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CAS 57-91-0 Raw Steroid Powders 17 alpha-Estradiol Alpha-estradiol 17A-estradiol

Categories Raw Steroid Powders
Brand Name: Zhenxiang
Model Number: 57-91-0
Certification: HSE, ISO 9001, USP, BP
Place of Origin: CHINA
MOQ: Negotiable
Price: Negotiable
Payment Terms: T/T, Western Union, Money Gram, Bitcoin
Supply Ability: 500kg/month
Delivery Time: Within 8 hours after payment is confirmed
Packaging Details: Specials
Molecular Formula: C18H24O2
Molecular Weight: 272.39
CAS Registry Number: 57-91-0
Assay: 99%min.
EINECS: 200-354-8
Synonyms: Alpha-estradiol; 17A-estradiol
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    CAS 57-91-0 Raw Steroid Powders 17 alpha-Estradiol Alpha-estradiol 17A-estradiol

    CAS 57-91-0 Raw Steroid Powders 17 alpha-Estradiol Alpha-estradiol 17A-estradiol



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    Quick Details

    SynonymsAlpha-estradiol; 17A-estradiol
    Molecular FormulaC18H24O2
    Molecular Weight27239%
    Appearancewhite or off-white crystalline powder
    Cosmeceutical useAnti-aging face creams.
    StorageStored in cool place, keep container tightly closed in a dry and well-ventilated place.
    Shelf life2 years in unopened container.


    17 alpha-Estradiol is a kind of estrogen that can promote and regulate the female sex organs and sexual characteristics of normal development. To promote development of ductal hyperplasia, but in larger doses, can inhibit the release of anterior pituitary prolactin, and reduction of milk secretion.

    The biological effects of 17 alpha-estradiol (17 alpha-E) and its interaction with estrogen receptors were studied in the MCF-7 human breast cancer cell line. Competition for [3H]17 beta-estradiol ([3H]17 beta-E) binding shows that 17 alpha-E binds to receptor with high affinity and has a dissociation constant (Kd) estimated to be 0.7 nM. Upon binding with 17 alpha-E, the cytosol receptor is translocated to the nucleus and is then rapidly depleted or processed in the same manner as the 17 beta-E-receptor complex.

    The nuclear 17 alpha-E-receptor complex was determined to be biologically active by its ability to stimulate an increase in the progesterone receptor content and to reverse antiestrogen inhibition of cellular proliferation and DNA polymerase activity. The estrogenic potency of 17 alpha-E, estimated from the dose-response curves as the median effective dose in stimulating progesterone receptor content and in reversing antiestrogen inhibition, is about one tenth the potency of 17 beta-E. Competition curves show that 17 alpha-E binds to the cytosol estrogen receptor with about one third the affinity of 17 beta-E, so the correlation between relative binding affinity and biological potency is not perfect.

    The correlation, however, is reasonably good compared with that in animal studies, in which 17 alpha-E displays negligible biological activity. Gas chromatography and mass spectrometry rule out the possibility that the observed estrogenic activity of 17 alpha-E was due to contamination of the preparation with the more active 17 beta-E. The enhanced estrogenic potency of 17 alpha-E in MCF-7 cells raises the question of whether the stereospecificity and, thus, the sensitivity of the estrogen receptors in breast cancer cells may be different than those in normal target tissues. Enhanced estrogenic activity may also be due simply to the nature of the tissue culture system, which allows continuous exposure of the cells to hormone; a condition which may not be achieved in some animal studies.
    Post-menopausal estrogen therapy is associated with a decreased incidence of Alzheimer disease and in vitro models have shown that 17beta-estradiol is effective in lowering amyloidogenic processing. To examine the effects of estrogen withdrawal and replacement on amyloid beta (Abeta) levels and amyloid beta-protein precursor (AbetaPP) processing in vivo, Swedish mutant AbetaPP transgenic mice were ovariectomized or sham ovariectomized at four weeks of age and treated with placebo or 17beta- or 17alpha-estradiol pellets, the latter being a weak estrogen receptor agonist. Compared to sham ovariectomized mice, ovariectomy with placebo did not alter Abeta levels; however, the levels of Abeta were decreased by 27% and 38% in mice treated with 17beta- and 17alpha- estradiol, respectively, with no change in AbetaPP holoprotein. Endogenous and exogenous estrogen both significantly increased the levels of sAbetaPPalpha, the secreted form of AbetaPP.

    The ratio of Abeta/sAbetaPPalpha, a measure of amyloidogenic processing, was reduced in all estrogen-containing groups. The Abeta lowering effect of 17beta- and 17alpha-estradiol was replicated when estrogens were administered at a more physiological dose in the drinking water, or when mice were ovariectomized at three months of age. The increased efficacy of 17alpha-estradiol versus 17beta-estradiol may help to develop safe and effective therapeutics.

    A comparative study of the proliferative effect of 17 beta-estradiol and 17 alpha-estradiol on human estrogen-sensitive cell lines was performed. When using charcoal-dextran stripped human female sera-supplemented media the administration of the hormones, 17 alpha-estradiol at 3 X 10(-10)M, and 17 beta-estradiol at 3 X 10(-11)M, resulted in a ten-fold increase in cell yield when compared with non-estrogen supplemented controls after cells were grown for periods between 10 to 14 days.

    No significant metabolization of 17 alpha-estradiol into 17 beta-estradiol occurred as measured by the E2 levels in the supernatants of the cell culture flasks. Increased concentrations of 17 beta-estradiol and 17 alpha-estradiol added to the media bathing C7MCF7-173 cells resulted in a triggering of a partially successful shut-off effect; this phenomenon was not observed with T47D-All cells. These results are compatible with predictions stemming from the indirect and direct negative working hypothesis for the regulation of cell proliferation.

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