2-oxo-nonadecanoic acid | 73506-87-3

• 分子结构分类: 有机化合物 - 脂质和类脂质分子 - 脂肪酰基
• 英文名称: 2-oxo-nonadecanoic acid
• 英文别名: 2-Oxo-nonadecansaeure；2-oxononadecanoic acid
• CAS: 73506-87-3
• 化学式: C₁₉H₃₆O₃
• 分子量: 312.493
• InChiKey: GLFSTVQYXPOBGJ-UHFFFAOYSA-N

计算性质

• 辛醇/水分配系数(LogP)：
  8.1
• 重原子数：
  22
• 可旋转键数：
  17
• 环数：
  0.0
• sp3杂化的碳原子比例：
  0.89
• 拓扑面积：
  54.4
• 氢给体数：
  1
• 氢受体数：
  3

反应信息

• 作为反应物：
  描述：

  2-oxo-nonadecanoic acid 生成 2-semicarbazono-nonadecanoic acid
  参考文献：
  名称：

  Schreiber, Comptes Rendus Hebdomadaires des Seances de l'Academie des Sciences, 1954, vol. 238, p. 1037

  摘要：

  DOI：
• 作为产物：
  描述：

  1-eicosen-3-one 在 potassium permanganate 、 丙酮 作用下， 生成 2-oxo-nonadecanoic acid
  参考文献：
  名称：

  Kaufmann; Stamm, Chemische Berichte, 1958, vol. 91, p. 2121,2125

  摘要：

  DOI：

文献信息

• Aldehyde-enamines from α-oxocarboxylic acids. A facile and general route to aldehydes via decarboxylation of α-oxocarboxylic acids carrying β-hydrogens
  作者：Ioannis K. Stamos

  DOI：10.1016/s0040-4039(00)86860-4

  日期：——
• Asano, Yakugaku Zasshi/Journal of the Pharmaceutical Society of Japan, 1958, vol. 78, p. 729,732
  作者：Asano

  DOI：——

  日期：——
• Schreiber, Bulletin de la Societe Chimique de France, 1956, p. 1361
  作者：Schreiber

  DOI：——

  日期：——
• Treatment with diazoxide causes prolonged improvement of β-cell function in rat islets transplanted to a diabetic environment
  作者：S. Hiramatsu、A. Höög、C. Möller、V. Grill

  DOI：10.1016/s0026-0495(00)80044-x

  日期：2000.5

  Prolonged hyperglycemia desensitizes beta cells. A role for hyperglycemia-induced excessive stimulation can be tested by diazoxide, which inhibits glucose-induced insulin secretion. Using diazoxide, we have investigated in a rat transplantation model whether excessive stimulation can induce lasting effects on beta cells. One batch with 150 islets and another with 20 islets isolated from Wistar-Furth rats were transplanted under the left-kidney capsule of syngeneic streptozotocin-diabetic recipients. In a first series, recipients were treated for 8 weeks with or without 0.2% diazoxide in the food. Graft-bearing kidneys were then perfused and excised. Diazoxide treatment increased by 5.5;fold the insulin response to 10 mmol/L arginine, by 4.1-fold the graft insulin content, and by 2.3-fold the preproinsulin mRNA versus nontreated diabetic controls. The persistence of these effects was assessed in a second series in which 8 weeks of diazoxide treatment was followed by 1 week of no treatment. Again, perfusion experiments showed a higher insulin response to arginine in diazoxide-treated rats (136.0 +/- 25.7 v 62.3 +/- 11.8 fmol/min, P < .05). Also, the response to 27.8 mmol/L glucose was increased (54.0 +/- 17.1 v 13.6 +/- 7.8 fmol/min, P < .05). The insulin content was increased (2.2 +/- 0.6 v 1.0 +/- 0.4 pmol/islet, P < .05), as well as the preproinsulin mRNA (0.60 +/- 0.08 v 0.22 +/- 0.02 pg/islet, P < .05). In a third series, we tested the impact of diazoxide treatment when given only during the first 2 weeks following transplantation. When tested 6 weeks later, insulin secretion was unaffected, whereas there was a strong tendency for a higher preproinsulin mRNA and insulin content in grafts of diazoxide;treated rats. In conclusion, this study demonstrates that beta-cell function in transplanted islets is improved by diazoxide long after the end of treatment, an effect that is likely due to removal of hyperglycemia induced excessive stimulation. Copyright (C) 2000 by W.B. Saunders Company.
• STAMOS, I. K., TETRAHEDRON LETT., 1982, 23, N 4, 459-462
  作者：STAMOS, I. K.

  DOI：——

  日期：——