3-[(1R,4S,5R,8S,9R,10R,12R,13R)-1,5,9-trimethyl-11,14,15,16-tetraoxatetracyclo[10.3.1.04,13.08,13]hexadecan-10-yl]-2-[[(1R,4S,5R,8S,9R,10R,12R,13R)-1,5,9-trimethyl-11,14,15,16-tetraoxatetracyclo[10.3.1.04,13.08,13]hexadecan-10-yl]methyl]propanal | 676620-78-3

• 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: 3-[(1R,4S,5R,8S,9R,10R,12R,13R)-1,5,9-trimethyl-11,14,15,16-tetraoxatetracyclo[10.3.1.04,13.08,13]hexadecan-10-yl]-2-[[(1R,4S,5R,8S,9R,10R,12R,13R)-1,5,9-trimethyl-11,14,15,16-tetraoxatetracyclo[10.3.1.04,13.08,13]hexadecan-10-yl]methyl]propanal
• CAS: 676620-78-3
• 化学式: C₃₄H₅₂O₉
• 分子量: 604.781
• InChiKey: LESMTKHHNIQQKR-MDAXRCBMSA-N

计算性质

• 辛醇/水分配系数(LogP)：
  6.2
• 重原子数：
  43
• 可旋转键数：
  5
• 环数：
  10.0
• sp3杂化的碳原子比例：
  0.97
• 拓扑面积：
  90.9
• 氢给体数：
  0
• 氢受体数：
  9

反应信息

• 作为反应物：
  描述：

  3-[(1R,4S,5R,8S,9R,10R,12R,13R)-1,5,9-trimethyl-11,14,15,16-tetraoxatetracyclo[10.3.1.04,13.08,13]hexadecan-10-yl]-2-[[(1R,4S,5R,8S,9R,10R,12R,13R)-1,5,9-trimethyl-11,14,15,16-tetraoxatetracyclo[10.3.1.04,13.08,13]hexadecan-10-yl]methyl]propanal 、 苯基溴化镁 以 四氢呋喃 、 乙醚 为溶剂， 反应 2.0h， 生成
  参考文献：
  名称：

  WO2007/67333

  摘要：

  公开号：
• 作为产物：
  描述：

  isobu-OH 在 重铬酸吡啶 作用下， 以85%的产率得到3-[(1R,4S,5R,8S,9R,10R,12R,13R)-1,5,9-trimethyl-11,14,15,16-tetraoxatetracyclo[10.3.1.04,13.08,13]hexadecan-10-yl]-2-[[(1R,4S,5R,8S,9R,10R,12R,13R)-1,5,9-trimethyl-11,14,15,16-tetraoxatetracyclo[10.3.1.04,13.08,13]hexadecan-10-yl]methyl]propanal
  参考文献：
  名称：

  WO2007/67333

  摘要：

  公开号：

文献信息

• Biological Mechanisms of Action of Novel C-10 Non-Acetal Trioxane Dimers in Prostate Cancer Cell Lines
  作者：Adebusola A. Alagbala、Andrew J. McRiner、Kristina Borstnik、Tanzina Labonte、Wonsuk Chang、John G. D'Angelo、Gary H. Posner、Barbara A. Foster

  DOI：10.1021/jm060803i

  日期：2006.12.1

  The mechanisms of action of three C-10 non-acetal trioxane dimers (TDs) were examined in human (LNCaP) and mouse (TRAMP-C1A and -C2H) prostate cancer cell lines. 1 (AJM3/23), 2 (GHP-TM-III-07w), and 3 (GHP-KB-06) inhibited cell growth with 3 being the most potent in C1A (GI(50) = 18.0 nM), C2H (GI(50) = 17.0 nM), and LNCaP (GI(50) = 17.9 nM) cells. In comparison to a standard cytotoxic agent such as doxorubicin (GI(50) = 45.3 nM), 3 (GI(50) = 17.9 nM) inhibited LNCaP cell growth more potently. TDs induced G(0)/G(1) cell cycle arrest in LNCaP cells and decreased cells in the S phase. These changes correlated with modulation of G(1) phase cell cycle proteins including decreased cyclin D1, cyclin E, and cdk2 and increased p21(waf1) and p27(Kip1). TDs also promoted apoptosis in LNCaP cells with increased expression of proapoptotic bax. These results demonstrate that TDs are potentially useful agents that warrant further preclinical development for treatment of prostate cancer.
• WO2007/67333
  申请人：——

  公开号：——

  公开（公告）日：——