3-[2-(3-Methoxy-4-morpholin-4-ylanilino)pyridin-4-yl]benzonitrile | 1417795-23-3

• 分子结构分类: 有机化合物 - 有机杂环化合物 - 恶嗪烷类
• 英文名称: 3-[2-(3-Methoxy-4-morpholin-4-ylanilino)pyridin-4-yl]benzonitrile
• 英文别名: 3-[2-(3-methoxy-4-morpholin-4-ylanilino)pyridin-4-yl]benzonitrile
• CAS: 1417795-23-3
• 化学式: C₂₃H₂₂N₄O₂
• 分子量: 386.453
• InChiKey: WYFRHLVGTKZBGO-UHFFFAOYSA-N

计算性质

• 辛醇/水分配系数(LogP)：
  3.8
• 重原子数：
  29
• 可旋转键数：
  5
• 环数：
  4.0
• sp3杂化的碳原子比例：
  0.22
• 拓扑面积：
  70.4
• 氢给体数：
  1
• 氢受体数：
  6

反应信息

• 作为产物：
  描述：

  3-氰基苯硼酸频哪醇酯 在 盐酸 、 四(三苯基膦)钯 、 sodium carbonate 作用下， 以 1,4-二氧六环 、 水 为溶剂， 反应 24.0h， 生成 3-[2-(3-Methoxy-4-morpholin-4-ylanilino)pyridin-4-yl]benzonitrile
  参考文献：
  名称：

  Discovery of 4-phenyl-2-phenylaminopyridine based TNIK inhibitors

  摘要：

  A series of compounds based on a 4-phenyl-2-phenylaminopyridine scaffold that are potent and selective inhibitors of Traf2- and Nck-interacting kinase (TNIK) activity are described. These compounds were used as tools to test the importance of TNIK kinase activity in signaling and proliferation in Wnt-activated colorectal cancer cells. The results indicate that pharmacological inhibition of TNIK kinase activity has minimal effects on either Wnt/TCF4/beta-catenin-driven transcription or viability. The findings suggest that the kinase activity of TNIK may be less important to Wnt signaling than other aspects of TNIK function, such as its putative role in stabilizing the TCF4/beta-catenin transcriptional complex. (C) 2012 Elsevier Ltd. All rights reserved.

  DOI：

  10.1016/j.bmcl.2012.11.013

文献信息

• Discovery of 4-phenyl-2-phenylaminopyridine based TNIK inhibitors
  作者：Koc-Kan Ho、K. Mark Parnell、Yi Yuan、Yong Xu、Steven G. Kultgen、Steven Hamblin、Thomas F. Hendrickson、Bai Luo、Jason M. Foulks、Michael V. McCullar、Steven B. Kanner

  DOI：10.1016/j.bmcl.2012.11.013

  日期：2013.1

  A series of compounds based on a 4-phenyl-2-phenylaminopyridine scaffold that are potent and selective inhibitors of Traf2- and Nck-interacting kinase (TNIK) activity are described. These compounds were used as tools to test the importance of TNIK kinase activity in signaling and proliferation in Wnt-activated colorectal cancer cells. The results indicate that pharmacological inhibition of TNIK kinase activity has minimal effects on either Wnt/TCF4/beta-catenin-driven transcription or viability. The findings suggest that the kinase activity of TNIK may be less important to Wnt signaling than other aspects of TNIK function, such as its putative role in stabilizing the TCF4/beta-catenin transcriptional complex. (C) 2012 Elsevier Ltd. All rights reserved.