(3E)-N-(4-(methylsulfonyl)phenyl)-N'-(2-oxo-3-((1-methyl-1H-imidazol-2-yl)methylene)indolin-5-yl)urea

• 分子结构分类: 有机化合物 - 苯类化合物 - 苯和取代衍生物
• 英文名称: (3E)-N-(4-(methylsulfonyl)phenyl)-N'-(2-oxo-3-((1-methyl-1H-imidazol-2-yl)methylene)indolin-5-yl)urea
• 英文别名: (E)-1-(3-((1-Methyl-1H-imidazol-2-yl)methylene)-2-oxoindolin-5-yl)-3-(4-(methylsulfonyl)phenyl)urea；1-[(3E)-3-[(1-methylimidazol-2-yl)methylidene]-2-oxo-1H-indol-5-yl]-3-(4-methylsulfonylphenyl)urea
• 化学式: C₂₁H₁₉N₅O₄S
• 分子量: 437.479
• InChiKey: ATIJRGHGXSCRHK-SFQUDFHCSA-N

计算性质

• 辛醇/水分配系数(LogP)：
  0.8
• 重原子数：
  31
• 可旋转键数：
  4
• 环数：
  4.0
• sp3杂化的碳原子比例：
  0.1
• 拓扑面积：
  131
• 氢给体数：
  3
• 氢受体数：
  5

反应信息

• 作为产物：
  描述：

  5-硝基-1,3-二氢-2H-吲哚-2-酮 在 哌啶 、 oxone||potassium monopersulfate triple salt 、 palladium 10% on activated carbon 、 氢气 作用下， 以 四氢呋喃 、 甲醇 、 乙醇 、 二氯甲烷 、 水 为溶剂， 反应 32.0h， 生成 (3E)-N-(4-(methylsulfonyl)phenyl)-N'-(2-oxo-3-((1-methyl-1H-imidazol-2-yl)methylene)indolin-5-yl)urea
  参考文献：
  名称：

  Design and synthesis of 2-oxindole based multi-targeted inhibitors of PDK1/Akt signaling pathway for the treatment of glioblastoma multiforme

  摘要：

  Aggressive behavior and diffuse infiltrative growth are the main features of Glioblastoma multiforme (GBM), together with the high degree of resistance and recurrence. Evidence indicate that GBM-derived stem cells (GSCs), endowed with unlimited proliferative potential, play a critical role in tumor development and maintenance. Among the many signaling pathways involved in maintaining GSC sternness, tumorigenic potential, and anti-apoptotic properties, the PDK1/Akt pathway is a challenging target to develop new potential agents able to affect GBM resistance to chemotherapy. In an effort to find new PDK1/Akt inhibitors, we rationally designed and synthesized a small family of 2-oxindole derivatives. Among them, compound 3 inhibited PDK1 kinase and downstream effectors such as CHK1, GS3K alpha and GS3K beta, which contribute to GCS survival. Compound 3 appeared to be a good tool for studying the role of the PDK1/Akt pathway in GCS self-renewal and tumorigenicity, and might represent the starting point for the development of more potent and focused multi-target therapies for GBM. (C) 2015 Elsevier Masson SAS. All rights reserved.

  DOI：

  10.1016/j.ejmech.2015.10.020