1-(4-氟苯基)-2,2-二甲基环丙烷羧酸 | 915921-31-2

• 分子结构分类: 有机化合物 - 苯类化合物 - 苯和取代衍生物
• 中文名称: 1-(4-氟苯基)-2,2-二甲基环丙烷羧酸
• 英文名称: 1-(4-fluorophenyl)-2,2-dimethylcyclopropanecarboxylic acid
• 英文别名: (4-fluorophenyl)-2,2-dimethylcyclopropanecarboxylic acid；1-(4-fluorophenyl)-2,2-dimethylcyclopropane-1-carboxylic acid
• CAS: 915921-31-2
• 化学式: C₁₂H₁₃FO₂
• mdl: MFCD08691455
• 分子量: 208.232
• InChiKey: RIOYANNPRFBSNF-UHFFFAOYSA-N

计算性质

• 辛醇/水分配系数(LogP)：
  2.7
• 重原子数：
  15
• 可旋转键数：
  2
• 环数：
  2.0
• sp3杂化的碳原子比例：
  0.416
• 拓扑面积：
  37.3
• 氢给体数：
  1
• 氢受体数：
  3

安全信息

• 海关编码：
  2916399090

反应信息

• 作为反应物：
  描述：

  1-(3-氨基丙基)咪唑 、 1-(4-氟苯基)-2,2-二甲基环丙烷羧酸 在 N,N'-羰基二咪唑 作用下， 以 四氢呋喃 为溶剂， 反应 72.0h， 生成 C10d
  参考文献：
  名称：

  Structure-activity and in vivo evaluation of a novel lipoprotein lipase (LPL) activator

  摘要：

  Elevated triglycerides (TG) contribute towards increased risk for cardiovascular disease. Lipoprotein lipase (LPL) is an enzyme that is responsible for the metabolism of core triglycerides of very-low density lipoproteins (VLDL) and chylomicrons in the vasculature. In this study, we explored the structure-activity relationships of our lead compound (C10d) that we have previously identified as an LPL agonist. We found that the cyclopropyl moiety of C10d is not absolutely necessary for LPL activity. Several substitutions were found to result in loss of LPL activity. The compound C10d was also tested in vivo for its lipid lowering activity. Mice were fed a high-fat diet (HFD) for four months, and treated for one week at 10 mg/kg. At this dose, C10d exhibited in vivo biological activity as indicated by lower TG and cholesterol levels as well as reduced body fat content as determined by ECHO-MRI. Furthermore, C10d also reduced the HFD induced fat accumulation in the liver. Our study has provided insights into the structural and functional characteristics of this novel LPL activator. (C) 2016 Elsevier Ltd. All rights reserved.

  DOI：

  10.1016/j.bmcl.2016.11.053

文献信息

• [EN] INDOLE DERIVATIVES AS CRTH2 RECEPTOR ANTAGONISTS<br/>[FR] DÉRIVÉS D'INDOLE COMME ANTAGONISTES DU RÉCEPTEUR CRTH2
  申请人：MERCK FROSST CANADA LTD

  公开号：WO2010031183A1

  公开（公告）日：2010-03-25

  Compound of formula I are antagonists of the PGD2 receptor, CRTH2, and as such are useful in the treatment and/or prevention of CRTH2-mediated diseases such as asthma.

  化合物I的拼合物是PGD2受体CRTH2的拮抗剂，因此在治疗和/或预防CRTH2介导的疾病如哮喘方面是有用的。
• AZAINDOLE DERIVATIVES AS CRTH2 RECEPTOR ANTAGONISTS
  申请人：Leblanc Yves

  公开号：US20110178115A1

  公开（公告）日：2011-07-21

  Compounds of formula I are antagonists of the PGD2 receptor, CRTH2, and as such are useful in the treatment and/or prevention of CRTH2-mediated diseases such as asthma.

  公式I的化合物是PGD2受体CRTH2的拮抗剂，因此在治疗和/或预防CRTH2介导的疾病如哮喘方面非常有用。
• INDOLE DERIVATIVES AS CRTH2 RECEPTOR ANTAGONISTS
  申请人：Colucci John

  公开号：US20110172263A1

  公开（公告）日：2011-07-14

  Compound of formula I are antagonists of the PGD2 receptor, CRTH2, and as such are useful in the treatment and/or prevention of CRTH2-mediated diseases such as asthma.

  I类化合物是PGD2受体CRTH2的拮抗剂，因此在治疗和/或预防CRTH2介导的疾病，如哮喘方面非常有用。
• Indole derivatives as CRTH2 receptor antagonists
  申请人：Colucci John

  公开号：US08637671B2

  公开（公告）日：2014-01-28

  Compound of formula I are antagonists of the PGD2 receptor, CRTH2, and as such are useful in the treatment and/or prevention of CRTH2-mediated diseases such as asthma.

  公式I的化合物是PGD2受体CRTH2的拮抗剂，因此在治疗和/或预防CRTH2介导的疾病，如哮喘方面有用。
• Azaindoles as potent CRTH2 receptor antagonists
  作者：Daniel Simard、Yves Leblanc、Carl Berthelette、M. Helmi Zaghdane、Carmela Molinaro、Zhaoyin Wang、Michel Gallant、Stephen Lau、Trinh Thao、Martine Hamel、Rino Stocco、Nicole Sawyer、Susan Sillaots、Francois Gervais、Robert Houle、Jean-François Lévesque

  DOI：10.1016/j.bmcl.2010.11.084

  日期：2011.1

  A new class of 7-azaindole analogs of MK-7246 as potent and selective CRTH2 antagonists is reported. The SAR leading to the identification of the optimal azaindole regioisomer as well as the pharmacokinetics and off-target activities of the most potent antagonists are disclosed. (C) 2010 Elsevier Ltd. All rights reserved.