product name Diethylstilbestrol
Description: Diethylstilbestrol (also called Stilbestrol) is a synthetic nonsteroidal form of estrogen used to prevent miscarriage and other pregnancy complications. Diethylstilbestrol is a well-known teratogen and carcinogen, that inhibits the hypothalamic-pituitary-gonadal axis, thereby blocking the testicular synthesis of testosterone, lowering plasma testosterone, and inducing a chemical castration. Diethylstilbestrol promotes coactivator release from orphan nuclear receptor ERR beta and inhibits its transcriptional activity in trophoblast stem cells.
References: Genes Dev. 2001 Apr 1;15(7):833-8; Mol Carcinog. 2003 Oct;38(2):78-84.
268.35
Formula
C18H20O2
CAS No.
56-53-1
Storage
-20℃ for 3 years in powder form
-80℃ for 2 years in solvent
Solubility (In vitro)
DMSO: 54 mg/mL (201.2 mM)
Water: <1 mg/mL
Ethanol: 54 mg/mL (201.2 mM)
Solubility (In vivo)
Synonyms
Stilbestrol
other peoduct :References PubMed ID：:http://www.ncbi.nlm.nih.gov/pubmed/19417665
| In Vitro |
In vitro activity: Diethylstilbestrol promotes coactivator release from orphan nuclear receptor ERR beta and inhibits its transcriptional activity in trophoblast stem cells. Kinase Assay: Cell Assay: |
|---|---|
| In Vivo | Diethylstilbestrol treated pregnant mice exhibits abnormal early placenta development associated with an overabundance of trophoblast giant cells and an absence of diploid trophoblast. Diethylstilbestrol causes epigenetic methylation changes that result in persistent alterations in gene expression, leading to tumorigenesis in mouse uterus. Diethylstilbestrol induces c-fos exon-4 hypomethylation at postnatal day 17 in mice uterus, while elevating its mRNA level from postnatal day 5. Diethylstilbestrol exposure leads to hypomethylation in the exon-4 region of c-fos mRNA. Diethylstilbestrol-treated rats exhibits more pronounced delay in maturational development of an adult pattern of immunoexpression of the three proteins compared with GnRHa-treated rats. Diethylstilbestrol results in similar reductions in both Sertoli cell numbers and suppression of testicular growth at 18 and 25 days, though by 35 days the suppression is more pronounced in DES-treated rats. Diethylstilbestrol treatment appears to imprint an abnormal, site-specific demethylation of CpG/-464, which requires ovarian hormones to occur in adult mice. Diethylstilbestrol (2.0 ng/g) per day increases adult prostate weight, whereas a 200 ng/g dose decreases adult prostate weight in male offspring mice. |
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| References | Genes Dev. 2001 Apr 1;15(7):833-8; Mol Carcinog. 2003 Oct;38(2):78-84. |
