Atpenin A5|CAS 119509-24-9|DC Chemicals

Cas No.:	119509-24-9
Chemical Name:	3-((2S,4S,5R)-5,6-dichloro-2,4-dimethylhexanoyl)-4-hydroxy-5,6-dimethoxypyridin-2(1H)-one
Synonyms:	Atpenin A5
SMILES:	c1(c(c(c(c([nH]1)OC)OC)O)C([C@H](C[C@@H]([C@H](CCl)Cl)C)C)=O)=O
Formula:	C₁₅H₂₁Cl₂NO₅
M.Wt:	366.24
Purity:	>95%
Sotrage:	Dry, dark and at 0 - 4 C for short term (days to weeks) or -20 C for long term (months to years).

Description:	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].
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: Neonatal mice[2] Dosage: 100 μg/kg Administration: Injected daily Result: Demonstrated myocardial thickness at the infarct zone and a significant reduction in scar size compared with controls.
In Vitro:	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].
References:	[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.

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