20-Hydroxyecdysone

2 years -80 in solvent

Orally administrated

10 mg/kg/day

In H4IIE cell culture, 20-Hydroxyecdysone treatment decreases expression of phosphoenolpyruvate carboxykinase (PEPCK) and glucose-6-phosphatase (G6Pase), reduces glucose production, and induces Akt2 phosphorylation sensitive to the phosphoinositide-3 kinase pathway-specific inhibitor LY-294002. [1] 20-Hydroxyecdysone treatment before or after CoCl2 exposure significantly ameliorates CoCl2-induced cellular injuries. 20-Hydroxyecdysone dramatically reduces the CoCl2-induced production of reactive oxygen species (ROS), decreases the depolarization of the mitochondrial membrane, inhibits the release of cytochrome c into the cytosol, increases the Bax/Bcl-2 ratio, and eliminates the CoCl2-induced activation of caspase-3. [2] 20-Hydroxyecdysone inhibits NF-kappaB activation in HeLa cells stably transfected with an IL-6-bound reporter gene with IC50 of 31.8 uM. [3] In vitro treatment of larval fat body tissues with 20-Hydroxyecdysone upregulates the apoptotic genes including Apaf-1, Nedd2 like1, Nedd2 like2, ICE1, ICE3, ICE5, Arp, and IAP. [4] 20-Hydroxyecdysone reverses TGF-beta1-induced increase in intracellular and extracellular fibronectin, and reverses TGF-beta1-induced down-regulation of Smad7. Additionally, 20-Hydroxyecdysone significantly attenuates TGF-beta1-induced upregulation of Smad2/3 and pSmad2/3, and downregulation of E-Cadherin. Moreover, 20-Hydroxyecdysone dramatically suppresses TGF-beta1-induced increases in the expression of Snail. [5]

DMSO 96 mg/mL, Water <1 mg/mL, Ethanol 96 mg/mL

(2S, 3R, 5R, 9R, 10R, 13R, 14S, 17S)-2, 3, 14-trihydroxy-10, 13-dimethyl-17-((2R, 3R)-2, 3, 6-trihydroxy-6-methylheptan-2-yl)-1, 2, 3, 4, 5, 10, 11, 12, 13, 15, 16, 17-dodecahydro-9H-cyclopenta[a]phenanthren-6(14H)-one