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Home > Products >  CAS 362-07-2 Raw Material Powder 2-Methoxyestradiol

CAS 362-07-2 Raw Material Powder 2-Methoxyestradiol CAS NO.362-07-2

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Keywords

  • 2-Methoxyestradiol
  • 2-Methoxyestradiol powder
  • 362-07-2

Quick Details

  • ProName: CAS 362-07-2 Raw Material Powder 2-Met...
  • CasNo: 362-07-2
  • Molecular Formula: C19H26O3
  • Appearance: White powder
  • Application: 2-Methoxyestradiol (2-ME2) is a natura...
  • DeliveryTime: Abiut 10 days
  • PackAge: Aluminum foil bag,fluorinated bottles,...
  • Port: Shenzhen port
  • Purity: 99%
  • Storage: Store in cool & dry place. Keep away f...
  • Transportation: 1) Door to Door Service by DHL/FEDEX/E...
  • LimitNum: 0
  • Moisture Content: <0.1%
  • Impurity: <0.1%

Superiority

1) Provide costomers with "one-stop"packaging service,from research,development,production,export and so on.
2) We have our own R&D and production base,equipped with advanced production equipment and precision testing the Unitef States Pharmacopoeia(USP),the Britis Pharmacopoeia(EP) and other international advanced standards.All products are through the KOSGER,HALAL certification,the ISO quality management system certification and the HACCP certification.
3) More than 12 years of export experience.
4)Competitive price in China market.

Details

2-Methoxyestradiol is an endogenous estrogen metabolite with low affinity for the estrogen receptor but which disrupts microtubule function. 2-Methoxyestradiol is formed by CYP450-mediated hydroxylation followed by catechol-O-methyltransferase (COMT)methylation of estradiol. 2-Methoxyestradiol is a derivative of an oestrogenic steroidal hormone and has demonstrated:potent inhibition of endothelial cell proliferation and migration and inhibition of bFGF and VEGF-induced corneal neovascularization in mice. In MDA-MB-231 cells, 2-Methoxyestradiol inhibits HIF mediated transcriptional activation of target genes without affecting the transcription of HIF-1α itself. 2-Methoxyestradiol has been shown to induce apoptosis through activation of the p53 pathway through either activation of p38 and NF-κB or JNK and AP-1 both leading to Bcl-2 phsophorylation.In addition the compound has also been observed to upregulate death receptor 5 and bind to tubulins.

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