SML4196
Piericidin A solution
≥95% (HPLC), Piericidin A 1% Solution in Ethanol
Synonym(s):
2-((2E,5E,7E,9R,10R,11E)-10-Hydroxy-3,7,9,11-tetramethyltrideca-2,5,7,11-tetraenyl)-5,6-dimethoxy-3-methylpyridin-4-ol, 2-[(2E,5E,7E,9R,10R,11E)-10-Hydroxy-3,7,9,11-tetramethyl-2,5,7,11-tridecatetraen-1-yl]-5,6-dimethoxy-3-methyl-4-pyridinol, Piericidine A
description
1%in Ethanol
Quality Level
Assay
≥95% (HPLC)
form
solution
concentration
10 mg/mL
color
colorless to yellow
storage temp.
-10 to -25°C
Biochem/physiol Actions
Potent irreversible inhibitor of mitochondrial complex I (NADH:ubiquinone oxidoreductase).
Piericidin A, an antibiotic isolated from Streptomyces mobaraensis, is a potent irreversible inhibitor of mitochondrial complex I (NADH:ubiquinone oxidoreductase). Piericidin A potently binds to ubiquinone binding sites in both mitochondrial and bacterial forms of the enzyme.
Piericidin A, an antibiotic isolated from Streptomyces mobaraensis, is a potent irreversible inhibitor of mitochondrial complex I (NADH:ubiquinone oxidoreductase). Piericidin A potently binds to ubiquinone binding sites in both mitochondrial and bacterial forms of the enzyme.
Regulatory Information
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Masatoshi Murai et al.
Biochimica et biophysica acta, 1857(7), 884-891 (2015-12-03)
There are a variety of chemicals which regulate the functions of bacterial and mitochondrial complex I. Some of them, such as rotenone and piericidin A, have been indispensable molecular tools in mechanistic studies on complex I. A large amount of
Hoi-Shan Wong et al.
Free radical biology & medicine, 143, 545-559 (2019-09-14)
Mitochondria are important sources of superoxide and hydrogen peroxide in cell signaling and disease. In particular, superoxide/hydrogen peroxide production during reverse electron transport from ubiquinol to NAD+ though Complex I is implicated in several physiological and pathological processes. S1QELs are
Brandt A Nichols et al.
Cancer research, 78(21), 6196-6208 (2018-09-07)
Cancer testis antigens (CTA) are expressed in testis and placenta and anomalously activated in a variety of tumors. The mechanistic contribution of CTAs to neoplastic phenotypes remains largely unknown. Using a chemigenomics approach, we find that the CTA HORMAD1 correlates
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