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    InvivoChem Cat #: V1767
    CAS #: 481-29-8Purity ≥98%

    Description: 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. 

    References: J Mol Cell Cardiol. 2002 Jun;34(6):679-88; Am J Physiol. 1999 Dec;277(6 Pt 1):L1124-32.

    Related CAS#: 53-43-0 (DHEA, Prasterone; Dehydroisoandrosterone; Dehydroepiandrosterone); 977-35-5 (Epiandrosterone sulfate); 28507-02-0 (16-bromo Epiandrosterone)

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    Molecular Weight (MW)290.44
    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)
    SMILESC[[email protected]]1([[email protected]](CC2)([H])[[email protected]]3([H])CC[[email protected]@]4([H])C[[email protected]@H](O)CC[[email protected]]4(C)[[email protected]@]3([H])CC1)C2=O
    Synonyms3β-androsterone, Epi; Epiandrosterone Sulfate, Epiandrosterone, 3β-Androsterone; trans-Androsterone; iso-Androsterone; Epiandrosterone 16-bromo, Epiandrosterone 16 bromo

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    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.

    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 Mice
    Formulation & Dosage Orally administered with 450 or 900 mg/k
    ReferencesJ Mol Cell Cardiol. 2002 Jun;34(6):679-88; Am J Physiol. 1999 Dec;277(6 Pt 1):L1124-32.

    These protocols are for reference only. InvivoChem does not independently validate these methods.


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