產(chǎn)品屬性：

Cas No.481-29-8

別名

化學(xué)名 (3S,5S,8R,9S,10S,13S,14S)-3-hydroxy-10,13-dimethyl-1,2,3,4,5,6,7,8,9,11,12,14,15,16-tetradecahydrocyclopenta[a]phenanthren-17-one

分子式 C19H30O2

分子量 290.44

溶解度 ≥ 12.35mg/mL in Ethanol

儲(chǔ)存條件 Store at -20°C
General tips  For obtaining a higher solubility , please warm the tube at 37 ℃ and shake it in the ultrasonic bath for a while.
Shipping Condition     Evaluation sample solution : ship with blue ice
All other available size: ship with RT , or blue ice upon request
產(chǎn)品描述：
IC50: Blocking L-type calcium channels of ventricular myocytes with an IC50 of 42 ± 6 M.

17-ketosteroid epiandrosterone (EPI) which formed in peripheral tissues is a metabolite of testosterone precursor dehydroepiandrosterone (DHEA). After circulation in vivo, EPI is ultimately excreted from urine. Serving as a weak androgen, EPI is proved to block the pentose phosphate pathway (PPP) and to down-regulate intracellular NADPH levels. Most importantly, EPI turns off L-type calcium channels of ventricular myocytes and restricts myocardial contractility. [1]

In vitro: It was reported that EPI, at concentrations from 10 to 100 mM, decreased left-ventricular developed pressure (LVDP) and myocardial contraction rate dose-dependently. In addition, EPI also increased CPP in isolated hearts, down-regulated levels of myocardial NADPH and nitrite, as well as relaxed rat aortic rings in the dose-dependent manner. Findings from whole cell clamp via electrophysiological analysis of single ventricular myocytes demonstrated that EPI could reversibly block L-type channel currents carried by Ba2+ in a dose-dependent manner with an IC50 of2 ± 6 M. Moreover, EPI, at a concentration of 30 mM, accelerated the decay of IBa during depolarization, which suggested this agent as a L-type Ca2+ channel antagonist with similar properties to those of 1, 4-dihydropyridine (DHP) Ca2+ channel blockers. [1]

In vivo: In vivo tests were performed using G-6-PD-low C57L/J mouse erythrocytes. Every other day, mice were orally administered with 450 or 900 mg/kg of tested agents including DHEA, EPI, pregnenolone (PREG) and androstanedione (ANDR) for seven days (four doses). Three hours after the final dose, mice were sacrificed. Findings from blood samples suggested that G-6-PD activity had no significant changes, which might be caused by the lack of receptor sites for the steroids on the erythrocyte membrane. [2]

Clinical trials: A double blind clinical trial was conducted to measure the effect of DHEA on eight psychiatric patients under conditions of constitutional inferiority, less confidence and social inadequacy. It was found that DHEA had no effect on behavior judged objectively nor did it regulated the performance in two productivity tests. [3]

References:

[1]Gupte SA, Tateyama M, Okada T, Oka M and Ochi R.  Epiandrosterone, a metabolite of testosterone precursor, blocks l-type calcium channels of ventricular myocytes and inhibits myocardial contractility. J Mol Cell Cardiol. 2002 Mar; 34: 679- 88.

[2]Calabrese EJ, Horton HM and Leonard DA.  The in vivo effects of four steroids on glucose-6-phosphate dehydrogenase activity of c57L/J mouse erythrocytes. J. Environ. Sci. Health. 1987; A22(6): 563-74.

[3]Forrest AD, Drewery J, Fotherby K and Laverty SG.  A clinical trial of dehydroepiandrosterone (diandrone). J. Neurol. Neurosurg. Psychiat. 1960; 23: 52-5.