(2E,4E,7E)-N-undeca-2,4,7-trienylhydroxylamine | 1560911-04-7

• 分子结构分类: 有机化合物 - 有机氮化合物
• 英文名称: (2E,4E,7E)-N-undeca-2,4,7-trienylhydroxylamine
• 英文别名: N-[(2E,4E,7E)-undeca-2,4,7-trienyl]hydroxylamine
• CAS: 1560911-04-7
• 化学式: C₁₁H₁₉NO
• 分子量: 181.278
• InChiKey: ILQSUHFMUPOUOZ-FAMOWBKMSA-N

计算性质

• 辛醇/水分配系数(LogP)：
  2.7
• 重原子数：
  13
• 可旋转键数：
  7
• 环数：
  0.0
• sp3杂化的碳原子比例：
  0.45
• 拓扑面积：
  32.3
• 氢给体数：
  2
• 氢受体数：
  2

反应信息

• 作为反应物：
  描述：

  (2E,4E,7E)-N-undeca-2,4,7-trienylhydroxylamine 在 sodium hydroxide 作用下， 以 1,4-二氧六环 、 二氯甲烷 、 水 为溶剂， 反应 21.0h， 生成 2-[(2E,4E,7E)-undeca-2,4,7-trienyl]-[1,2,4]oxadiazolidine-3,5-dione
  参考文献：
  名称：

  Inhibition of long chain fatty acyl-CoA synthetase (ACSL) and ischemia reperfusion injury

  摘要：

  Various triacsin C analogs, containing different alkenyl chains and carboxylic acid bioisoteres including 4-aminobenzoic acid, isothiazolidine dioxide, hydroxylamine, hydroxytriazene, and oxadiazolidine dione, were synthesized and their inhibitions of long chain fatty acyl-CoA synthetase (ACSL) were examined. Two methods, a cell-based assay of ACSL activity and an in situ [C-14]-palmitate incorporation into extractable lipids were used to study the inhibition. Using an in vivo leukocyte recruitment inhibition protocol, the translocation of one or more cell adhesion molecules from the cytoplasm to the plasma membrane on either the endothelium or leukocyte or both was inhibited by inhibitors 1, 9, and triacsin C. The results suggest that inhibition of ACSL may attenuate the vascular inflammatory component associated with ischemia reperfusion injury and lead to a decrease of infarct expansion. (C) 2014 Elsevier Ltd. All rights reserved.

  DOI：

  10.1016/j.bmcl.2014.01.016
• 作为产物：
  描述：

  (E,E,E)-2,4,7-undecatrienal 在 盐酸 、 盐酸羟胺 、 sodium acetate 、 sodium cyanoborohydride 作用下， 以 甲醇 、 乙醇 、 水 为溶剂， 反应 74.0h， 生成 (2E,4E,7E)-N-undeca-2,4,7-trienylhydroxylamine
  参考文献：
  名称：

  Inhibition of long chain fatty acyl-CoA synthetase (ACSL) and ischemia reperfusion injury

  摘要：

  Various triacsin C analogs, containing different alkenyl chains and carboxylic acid bioisoteres including 4-aminobenzoic acid, isothiazolidine dioxide, hydroxylamine, hydroxytriazene, and oxadiazolidine dione, were synthesized and their inhibitions of long chain fatty acyl-CoA synthetase (ACSL) were examined. Two methods, a cell-based assay of ACSL activity and an in situ [C-14]-palmitate incorporation into extractable lipids were used to study the inhibition. Using an in vivo leukocyte recruitment inhibition protocol, the translocation of one or more cell adhesion molecules from the cytoplasm to the plasma membrane on either the endothelium or leukocyte or both was inhibited by inhibitors 1, 9, and triacsin C. The results suggest that inhibition of ACSL may attenuate the vascular inflammatory component associated with ischemia reperfusion injury and lead to a decrease of infarct expansion. (C) 2014 Elsevier Ltd. All rights reserved.

  DOI：

  10.1016/j.bmcl.2014.01.016

文献信息

• Inhibition of long chain fatty acyl-CoA synthetase (ACSL) and ischemia reperfusion injury
  作者：Allan M. Prior、Man Zhang、Nina Blakeman、Palika Datta、Hung Pham、Qian Chen、Lindon H. Young、Margaret T. Weis、Duy H. Hua

  DOI：10.1016/j.bmcl.2014.01.016

  日期：2014.2

  Various triacsin C analogs, containing different alkenyl chains and carboxylic acid bioisoteres including 4-aminobenzoic acid, isothiazolidine dioxide, hydroxylamine, hydroxytriazene, and oxadiazolidine dione, were synthesized and their inhibitions of long chain fatty acyl-CoA synthetase (ACSL) were examined. Two methods, a cell-based assay of ACSL activity and an in situ [C-14]-palmitate incorporation into extractable lipids were used to study the inhibition. Using an in vivo leukocyte recruitment inhibition protocol, the translocation of one or more cell adhesion molecules from the cytoplasm to the plasma membrane on either the endothelium or leukocyte or both was inhibited by inhibitors 1, 9, and triacsin C. The results suggest that inhibition of ACSL may attenuate the vascular inflammatory component associated with ischemia reperfusion injury and lead to a decrease of infarct expansion. (C) 2014 Elsevier Ltd. All rights reserved.