5-(4-(bicyclo[2.2.1]hept-2-ylmethoxy)-3-chlorobenzylidene)-1,3-thiazolidine-2,4-dione | 1446520-30-4

• 分子结构分类: 有机化合物 - 脂质和类脂质分子 - 异戊烯醇脂质
• 英文名称: 5-(4-(bicyclo[2.2.1]hept-2-ylmethoxy)-3-chlorobenzylidene)-1,3-thiazolidine-2,4-dione
• 英文别名: 5-[[4-(2-bicyclo[2.2.1]heptanylmethoxy)-3-chlorophenyl]methylidene]-1,3-thiazolidine-2,4-dione
• CAS: 1446520-30-4
• 化学式: C₁₈H₁₈ClNO₃S
• 分子量: 363.865
• InChiKey: KEBLMCRLTPTWEZ-UHFFFAOYSA-N

计算性质

• 辛醇/水分配系数(LogP)：
  4.48
• 重原子数：
  24.0
• 可旋转键数：
  4.0
• 环数：
  4.0
• sp3杂化的碳原子比例：
  0.44
• 拓扑面积：
  55.4
• 氢给体数：
  1.0
• 氢受体数：
  4.0

反应信息

• 作为产物：
  描述：

  3-氯-4-羟基苯甲醛 、 2-降莰烷甲醇 在 哌啶 、 溶剂黄146 、 三苯基膦 、 偶氮二甲酸二乙酯 作用下， 以 四氢呋喃 、 甲苯 为溶剂， 生成 5-(4-(bicyclo[2.2.1]hept-2-ylmethoxy)-3-chlorobenzylidene)-1,3-thiazolidine-2,4-dione
  参考文献：
  名称：

  Control of the intracellular levels of prostaglandin E2 through inhibition of the 15-hydroxyprostaglandin dehydrogenase for wound healing

  摘要：

  Excessive scar formation is an aberrant form of wound healing and is an indication of an exaggerated function of fibroblasts and excess accumulation of extracellular matrix during wound healing. Much experimental data suggests that prostaglandin E-2 (PGE(2)) plays a role in the prevention of excessive scarring. However, it has a very short half-live in blood, its oxidization to 15-ketoprostaglandins is catalyzed by 15-hydroxyprostaglandin dehydrogenase (15-PGDH). Previously, we reported that 15-PGDH inhibitors significantly increased PGE(2) levels in A549 cells. In our continuing attempts to develop highly potent 15-PGDH inhibitors, we newly synthesized various thiazolidine-2,4-dione derivatives. Compound 27, 28, 29, and 30 demonstrated IC50 values of 0.048, 0.020, 0.038 and 0.048 mu M, respectively. They also increased levels of PGE(2) in A549 cells. Especially, compound 28 significantly increased level of PGE(2) at 260 pg/mL, which was approximately fivefold higher than that of control. Scratch wounds were analyzed in confluent monolayers of HaCaT cells. Cells exposed to compound 28 showed significantly improved wound healing with respect to control. (C) 2013 The Authors. Published by Elsevier Ltd. All rights reserved.

  DOI：

  10.1016/j.bmc.2013.05.049

文献信息

• Control of the intracellular levels of prostaglandin E2 through inhibition of the 15-hydroxyprostaglandin dehydrogenase for wound healing
  作者：Dubok Choi、Yu Lan Piao、Ying Wu、Hoon Cho

  DOI：10.1016/j.bmc.2013.05.049

  日期：2013.8

  Excessive scar formation is an aberrant form of wound healing and is an indication of an exaggerated function of fibroblasts and excess accumulation of extracellular matrix during wound healing. Much experimental data suggests that prostaglandin E-2 (PGE(2)) plays a role in the prevention of excessive scarring. However, it has a very short half-live in blood, its oxidization to 15-ketoprostaglandins is catalyzed by 15-hydroxyprostaglandin dehydrogenase (15-PGDH). Previously, we reported that 15-PGDH inhibitors significantly increased PGE(2) levels in A549 cells. In our continuing attempts to develop highly potent 15-PGDH inhibitors, we newly synthesized various thiazolidine-2,4-dione derivatives. Compound 27, 28, 29, and 30 demonstrated IC50 values of 0.048, 0.020, 0.038 and 0.048 mu M, respectively. They also increased levels of PGE(2) in A549 cells. Especially, compound 28 significantly increased level of PGE(2) at 260 pg/mL, which was approximately fivefold higher than that of control. Scratch wounds were analyzed in confluent monolayers of HaCaT cells. Cells exposed to compound 28 showed significantly improved wound healing with respect to control. (C) 2013 The Authors. Published by Elsevier Ltd. All rights reserved.