Quinestrol
mRNA synthesis
In vitro transcription of capped mRNA with modified nucleotides and Poly(A) tail
Tyramide Signal Amplification (TSA)
TSA (Tyramide Signal Amplification), used for signal amplification of ISH, IHC and IC etc.
Phos Binding Reagent Acrylamide
Separation of phosphorylated and non-phosphorylated proteins without phospho-specific antibody
Cell Counting Kit-8 (CCK-8)
A convenient and sensitive way for cell proliferation assay and cytotoxicity assay
SYBR Safe DNA Gel Stain
Safe and sensitive stain for visualization of DNA or RNA in agarose or acrylamide gels.
Inhibitor Cocktails
Protect the integrity of proteins from multiple proteases and phosphatases for different applications.
Quinestrol is a synthetic estrogen that is effective in hormone replacement therapy after the menopause [1][2].
Estrogen has extraordinarily complex biological effects in diverse tissues such as skeletal, urogenital, digestive, cardiovascular, ocular and nervous systems. Apart from estrogens, selective estrogen receptor modulators may be used for prevention of some of the long-term consequences of estrogen deficiency [2].
Quinestrol is 3-cyclopentyl ether of ethynyl estradiol. After gastrointestinal absorption, Quinestrol is stored in adipose tissue, where it is slowly released and metabolized in the liver to its active form, ethinyl estradiol.
In adult male mice, quinestrol reduced sperm counts and increased the number of abnormal spermatozoa. Quinestrol stimulated oxidative stress to induce apoptosis in spermatogenic cells through the mitochondrial and death receptor pathways [3]. In adult male rat, quinestrol significantly increased the number of germ cells expressing caspase-3, Bax, Fas and FasL, and reduced the number of cells expressing Bcl-2 and PCNA. These results suggested that quinestrol induced abnormal spermatogenesis through the mitochondrial- and Fas-L-mediated pathways [4].
References:
[1]. Baumgardner SB, Condrea H, Daane TA, et al. Replacement estrogen therapy for menopausal vasomotor flushes. Comparison of quinestrol and conjugated estrogens. Obstet Gynecol. 1978 Apr;51(4):445-52.
[2]. Skouby, S.O. Criteria for the selection of an optimal estrogen replacement. Gynecological Endocrinology 15, 60-67 (2001).
[3]. Li J, Chen F, Li C,et al. Quinestrol induces spermatogenic apoptosis in vivo via increasing pro-apoptotic proteins in adult male mice. Tissue Cell. 2014 Oct;46(5):318-25.
[4]. Li J, Chen F, Chen Y, et al. Mitochondrial- and Fas-L-mediated pathways involved in quinestrol induced spermatogenic apoptosis in adult rat testes. Toxicol Mech Methods. 2014 Dec;24(9):609-15.
Storage | Store at -20°C |
M.Wt | 364.5 |
Cas No. | 152-43-2 |
Formula | C25H32O2 |
Synonyms | Estrovis®,Ethynyl Estradiol-3-cyclopentyl ether,W 3566 |
Solubility | insoluble in H2O; ≥12.15 mg/mL in DMSO; ≥16.57 mg/mL in EtOH |
Chemical Name | 3-(cyclopentyloxy)-19-norpregna-1,3,5(10)-trien-20-yn-17α-ol |
SDF | Download SDF |
Canonical SMILES | C[C@@]12[C@@]([H])(CC[C@@]2(O)C#C)[C@]([C@]3([H])CC1)([H])CCC4=C3C=CC(OC5CCCC5)=C4 |
运输条件 | 蓝冰运输或根据您的需求运输。 |
一般建议 | 不同厂家不同批次产品溶解度各有差异,仅做参考。若实验所需浓度过大至产品溶解极限,请添加助溶剂助溶或自行调整浓度。溶液形式一般不宜长期储存,请尽快用完。 |
Quality Control & MSDS
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