Bioactivity | Atpenin A5 is a potent and highly specific complex II inhibitor (IC50 ~10 nM), and is an effective mKATP channel agonist and cardioprotective agent[1]. |
Invitro | Atpenin A5 shows the inhibition profile for submitochondrial particles (SMPs), mitochondria, and cardiomyocytes, with IC50 values of 8.3, 9.3, and 8.5 nM, respectively. Atpenin A5 (AA5) is a potent and specific complex II inhibitor. Atpenin A5 (1 nM) also activates the mKATP channel and protects against simulated ischemia-reperfusion (IR) injury in isolated cardiomyocytes[1]. |
In Vivo | Atpenin A5 is a potent inhibitor of succinate dehydrogenase (SDH). Succinate dehydrogenase inhibition by Atpenin A5 promotes cardiomyocyte mitosis and regeneration in the postnatal heart after myocardial infarction (MI). Atpenin A5-injected mice demonstrated myocardial thickness at the infarct zone and a significant reduction in scar size compared with controls[2]. Animal Model: |
Name | Atpenin A5 |
CAS | 119509-24-9 |
Formula | C15H21Cl2NO5 |
Molar Mass | 366.24 |
Appearance | Solid |
Transport | Room temperature in continental US; may vary elsewhere. |
Storage | -20°C, protect from light, stored under nitrogen *In solvent : -80°C, 6 months; -20°C, 1 month (protect from light, stored under nitrogen) |
Reference | [1]. Andrew P Wojtovich, et al. The complex II inhibitor atpenin A5 protects against cardiac ischemia-reperfusion injury via activation of mitochondrial KATP channels. Basic Res Cardiol. 2009 Mar;104(2):121-9. [2]. Jiyoung Bae, et al. Malonate Promotes Adult Cardiomyocyte Proliferation and Heart Regeneration. Circulation. 2021 May 18;143(20):1973-1986. |