Epiandrosterone [also known as 3β-androsterone, Epi (17-ketosteroid epiandrosterone)] is a naturally occuring/endogenous steroid hormone with weak androgenic activity. It is also a natural/endogenous metabolite of Dehydroepiandrosterone (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.
理化性质和储存条件
| Molecular Weight (MW) | 290.44 |
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| Formula | C19H30O2 |
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| CAS No. | 481-29-8 |
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| Storage | -20℃ for 3 years in powder form |
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| -80℃ for 2 years in solvent |
| Solubility (In vitro) | DMSO: 29 mg/mL (99.8 mM) |
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| Water: <1 mg/mL |
| Ethanol: 58 mg/mL (199.7 mM) |
| SMILES | C[C@]1([C@](CC2)([H])[C@]3([H])CC[C@@]4([H])C[C@@H](O)CC[C@]4(C)[C@@]3([H])CC1)C2=O |
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| Synonyms | 3β-androsterone, Epi; Epiandrosterone Sulfate, Epiandrosterone, 3β-Androsterone; trans-Androsterone; iso-Androsterone; Epiandrosterone 16-bromo, Epiandrosterone 16 bromo |
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实验参考方法
| 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.
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. |
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| 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. |
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| Animal model | Mice |
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| Formulation & Dosage | Orally administered with 450 or 900 mg/k |
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| References | J Mol Cell Cardiol. 2002 Jun;34(6):679-88; Am J Physiol. 1999 Dec;277(6 Pt 1):L1124-32. |
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