ethyl 4-((6-(benzyloxy)-9H-purin-2-yl)diazenyl)benzoate | 1421330-72-4

• 分子结构分类: 有机化合物 - 有机杂环化合物 - 咪唑并嘧啶类
• 英文名称: ethyl 4-((6-(benzyloxy)-9H-purin-2-yl)diazenyl)benzoate
• 英文别名: ethyl 4-[(6-phenylmethoxy-7H-purin-2-yl)diazenyl]benzoate
• CAS: 1421330-72-4
• 化学式: C₂₁H₁₈N₆O₃
• 分子量: 402.412
• InChiKey: LXTVLRZPDDFWNE-UHFFFAOYSA-N

计算性质

• 辛醇/水分配系数(LogP)：
  4.2
• 重原子数：
  30
• 可旋转键数：
  8
• 环数：
  4.0
• sp3杂化的碳原子比例：
  0.14
• 拓扑面积：
  115
• 氢给体数：
  1
• 氢受体数：
  8

反应信息

• 作为产物：
  描述：

  6-苄氧基嘌呤 在 哌啶 、 4-二甲氨基吡啶 、 sodium periodate 、 10% Pt/activated carbon 、 氢气 、 四丁基硝酸铵 、 溶剂黄146 、 三氟乙酸酐 作用下， 以 甲醇 、 二氯甲烷 、 水 、 乙酸乙酯 为溶剂， 20.0 ℃ 、101.33 kPa 条件下， 反应 55.5h， 生成 ethyl 4-((6-(benzyloxy)-9H-purin-2-yl)diazenyl)benzoate
  参考文献：
  名称：

  Hypoxia-Selective O⁶-Alkylguanine-DNA Alkyltransferase Inhibitors: Design, Synthesis, and Evaluation of 6-(Benzyloxy)-2-(aryldiazenyl)-9H-purines as Prodrugs of O⁶-Benzylguanine

  摘要：

  O-6-Alkylguanine-DNA alkyltransferase (AGT) is a DNA repair protein which removes alkyl groups from the O-6 position of guanine, thereby providing strong resistance to anticancer agents which alkylate this position. The clinical usefulness of these anticancer agents would be substantially augmented if AGT could be selectively inhibited in tumor tissue, without a corresponding depletion in normal tissue. We report the synthesis of a new AGT inhibitor (5c) which selectively depletes AGT in hypoxic tumor cells.

  DOI：

  10.1021/jm301804p

文献信息

• Hypoxia-Selective <i>O</i>⁶-Alkylguanine-DNA Alkyltransferase Inhibitors: Design, Synthesis, and Evaluation of 6-(Benzyloxy)-2-(aryldiazenyl)-9<i>H</i>-purines as Prodrugs of <i>O</i>⁶-Benzylguanine
  作者：Rui Zhu、Raymond P. Baumann、Philip G. Penketh、Krishnamurthy Shyam、Alan C. Sartorelli

  DOI：10.1021/jm301804p

  日期：2013.2.14

  O-6-Alkylguanine-DNA alkyltransferase (AGT) is a DNA repair protein which removes alkyl groups from the O-6 position of guanine, thereby providing strong resistance to anticancer agents which alkylate this position. The clinical usefulness of these anticancer agents would be substantially augmented if AGT could be selectively inhibited in tumor tissue, without a corresponding depletion in normal tissue. We report the synthesis of a new AGT inhibitor (5c) which selectively depletes AGT in hypoxic tumor cells.