ethyl 2-<(1,3-bis(N-(tert-butoxycarbonyl)amino))-2-propyl>thiazole-4-carboxylate | 167105-73-9

• 分子结构分类: 有机化合物 - 有机杂环化合物 - 唑类
• 英文名称: ethyl 2-<(1,3-bis(N-(tert-butoxycarbonyl)amino))-2-propyl>thiazole-4-carboxylate
• CAS: 167105-73-9
• 化学式: C₁₉H₃₁N₃O₆S
• 分子量: 429.538
• InChiKey: HHHSUUPWNBDGDW-UHFFFAOYSA-N

计算性质

• 辛醇/水分配系数(LogP)：
  3.45
• 重原子数：
  29.0
• 可旋转键数：
  7.0
• 环数：
  1.0
• sp3杂化的碳原子比例：
  0.68
• 拓扑面积：
  115.85
• 氢给体数：
  2.0
• 氢受体数：
  8.0

反应信息

• 作为反应物：
  描述：

  ethyl 2-<(1,3-bis(N-(tert-butoxycarbonyl)amino))-2-propyl>thiazole-4-carboxylate 在 劳森试剂 、 氨 作用下， 以 四氢呋喃 、 甲醇 、 乙二醇二甲醚 、 水 为溶剂， 反应 28.0h， 生成 ethyl 2'-<(1,3-bis-(N-(tert-butoxycarbonyl)amino))-2-propyl>-2,4'-bithiazole-4-carboxylate
  参考文献：
  名称：

  Guanosine-Specific DNA Damage by a Co(II).cntdot.Bithiazole Complex

  摘要：

  A bithiazole derivative structurally related to the bithiazole moiety of bleomycin (BLM) A(2) was prepared. This derivative contained a 2-(1,3-diaminopropyl) substituent, rather than the 2-(2-aminoethyl) substituent normally present in BLM, in order to facilitate metal coordination by the bithiazole moiety itself. In the presence of Co2+, th, modified bithiazole mediated the production of alkali labile lesions on double-stranded DNA. Following treatment with alkali, guanosine-specific DNA strand scission was observed. DNA degradation by this Co(II). bithiazole complex was not light dependent but did require molecular oxygen. DNA cleavage studies employing scavengers of activated oxygen species suggested that the observed DNA damage did not result from diffusible, activated forms of oxygen. Moreover, ESR spectroscopy utilizing a spin trapping reagent demonstrated conclusively that the Co(II). bithiazole complex did not produce diffusible oxygen radicals. Absorption spectroscopy with a thiazole analog of the modified bithiazole suggested that, in the presence of oxygen, a O-2 . Co . thiazole complex was formed. These mechanistic studies suggested that the (oxygenated) Co(II). bithiazole complex mediated the oxidative alteration or liberation of the guanine base, producing an alkali labile site. Further, the guanosine specificity appeared to derive from preferential reactivity at guanosine sites, as opposed to a guanosine binding selectivity of the bithiazole. The oxidative degradation of G residues in DNA appears to proceed by an inner sphere mechanism.

  DOI：

  10.1021/ja00141a001
• 作为产物：
  描述：

  1,3-二-(Boc-氨基)-2-羟基丙烷 在 吡啶 、 硫化氢 、 三乙胺 作用下， 以 乙醇 、 二甲基亚砜 、 N,N-二甲基甲酰胺 为溶剂， 反应 124.0h， 生成 ethyl 2-<(1,3-bis(N-(tert-butoxycarbonyl)amino))-2-propyl>thiazole-4-carboxylate
  参考文献：
  名称：

  Guanosine-Specific DNA Damage by a Co(II).cntdot.Bithiazole Complex

  摘要：

  A bithiazole derivative structurally related to the bithiazole moiety of bleomycin (BLM) A(2) was prepared. This derivative contained a 2-(1,3-diaminopropyl) substituent, rather than the 2-(2-aminoethyl) substituent normally present in BLM, in order to facilitate metal coordination by the bithiazole moiety itself. In the presence of Co2+, th, modified bithiazole mediated the production of alkali labile lesions on double-stranded DNA. Following treatment with alkali, guanosine-specific DNA strand scission was observed. DNA degradation by this Co(II). bithiazole complex was not light dependent but did require molecular oxygen. DNA cleavage studies employing scavengers of activated oxygen species suggested that the observed DNA damage did not result from diffusible, activated forms of oxygen. Moreover, ESR spectroscopy utilizing a spin trapping reagent demonstrated conclusively that the Co(II). bithiazole complex did not produce diffusible oxygen radicals. Absorption spectroscopy with a thiazole analog of the modified bithiazole suggested that, in the presence of oxygen, a O-2 . Co . thiazole complex was formed. These mechanistic studies suggested that the (oxygenated) Co(II). bithiazole complex mediated the oxidative alteration or liberation of the guanine base, producing an alkali labile site. Further, the guanosine specificity appeared to derive from preferential reactivity at guanosine sites, as opposed to a guanosine binding selectivity of the bithiazole. The oxidative degradation of G residues in DNA appears to proceed by an inner sphere mechanism.

  DOI：

  10.1021/ja00141a001