5-(4-羟基苯基)戊酸乙酯 | 154044-13-0

• 分子结构分类: 有机化合物 - 脂质和类脂质分子 - 脂肪酰基
• 中文名称: 5-(4-羟基苯基)戊酸乙酯
• 中文别名: 4-羟基苯戊酸乙酯
• 英文名称: ethyl 5-(4-(hydroxyl)phenyl)pentanoate
• 英文别名: ethyl 5-(4-hydroxyphenyl)pentanoate
• CAS: 154044-13-0
• 化学式: C₁₃H₁₈O₃
• 分子量: 222.284
• InChiKey: XFWCPDUOSYVHTR-UHFFFAOYSA-N

物化性质

• 沸点：
  345.0±25.0 °C(Predicted)
• 密度：
  1.075

计算性质

• 辛醇/水分配系数(LogP)：
  2.9
• 重原子数：
  16
• 可旋转键数：
  7
• 环数：
  1.0
• sp3杂化的碳原子比例：
  0.46
• 拓扑面积：
  46.5
• 氢给体数：
  1
• 氢受体数：
  3

安全信息

• 海关编码：
  2918290000

反应信息

• 作为反应物：
  描述：

  5-(4-羟基苯基)戊酸乙酯 在 sodium hydroxide 、 potassium carbonate 、 1-羟基苯并三唑 、 盐酸-N-乙基-Nˊ-(3-二甲氨基丙基)碳二亚胺 作用下， 以 四氢呋喃 、 甲醇 、 N,N-二甲基甲酰胺 为溶剂， 反应 3.0h， 生成 5-{4-[(3-fluorobenzyl)oxy]phenyl}-N-(pyridin-4-ylmethyl)pentanamide
  参考文献：
  名称：

  Discovery of N-(3-{4-[(3-Fluorobenzyl)oxy]phenoxy}propyl)-2-pyridin-4-ylacetamide as a Potent and Selective Reverse NCX Inhibitor

  摘要：

  在心力衰竭和心肌缺血再灌注的情况下，钠钙交换机（NCX）会导致钙超载，从而引起收缩功能障碍和心律失常。NCX 是治疗心力衰竭和心肌缺血再灌注的一个有吸引力的靶点。我们以化合物 3 为基础，设计并合成了一系列苄氧基苯基衍生物。我们评估了这些衍生物对 NCX 反向和正向模式的抑制活性。我们发现了一种新型强效选择性反向 NCX 抑制剂 (12)，其对反向 NCX 的 IC50 值为 0.085 μM。

  DOI：

  10.1248/cpb.53.1043
• 作为产物：
  描述：

  5-(4-甲氧基苯基)-5-氧代戊酸 在 硫酸 、 palladium 10% on activated carbon 、 氢溴酸 、 氢气 、 溶剂黄146 作用下， 以 水 为溶剂， 20.0 ℃ 、101.33 kPa 条件下， 反应 36.0h， 生成 5-(4-羟基苯基)戊酸乙酯
  参考文献：
  名称：

  通过dl-脯氨酸催化的Knoevenagel缩合反应/ [4 + 2]环加成级联反应进行外消旋的全环糊精和去甲基全环糊精合成†

  摘要：

  朝dactyloidin（第一外消旋全合成的有效方法2）和demethyldactyloidin（3）进行说明。他们的氧桥联的三环缩酮系统是通过使用卓越的仿生Knoevenagel缩合/ [4 + 2]环加成级联反应作为关键策略而快速构建的，并且通过格利雅（Grignard）加成组装了1,5-二羰基链段。

  DOI：

  10.1039/c5ob01636c

文献信息

• Structural Determinants of 4-Chloro-<i>m</i>-cresol Required for Activation of Ryanodine Receptor Type 1
  作者：Alan R. Jacobson、Scott T. Moe、P. D. Allen、James D. Fessenden

