inhibitor Authipyrin

Nadine Kaiser, Dale Corkery, Yaowen Wu, Luca Laraia, Herbert Waldmann*

*Corresponding author for this work

Research output: Contribution to journalJournal articleResearchpeer-review


Autophagy ensures cellular homeostasis by the degradation of long-lived proteins, damaged organelles and pathogens. This catabolic process provides essential cellular building blocks upon nutrient deprivation. Cellular metabolism, especially mitochondrial respiration, has a significant influence on autophagic flux, and complex I function is required for maximal autophagy. In Parkinson's disease mitochondrial function is frequently impaired and autophagic flux is altered. Thus, dysfunctional organelles and protein aggregates accumulate and cause cellular damage. In order to investigate the interdependency between mitochondrial function and autophagy, novel tool compounds are required. Herein, we report the discovery of a structurally novel autophagy inhibitor (Authipyrin) using a high content screening approach. Target identification and validation led to the discovery that Authipyrin targets mitochondrial complex I directly, leading to the potent inhibition of mitochondrial respiration as well as autophagy.

Original languageEnglish
JournalBioorganic and Medicinal Chemistry
Issue number12
Pages (from-to)2444-2448
Number of pages5
Publication statusPublished - 2019


  • Autophagy
  • Complex I
  • Inhibitor
  • Mitochondrial respiration
  • Thienopyrimidines

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