S-methyl N-cyano-N'-(2-methoxy-5-pyridyl)isothiourea | 216958-97-3

• 分子结构分类: 有机化合物 - 有机氧化合物
• 英文名称: S-methyl N-cyano-N'-(2-methoxy-5-pyridyl)isothiourea
• 英文别名: methyl N-cyano-N'-(6-methoxypyridin-3-yl)carbamimidothioate
• CAS: 216958-97-3
• 化学式: C₉H₁₀N₄OS
• 分子量: 222.271
• InChiKey: RKMYZXUXLVFJAK-UHFFFAOYSA-N

计算性质

• 辛醇/水分配系数(LogP)：
  1.6
• 重原子数：
  15
• 可旋转键数：
  4
• 环数：
  1.0
• sp3杂化的碳原子比例：
  0.22
• 拓扑面积：
  95.6
• 氢给体数：
  1
• 氢受体数：
  5

反应信息

• 作为反应物：
  描述：

  S-methyl N-cyano-N'-(2-methoxy-5-pyridyl)isothiourea 、 癸二胺 在 吡啶 、 4-二甲氨基吡啶 、 三乙胺 作用下， 反应 11.0h， 生成 N-(10-aminodecyl)-N'-cyano-N"-(2-methoxy-5-pyridyl)guanidine
  参考文献：
  名称：

  Cyanoguanidines as cell proliferation inhibitors

  摘要：

  本发明涉及式（I）或其互变异构体的迄今未知的化合物，其中吡啶环的连接位于3-或4-位置，其中R代表一个或多个取代基，可以相同也可以不同，选自以下群组：氢，卤素，三氟甲基，羧基，C1-C4烷基，烷氧基或烷氧羰基，硝基，氨基或氰基，Q代表C5-C14双价的碳氢基团，可以是直链，支链，环状，饱和或不饱和的，X代表羧基，C1-C4烷氧羰基，二（C1-C4烷氧基）膦酰氧基，氨基，C1-C4烷氧羰胺基或四氢吡喃氧基；以及其药学上可接受的、无毒的盐和N-氧化物。这些化合物在人和兽医学实践中具有价值。

  公开号：

  US06346520B1
• 作为产物：
  描述：

  5-氨基-2-甲氧基吡啶 、 N-氰亚胺基-S,S-二硫代碳酸二甲酯 在 sodium hydride 作用下， 以 N,N-二甲基甲酰胺 为溶剂， 反应 78.0h， 以55%的产率得到S-methyl N-cyano-N'-(2-methoxy-5-pyridyl)isothiourea
  参考文献：
  名称：

  Early stimulation of acidification rate by novel cytotoxic pyridyl cyanoguanidines in human tumor cells: comparison with m-Iodobenzylguanidine

  摘要：

  CHS 828, a newly recognized pyridyl cyanoguanidine, has shown promising antitumor activity both in vitro and in vivo and is presently in early phase I clinical trial in collaboration with EORTC. In this study, the effects of CHS 828 and a series of analogues on extracellular acidification and cytotoxicity were compared with those of m-iodobenzylguanidine (MIBG) in human tumor cells. The extracellular acidification rate was measured using the Cytosensor microphysiometer, and determination of cytotoxicity and proliferation was [C-14] performed by the fluorometric microculture cytotoxicity assay (FMCA) and measurement of [C-14]thymidine and leucine uptake. CHS 828 significantly increased the acidification rate during the first 15-24 hr in a concentration-dependent manner. This effect was abolished by removal of glucose from the medium, substituted with 10 mM of pyruvate, indicating stimulated glycolysis as the source of the increased acidification rate. However, CHS 828 induced cytotoxicity at concentrations well below those that affected the rate of acidification; when a series of closely related pyridylguanidine analogues were tested and compared, no apparent relationship between cytotoxicity and acidification could be discerned. Furthermore, comparable increases in the acidification rate were evident in one subline with high-grade resistance to the cytotoxic actions of CHS 828. The results indicate that CHS 828 may share the inhibitory actions of MIBG on mitochondrial respiration with a subsequent increase in glycolysis and acidification rate. However, this mechanism of action appears neither necessary nor sufficient to fully explain the cytotoxic actions of CHS 828 in human tumor cells, actions which remain to be mechanistically clarified. (C) 2000 Elsevier Science Inc.

  DOI：

  10.1016/s0006-2952(00)00382-8