  DOI：10.1124/mol.106.022491

  日期：2006.7

  4-Chloro- m -cresol (4-C m C) is a clinically relevant activator of the intracellular Ca2+ release channel, the ryanodine receptor isoform 1 (RyR1). In this study, the chemical moieties on the 4-C m C molecule required for its activation of RyR1 were determined using structure-activity relationship analysis with a set of commercially available 4-C m C analogs. Separate compounds each lacking one of the three functional groups of 4-C m C (1-hydroxyl, 3-methyl, or 4-chloro) were poor activators of RyR1. Substitution of different chemical groups for the 1-hydroxyl of 4-C m C resulted in compounds that were poor activators of RyR1, suggesting that the hydroxyl group is preferred at this position. Substitution of hydrophobic groups at the 3-position enhanced bioactivity of the compound relative to 4-C m C, whereas substitution with hydrophilic groups abolished bioactivity. Likewise, 4-C m C analogs with hydrophobic groups substituted into the 4-position enhanced bioactivity, whereas hydrophilic or charged groups diminished bioactivity. 4-C m C analogs containing a single hydrophobic group at either the 3- or 4-position as well as 3,5-disubstituted or 3,4,5-trisubstituted phenols were also effective activators of RyR1. These results indicate that the 1-hydroxyl group of 4-C m C is required for activation of RyR1 and that hydrophobic groups at the 3,4- and 5-positions are preferred. These findings suggest that the 4-C m C binding site on RyR1 most likely consists of a hydrophilic region to interact with the 1-hydroxyl as well as a hydrophobic region(s) to interact with chemical groups at the 3- and/or 4-positions of 4-C m C.

  4-Chloro- m -cresol (4-C m C) 是细胞内 Ca2+ 释放通道（兰尼碱受体亚型 1 (RyR1)）的临床相关激活剂。在这项研究中，使用一组市售的 4-C m C 类似物进行结构-活性关系分析，确定了 4-C m C 分子上激活 RyR1 所需的化学部分。各自缺乏 4-C m C 三个官能团（1-羟基、3-甲基或 4-氯）之一的单独化合物是 RyR1 的不良激活剂。用不同的化学基团取代 4-C m C 的 1-羟基产生的化合物是 RyR1 的不良激活剂，表明在该位置优选羟基。相对于4-C m C，3位疏水基团的取代增强了化合物的生物活性，而亲水基团的取代消除了生物活性。同样，4-位疏水基团取代的4-C m C类似物增强了生物活性，而亲水或带电基团降低了生物活性。在3-位或4-位含有单个疏水基团的4-C m C类似物以及3,5-二取代或3,4,5-三取代酚也是RyR1的有效激活剂。这些结果表明，4-C m C 的 1-羟基是 RyR1 活化所必需的，并且优选 3,4-和 5-位的疏水基团。这些发现表明，RyR1 上的 4-C m C 结合位点很可能由与 1-羟基相互作用的亲水区域以及与 3-和/或 4-羟基相互作用的疏水区域组成。 -4-C m C的位置。
• 2,3-Dihydro-6-nitroimidazo[2,1-b]oxazoles
  申请人：Tsubouchi Hidetsugu

  公开号：US20060094767A1

  公开（公告）日：2006-05-04

  The present invention provides a 2,3-dihydro-6-nitroimidazo[2,1-b]oxazole compound represented by the following general formula: wherein R 1 represents a hydrogen atom or C1-C6 alkyl group, n represents an integer of 0 to 6, R 2 represents a group —OR 3 or the like, and R 3 represents a hydrogen atom, C1-C6 alkyl group or the like, or R 1 and —(CH 2 ) n R 2 may bind to each other together with carbon atoms adjacent thereto through nitrogen atoms so as to form a spiro ring represented by the general formula (H): wherein R 41 is hydrogen, C1-C6 alkyl group or the like. The present compound has an excellent bactericidal action against Mycobacterium tuberculosis , multi-drug-resistant Mycobacterium tuberculosis , and atypical acid-fast bacteria.

  本发明提供了一种2,3-二氢-6-硝基咪唑并[2,1-b]噁唑化合物，其通式如下：其中，R1代表氢原子或C1-C6烷基，n代表0到6的整数，R2代表—OR3或类似的基团，R3代表氢原子、C1-C6烷基或类似的基团，或者R1和—(CH2)nR2可以通过相邻的碳原子通过氮原子结合在一起形成一个螺环，其通式为（H）：其中，R41为氢、C1-C6烷基或类似的基团。该化合物对结核分枝杆菌、多药耐药结核分枝杆菌和非典型酸性快速细菌具有优异的杀菌作用。
• 2,3-DIHYDRO-6-NITROIMIDAZO 2,1-b OXAZOLES
  申请人：OTSUKA PHARMACEUTICAL CO., LTD.

