6Beta-羟基雌酚酮 | 1229-25-0

• 分子结构分类: 有机化合物 - 脂质和类脂质分子 - 类固醇和类固醇衍生物
• 中文名称: 6Beta-羟基雌酚酮
• 英文名称: 6beta-Hydroxyestrone
• 英文别名: (6R,8R,9S,13S,14S)-3,6-dihydroxy-13-methyl-7,8,9,11,12,14,15,16-octahydro-6H-cyclopenta[a]phenanthren-17-one
• CAS: 1229-25-0
• 化学式: C₁₈H₂₂O₃
• 分子量: 286.4
• InChiKey: HTORTGVWUGQTHQ-UHOVARLQSA-N

物化性质

• 熔点：
  265-267 °C
• 沸点：
  492.1±45.0 °C(Predicted)
• 密度：
  1.249±0.06 g/cm3(Predicted)

计算性质

• 辛醇/水分配系数(LogP)：
  1.8
• 重原子数：
  21
• 可旋转键数：
  0
• 环数：
  4.0
• sp3杂化的碳原子比例：
  0.61
• 拓扑面积：
  57.5
• 氢给体数：
  2
• 氢受体数：
  3

ADMET

代谢

6beta-雌酮是雌酮的一个已知的人类代谢物。

6beta-estrone is a known human metabolite of estrone.

来源:NORMAN Suspect List Exchange

反应信息

• 作为产物：
  描述：

  雌酚酮 、 氧气 、 1-Deoxy-1-(7,8-dimethyl-2,4-dioxidobenzo[g]pteridin-10(5H)-yl)-5-O-phosphonopentitol 生成 6Beta-羟基雌酚酮 、 氢(+1)阳离子 、 水 、 FMN
  参考文献：
  名称：

  Characterization of the Oxidative Metabolites of 17β-Estradiol and Estrone Formed by 15 Selectively Expressed Human Cytochrome P450 Isoforms

  摘要：

  22-0.51)。

  DOI：

  10.1210/en.2003-0192

文献信息

• Remedy for hormone-dependent cancer
  申请人：Shiotsu Yukimasa

  公开号：US20060035875A1

  公开（公告）日：2006-02-16

  A therapeutic agent for a hormone-dependent cancer, which comprises (a) a steroid-sulfatase inhibitor and (b) an agent for hormone therapy and/or an agent for chemotherapy, which may be administered together or separately at an interval, is provided. A method for treating a hormone-dependent cancer, which comprises administering (a) a steroid-sulfatase inhibitor and (b) an agent for hormone therapy and/or an agent for chemotherapy together or separately at an interval, is also provided. A steroid-sulfatase inhibitor which is used in combination with an agent for hormone therapy and/or an agent for chemotherapy, and which is administered together therewith or separately therefrom at an interval, is also provided. A kit for treating a hormone-dependent cancer, which comprises a first component comprising (a) a steroid-sulfatase inhibitor and a second component comprising (b) an agent for hormone therapy and/or an agent for chemotherapy, is also provided. A pharmaceutical composition, which comprises (a) a steroid-sulfatase inhibitor and (b) an agent for hormone therapy and/or an agent for chemotherapy, is also provided. Further, use of (a) a steroid-sulfatase inhibitor and (b) an agent for hormone therapy and/or an agent for chemotherapy for the manufacture of a therapeutic agent for a hormone-dependent cancer is provided.
• Characterization of the Oxidative Metabolites of 17β-Estradiol and Estrone Formed by 15 Selectively Expressed Human Cytochrome P450 Isoforms
  作者：Anthony J. Lee、May Xiaoxin Cai、Paul E. Thomas、Allan H. Conney、Bao Ting Zhu

  DOI：10.1210/en.2003-0192

  日期：2003.8.1

  We systematically characterized the oxidative metabolites of 17β-estradiol and estrone formed by 15 human cytochrome P450 (CYP) isoforms. CYP1A1 had high activity for 17β-estradiol 2-hydroxylation, followed by 15α-, 6α-, 4-, and 7α-hydroxylation. However, when estrone was the substrate, CYP1A1 formed more 4-hydroxyestrone than 15α- or 6α-hydroxyestrone, with 2-hydroxyestrone as the major metabolite. CYP1A2 had the highest activity for the 2-hydroxylation of both 17β-estradiol and estrone, although it also had considerable activity for their 4-hydroxylation (9–13% of 2-hydroxylation). CYP1B1 mainly catalyzed the formation of catechol estrogens, with 4-hydroxyestrogens predominant. CYP2A6, 2B6, 2C8, 2C9, 2C19, and 2D6 each showed a varying degree of low catalytic activity for estrogen 2-hydroxylation, whereas CYP2C18 and CYP2E1 did not show any detectable estrogen-hydroxylating activity. CYP3A4 had strong activity for the formation of 2-hydroxyestradiol, followed by 4-hydroxyestradiol and an unknown polar metabolite, and small amounts of 16α- and 16β-hydroxyestrogens were also formed. The ratio of 4- to 2-hydroxylation of 17β-estradiol or estrone with CYP3A4 was 0.22 or 0.51, respectively. CYP3A5 had similar catalytic activity for the formation of 2- and 4- hydroxyestrogens. Notably, CYP3A5 had an unusually high ratio of 4- to 2-hydroxylation of 17β-estradiol or estrone (0.53 or 1.26, respectively). CYP3A4 and 3A5 also catalyzed the formation of nonpolar estrogen metabolite peaks (chromatographically less polar than estrone). CYP3A7 had a distinct catalytic activity for the 16α-hydroxylation of estrone, but not 17β-estradiol. CYP4A11 had little catalytic activity for the metabolism of 17β-estradiol and estrone. In conclusion, many human CYP isoforms are involved in the oxidative metabolism of 17β-estradiol and estrone, with a varying degree of catalytic activity and distinct regioselectivity.

  22-0.51)。