2-oxopentadecanoic acid | 92857-44-8

• 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-oxopentadecanoic acid
• 英文别名: α-Oxo-n-pentadecansaeure；2-Oxo-pentadecansaeure；2-Oxo-pentadecanoic acid
• CAS: 92857-44-8
• 化学式: C₁₅H₂₈O₃
• 分子量: 256.386
• InChiKey: AHYSGMPLGXUBBV-UHFFFAOYSA-N

计算性质

• 辛醇/水分配系数(LogP)：
  5.9
• 重原子数：
  18
• 可旋转键数：
  13
• 环数：
  0.0
• sp3杂化的碳原子比例：
  0.87
• 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-oxopentadecanoic acid 在 三氯氧磷 作用下， 生成 3-十三烷基-1H-喹喔啉-2-硫酮
  参考文献：
  名称：

  Asano, Yakugaku Zasshi/Journal of the Pharmaceutical Society of Japan, 1958, vol. 78, p. 729,732

  摘要：

  DOI：
• 作为产物：
  描述：

  肉豆蔻酸 在 oxone 、 N,N-二异丙基乙胺 、 N-[(dimethylamino)-3-oxo-1H-1,2,3-triazolo[4,5-b]pyridin-1-yl-methylene]-N-methylmethanaminium hexafluorophosphate 作用下， 以 四氢呋喃 、 水 、 N,N-二甲基甲酰胺 为溶剂， 反应 4.34h， 生成 2-oxopentadecanoic acid
  参考文献：
  名称：

  通过元素硫的亲核活化实现胺的温和和化学选择性硫酰化

  摘要：

  已经开发了一种使用 α-酮酸和元素硫对胺进行硫代酰化的温和且化学选择性的方法。这种转化成功的关键是硫醇（如 1-十二烷硫醇）对元素硫的亲核活化。在所应用的反应条件下，可以耐受各种官能团，包括未保护的羟基、羧基、酰胺、硫化物和叔胺部分。为了证明与使用 Lawesson 试剂或 P2S5 的传统 OS 交换反应相比，该方法的优势，将硫代酰胺部分特定地引入到生物活性化合物中。

  DOI：

  10.1021/jacs.0c03256

文献信息

• Kaufmann; Stamm, Chemische Berichte, 1958, vol. 91, p. 2121,2125
  作者：Kaufmann、Stamm

  DOI：——

  日期：——
• Adickes; Andresen, Justus Liebigs Annalen der Chemie, 1944, vol. 555, p. 41,49
  作者：Adickes、Andresen

  DOI：——

  日期：——
• SPIROQUINONE COMPOUND AND PHARMACEUTICAL COMPOSITION
  申请人：Hykes Laboratories LLC

  公开号：EP2070919B1

  公开（公告）日：2012-10-10
• 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.