52840-12-7

• 常用中文名：Chenodeoxycholic acid-d5
• 常用英文名：Chenodeoxycholic acid-d5
• CAS号：52840-12-7
• 分子式：C₂₄H₃₅D₅O₄
• 分子量：397.60300
• 发布时间：2016-12-13 21:09:46
• 更新时间：2024-01-04 11:50:04
• 鹅去氧胆酸-d5(CDCA-d5)是氘标记的鹅去氧胆酸。鹅去氧胆酸是一种疏水性初级胆汁酸,可激活参与胆固醇代谢的核受体(FXR)。

名称

• 英文名: (4R)-4-[(3R,5R,7R,8R,9S,10S,13R,14S,17R)-2,2,3,4,4-pentadeuterio-3,7-dihydroxy-10,13-dimethyl-1,5,6,7,8,9,11,12,14,15,16,17-dodecahydrocyclopenta[a]phenanthren-17-yl]pentanoic acid
• 英文别名: Chenocol-d5; Chenodiol-d5; Chenodeoxycholic Acid-d5; Fluibil-d5; CDC-d5; Chendol-d5

物化性质

• 分子式: C₂₄H₃₅D₅O₄
• 分子量: 397.60300
• 精确质量: 397.32400
• PSA: 77.76000
• LogP: 4.47790

生物活性

• 描述: 鹅去氧胆酸-d5(CDCA-d5)是氘标记的鹅去氧胆酸。鹅去氧胆酸是一种疏水性初级胆汁酸,可激活参与胆固醇代谢的核受体(FXR)。
• 相关类别:
  研究领域 >> 癌症
  信号通路 >> 代谢酶/蛋白酶 >> FXR
  信号通路 >> 自噬 >> 自噬
  研究领域 >> 代谢疾病
• 体外研究: 氢、碳和其他元素的稳定重同位素已被纳入药物分子中,主要作为药物开发过程中定量的示踪剂。氘化因其可能影响药物的药代动力学和代谢特征而受到关注[1]。
• 参考文献:

  [1]. Russak EM, et al. Impact of Deuterium Substitution on the Pharmacokinetics of Pharmaceuticals. Ann Pharmacother. 2019;53(2):211-216.

  [2]. Stauffer AT, et al. Chenodeoxycholic acid and deoxycholic acid inhibit 11 beta-hydroxysteroid dehydrogenase type 2 and cause cortisol-induced transcriptional activation of the mineralocorticoid receptor. J Biol Chem. 2002 Jul 19;277(29):26286-92

  [3]. Casaburi I, et al. Chenodeoxycholic acid through a TGR5-dependent CREB signaling activation enhances cyclin D1 expression and promotes human endometrial cancer cell proliferation. Cell Cycle. 2012 Jul 15;11(14):2699-710

  [4]. Kawabe Y, et al. The molecular mechanism of the induction of the low density lipoprotein receptor by chenodeoxycholic acid in cultured human cells. Biochem Biophys Res Commun. 1995 Mar 8;208(1):405-11.

  [5]. Ao M, et al. Chenodeoxycholic acid stimulates Cl(-) secretion via cAMP signaling and increases cystic fibrosis transmembrane conductance regulator phosphorylation in T84 cells. Am J Physiol Cell Physiol. 2013 Aug 15;305(4):C447-56

  [6]. Noh K, et al. Farnesoid X receptor activation by chenodeoxycholic acid induces detoxifying enzymes through AMP-activated protein kinase and extracellular signal-regulated kinase 1/2-mediated phosphorylation of CCAAT/enhancer binding protein β. Drug Metab