product name Epiandrosterone
Description: Epiandrosterone [also known as 3β-androsterone, Epi (17-ketosteroid epiandrosterone)] is a steroid hormone with weak androgenic activity, and is also a natural metabolite of DHEA. EPI formed in peripheral tissues is a metabolite of testosterone precursor 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 and to down-regulate intracellular NADPH levels.
References: J Mol Cell Cardiol. 2002 Jun;34(6):679-88; Am J Physiol. 1999 Dec;277(6 Pt 1):L1124-32.
290.44
Formula
C19H30O2
CAS No.
481-29-8
Storage
-20℃ for 3 years in powder form
-80℃ for 2 years in solvent
Solubility (In vitro)
DMSO: 29 mg/mL (99.8 mM)
Water: <1 mg/mL
Ethanol: 58 mg/mL (199.7 mM)
Solubility (In vivo)
Synonyms
3β-androsterone, Epi
other peoduct :References PubMed ID：:http://www.ncbi.nlm.nih.gov/pubmed/1939489
| In Vitro |
In vitro activity: Epiandrosterone is a natural metabolite of dehydroepiandrosterone (DHEA) via the 5α-reductaseenzyme. Epiandrosterone is formed in peripheral tissues, from which it is released into the circulation and is ultimately excreted in the urine. Epiandrosterone is only a weak androgen, but it is widely recognized to inhibit the pentose phosphate pathway (PPP) and to decrease intracellular NADPH levels. Epiandrosterone attenuates NO-evoked relaxation of pulmonary artery, although it inhibits angiotensin II- and hypoxia-induced vasoconstriction in isolated lungs and relaxes isolated pulmonary arteries pre-constricted with KCl. Kinase Assay: Cell Assay: 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. |
|---|---|
| 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. |
| Animal model | |
| Formulation & Dosage | |
| References | J Mol Cell Cardiol. 2002 Jun;34(6):679-88; Am J Physiol. 1999 Dec;277(6 Pt 1):L1124-32. |
Related Posts
product name Epiandrosterone
Description: Epiandrosterone [also known as 3β-androsterone, Epi (17-ketosteroid epiandrosterone)] is a steroid hormone with weak androgenic activity, and is also a natural metabolite of DHEA. EPI formed in peripheral tissues is a metabolite of testosterone precursor 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 and to down-regulate intracellular NADPH levels.
References: J Mol Cell Cardiol. 2002 Jun;34(6):679-88; Am J Physiol. 1999 Dec;277(6 Pt 1):L1124-32.
290.44
Formula
C19H30O2
CAS No.
481-29-8
Storage
-20℃ for 3 years in powder form
-80℃ for 2 years in solvent
Solubility (In vitro)
DMSO: 29 mg/mL (99.8 mM)
Water: <1 mg/mL
Ethanol: 58 mg/mL (199.7 mM)
Solubility (In vivo)
Synonyms
3β-androsterone, Epi
other peoduct :References PubMed ID：:http://www.ncbi.nlm.nih.gov/pubmed/1939489
| In Vitro |
In vitro activity: Epiandrosterone is a natural metabolite of dehydroepiandrosterone (DHEA) via the 5α-reductaseenzyme. Epiandrosterone is formed in peripheral tissues, from which it is released into the circulation and is ultimately excreted in the urine. Epiandrosterone is only a weak androgen, but it is widely recognized to inhibit the pentose phosphate pathway (PPP) and to decrease intracellular NADPH levels. Epiandrosterone attenuates NO-evoked relaxation of pulmonary artery, although it inhibits angiotensin II- and hypoxia-induced vasoconstriction in isolated lungs and relaxes isolated pulmonary arteries pre-constricted with KCl. Kinase Assay: Cell Assay: 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. |
|---|---|
| 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. |
| Animal model | |
| Formulation & Dosage | |
| References | J Mol Cell Cardiol. 2002 Jun;34(6):679-88; Am J Physiol. 1999 Dec;277(6 Pt 1):L1124-32. |