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    Estradiol (β-Estradiol)
    Estradiol (β-Estradiol)

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    This product is for research use only, not for human use. We do not sell to patients.
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    InvivoChem Cat #: V1724
    CAS #: 50-28-2Purity ≥98%

    Description: Estradiol (Oestradiol; Estrace; Dihydrofolliculin; β-Estradiol; 17β-estradiol, β-Estradiol; E2; 17β-Oestradiol), the 17-beta-isomer of estradiol, is an endogenous/naturally occuring estrogen steroid hormone and a primary female sex hormone that is involved in the regulation of the estrous and menstrual female reproductive cycles. 

    References: J Neurosci. 1997 Mar 1;17(5):1848-59; J Neurosci. 1992 Jul;12(7):2549-54.

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    Molecular Weight (MW)272.38
    CAS No.50-28-2
    Storage-20℃ for 3 years in powder form
    -80℃ for 2 years in solvent
    Solubility (In vitro)DMSO: 54 mg/mL (198.3 mM)
    Water: <1 mg/mL
    Ethanol: 5 mg/mL (18.4 mM)
    Other info

    Chemical Name: (8R,9S,13S,14S,17S)-13-methyl-6,7,8,9,11,12,14,15,16,17-decahydrocyclopenta[a]phenanthrene-3,17-diol


    InChi Code: InChI=1S/C18H24O2/c1-18-9-8-14-13-5-3-12(19)10-11(13)2-4-15(14)16(18)6-7-17(18)20/h3,5,10,14-17,19-20H,2,4,6-9H2,1H3/t14-,15-,16+,17+,18+/m1/s1

    SMILES Code: C[[email protected]]12CC[[email protected]]3[[email protected]]([[email protected]@H]1CC[[email protected]@H]2O)CCC4=C3C=CC(=C4)O


    Oestradiol; Estrace; Dihydrofolliculin; β-Estradiol; Beta-Estradiol; 17beta-Estradiol; Estradiol; 17β-Oestradiol

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    In Vitro

    In vitro activity: Estradiol induces new dendritic spines and synapses on hippocampal CA1 pyramidal cells. Estradiol treatment resulted in a 46% increase in NMDA receptor binding. Estradiol treatment increases NMDA receptor binding in parallel with dendritic spine and synapse density. Estradiol treatment results in increased sensitivity of CA1 pyramidal cells to NMDA receptor-mediated synaptic input and that this increase is well correlated with the estradiol-induced increase in dendritic spine density in the apical dendritic tree of these cells. 17 beta-estradiol is found to reduce Ba2+ entry reversibly via Ca2+ channels in acutely dissociated and cultured neostriatal neurons. 17 alpha-Estradiol also reduces Ba2+ currents but is significantly less effective than 17 beta-estradiol in rat neostriatal neurons. 17 beta-estradiol exerts a dose-dependent inhibition of IL-1-, TNF-, and IL-1 and TNF-induced production of bioassayable IL-6. Estradiol inhibits both TNF-induced IL-6 production and osteoclast development in primary bone cell cultures derived from neonatal murine calvaria.

    Cell Assay: With treatment of estradiol, ERβ-specific effects on gene expression have been investigated in three different cell lines lacking expression of endogenous ERα and ERβ, namely U2OS (25), HEK293 (26), and Hs578T (23) cells. 17 genes of the 76   ERβ-regulated genes were commonly regulated by both ERα and ERβ, suggesting that the transcriptional effects of estradiol via ERα or ERβ are largely distinct in U2OS cells. 95 and 61  genes were identified as ERβ-regulated genes in Hs578T cells and HEK293 cells in a 24-h estradiol treatment, respectively. Only three genes (PTGER4, ENPP2, and DKK1) commonly regulated in both HEK293 and Hs578T cells, suggesting that ERβ evokes distinct gene responses in different types of target cells. By using estradiol, new roles of ERβ signaling was established, including protective functions in the epithelial-mesenchymal transition,as well as regulation of cell proliferation in the colon.

    In VivoEstradiol mediates fluctuation in hippocampal synapse density during the estrous cycle in the adult rat. Estradiol alone can reverse the ovariectomy-induced decrease in spine density. Estradiol combined with Progesterone initially increases spine density for a period of 2 to 6 hours but then results in a much sharper decrease than is observed following estradiol alone.
    Animal modelRats
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    J Neurosci. 1997 Mar 1;17(5):1848-59; J Neurosci. 1992 Jul;12(7):2549-54.

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


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