  公开号：EP1555267A1

  公开（公告）日：2005-07-20

  The present invention provides a 2,3-dihydro-6-nitroimidazo[2,1-b]oxazole compound represented by the following general formula: wherein R1 represents a hydrogen atom or C1-C6 alkyl group, n represents an integer of 0 to 6, R2 represents a group -OR3 or the like, and R3 represents a hydrogen atom, C1-C6 alkyl group or the like, or R1 and -(CH2)nR2 may bind to each other together with carbon atoms adjacent thereto through nitrogen atoms so as to form a spiro ring represented by the general formula (H): wherein R41 is hydrogen, C1-C6 alkyl group or the like. The present compound has an excellent bactericidal action against Mycobacterium tuberculosis, multi-drug-resistant Mycobacterium tuberculosis, and a typical acid-fast bacteria.

  本发明提供了由以下通式代表的 2，3-二氢-6-硝基咪唑并[2，1-b]恶唑化合物： 其中R1代表氢原子或C1-C6烷基，n代表0至6的整数，R2代表基团-OR3或类似基团，R3代表氢原子、C1-C6烷基或类似基团，或者R1和-(CH2)nR2可以通过氮原子与相邻的碳原子相互结合，从而形成通式(H)代表的螺环： 其中 R41 为氢、C1-C6 烷基或类似基团。本化合物对结核分枝杆菌、多重耐药结核分枝杆菌和典型的耐酸细菌有很好的杀菌作用。
• 2,3-dihydro-6-nitroimidazo[2,1-b]oxazoles compound
  申请人：OTSUKA PHARMACEUTICAL CO., LTD.

  公开号：EP2570418A2

  公开（公告）日：2013-03-20

  The present invention provides a 2,3-dihydro-6-nitroimidazo[2,1-b]oxazole compound represented by the following general formula: wherein R1 represents a hydrogen atom or C1-C6 alkyl group, n represents an integer of 0 to 6, R2 represents a group -OR3 or the like, and R3 represents a hydrogen atom, C1-C6 alkyl group or the like, or R1 and -(CH2)nR2 may bind to each other together with carbon atoms adjacent thereto through nitrogen atoms so as to form a spiro ring represented by the general formula (H): wherein R41 is hydrogen, C1-C6 alkyl group or the like. The present compound has an excellent bactericidal action against Mycobacterium tuberculosis, multi-drug-resistant Mycobacterium tuberculosis, and atypical acid-fast bacteria.

  本发明提供了一种由以下通式表示的 2,3-二氢-6-硝基咪唑并[2,1-b]恶唑化合物： 其中R1代表氢原子或C1-C6烷基，n代表0至6的整数，R2代表基团-OR3或类似基团，R3代表氢原子、C1-C6烷基或类似基团，或者R1和-(CH2)nR2可以通过氮原子与相邻的碳原子相互结合，从而形成通式(H)代表的螺环： 其中 R41 为氢、C1-C6 烷基或类似基团。本化合物对结核分枝杆菌、多重耐药结核分枝杆菌和非典型耐酸菌有很好的杀菌作用。
• Design and Structural Optimization of Dual FXR/PPARδ Activators
  作者：Simone Schierle、Sebastian Neumann、Pascal Heitel、Sabine Willems、Astrid Kaiser、Julius Pollinger、Daniel Merk

  DOI：10.1021/acs.jmedchem.0c00618

  日期：2020.8.13

  Nonalcoholic steatohepatitis (NASH) is considered as severe hepatic manifestation of the metabolic syndrome and has alarming global prevalence. The ligand-activated transcription factors farnesoid X receptor (FXR) and peroxisome proliferator-activated receptor (PPAR) delta have been validated as molecular targets to counter NASH. To achieve robust therapeutic efficacy in this multifactorial pathology, combined peripheral PPAR delta-mediated activity and hepatic effects of FXR activation appear as a promising multitarget approach. We have designed a minimal dual FXR/PPAR delta activator scaffold by rational fusion of pharmacophores derived from selective agonists. Our dual agonist lead compound exhibited weak agonism on FXR and PPAR delta and was structurally refined to a potent and balanced FXR/PPAR delta activator in a computer-aided fashion. The resulting dual FXR/PPAR delta modulator comprises high selectivity over related nuclear receptors and activates the two target transcription factors in native cellular settings.