1-(2-benzyl-6-phenyl-2H-pyrazolo[3,4-d]pyrimidin-4-yl)-3-phenylurea | 1224256-55-6

• 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: 1-(2-benzyl-6-phenyl-2H-pyrazolo[3,4-d]pyrimidin-4-yl)-3-phenylurea
• 英文别名: 1-(2-benzyl-6-phenylpyrazolo[3,4-d]pyrimidin-4-yl)-3-phenylurea
• CAS: 1224256-55-6
• 化学式: C₂₅H₂₀N₆O
• 分子量: 420.473
• InChiKey: RPQTVLZPPZHYEE-UHFFFAOYSA-N

计算性质

• 辛醇/水分配系数(LogP)：
  4.3
• 重原子数：
  32
• 可旋转键数：
  5
• 环数：
  5.0
• sp3杂化的碳原子比例：
  0.04
• 拓扑面积：
  84.7
• 氢给体数：
  2
• 氢受体数：
  4

反应信息

• 作为产物：
  描述：

  2-benzyl-6-phenyl-2H-pyrazolo[3,4-d]pyrimidin-4-amine 、 异氰酸苯酯 反应 0.05h， 以65%的产率得到1-(2-benzyl-6-phenyl-2H-pyrazolo[3,4-d]pyrimidin-4-yl)-3-phenylurea
  参考文献：
  名称：

  NovelN²-Substituted Pyrazolo[3,4-d]pyrimidine Adenosine A₃Receptor Antagonists: Inhibition of A₃-Mediated Human Glioblastoma Cell Proliferation^†

  摘要：

  Adenosine induces glioma cell proliferation by means of an antiapoptotic effect, which is blocked by cotreatment with selective A(3) AR antagonists. In this study, a novel series of N-2-substituted pyrazolo[3,4-d]pyrimidines 2a-u was developed as highly potent and selective A(3) AR antagonists. The most performing compounds were derivatives 2a (R-1 = CH3 and R-2 = COC6H5; K-i 334, 728, and 0.60 nM at the human A(1), A(2A), and A(3) ARs, respectively) and 2b (R-1 = CH3 and R-2 = COC6H4-4-OCH3; K-i 1037, 3179, and 0.18 nM at the human A(1), A(2A), and A(3) ARs, respectively), which counteracted the effect of the A(3) AR agonists Cl-IB-MECA and IB-MECA on human glioma U87MG cell proliferation. This effect was concentration-dependent, with IC50 values comparable to A(3) AR binding affinity values of 2a and 2b, thereby suggesting that their effects were receptor-mediated. Furthermore, the antiproliferative activity of the new compounds was demonstrated to be mediated by the block of A(3) AR agonist activation of intracellular kinases ERK 1/2.

  DOI：

  10.1021/jm901785w

文献信息

• Novel<i>N</i>²-Substituted Pyrazolo[3,4-<i>d</i>]pyrimidine Adenosine A₃Receptor Antagonists: Inhibition of A₃-Mediated Human Glioblastoma Cell Proliferation^†
  作者：Sabrina Taliani、Concettina La Motta、Laura Mugnaini、Francesca Simorini、Silvia Salerno、Anna Maria Marini、Federico Da Settimo、Sandro Cosconati、Barbara Cosimelli、Giovanni Greco、Vittorio Limongelli、Luciana Marinelli、Ettore Novellino、Osele Ciampi、Simona Daniele、Maria Letizia Trincavelli、Claudia Martini

  DOI：10.1021/jm901785w

  日期：2010.5.27

  Adenosine induces glioma cell proliferation by means of an antiapoptotic effect, which is blocked by cotreatment with selective A(3) AR antagonists. In this study, a novel series of N-2-substituted pyrazolo[3,4-d]pyrimidines 2a-u was developed as highly potent and selective A(3) AR antagonists. The most performing compounds were derivatives 2a (R-1 = CH3 and R-2 = COC6H5; K-i 334, 728, and 0.60 nM at the human A(1), A(2A), and A(3) ARs, respectively) and 2b (R-1 = CH3 and R-2 = COC6H4-4-OCH3; K-i 1037, 3179, and 0.18 nM at the human A(1), A(2A), and A(3) ARs, respectively), which counteracted the effect of the A(3) AR agonists Cl-IB-MECA and IB-MECA on human glioma U87MG cell proliferation. This effect was concentration-dependent, with IC50 values comparable to A(3) AR binding affinity values of 2a and 2b, thereby suggesting that their effects were receptor-mediated. Furthermore, the antiproliferative activity of the new compounds was demonstrated to be mediated by the block of A(3) AR agonist activation of intracellular kinases ERK 1/2.