4-[(5R)-2,2-dimethyl-3-[(2-methylpropan-2-yl)oxycarbonyl]-1,3-oxazolidin-5-yl]butanoic acid | 1230070-52-6

• 分子结构分类: 有机化合物 - 有机氧化合物
• 英文名称: 4-[(5R)-2,2-dimethyl-3-[(2-methylpropan-2-yl)oxycarbonyl]-1,3-oxazolidin-5-yl]butanoic acid
• CAS: 1230070-52-6
• 化学式: C₁₄H₂₅NO₅
• 分子量: 287.356
• InChiKey: XJOUFFBYBGFKEP-SNVBAGLBSA-N

计算性质

• 辛醇/水分配系数(LogP)：
  1.7
• 重原子数：
  20
• 可旋转键数：
  6
• 环数：
  1.0
• sp3杂化的碳原子比例：
  0.86
• 拓扑面积：
  76.1
• 氢给体数：
  1
• 氢受体数：
  5

反应信息

• 作为反应物：
  描述：

  4-[(5R)-2,2-dimethyl-3-[(2-methylpropan-2-yl)oxycarbonyl]-1,3-oxazolidin-5-yl]butanoic acid 、 甘氨酸叔丁酯盐酸盐 在 1-羟基苯并三唑 、 盐酸-N-乙基-Nˊ-(3-二甲氨基丙基)碳二亚胺 、 三乙胺 作用下， 以 N,N-二甲基甲酰胺 为溶剂， 以63%的产率得到tert-butyl (R)-5-(4-((2-(tert-butoxy)-2-oxoethyl)amino)-4-oxobutyl)-2,2-dimethyloxazolidine-3-carboxylate
  参考文献：
  名称：

  Negamycin Analogue with Readthrough-Promoting Activity as a Potential Drug Candidate for Duchenne Muscular Dystrophy

  摘要：

  A series of (+)-negamycin 1 analogues were synthesized, and their readthrough-promoting activity was evaluated for nonsense mutations in Duchenne muscular dystrophy 3 (DMD). A structure activity relationship study indicated that 11b was the most potent drug 0 candidate. Immunohistochemical analyses suggested that treatment with 11b restored dystrophin expression in mdx mice, a DMD mouse model. Furthermore, lib decreased serum creatine kinase (CK) levels, an indicator of muscle fiber destruction. Most importantly, 11b demonstrated lower toxicity than 1, and thus, it could be a useful candidate for long-term treatment of DMD.

  DOI：

  10.1021/ml200245t
• 作为产物：
  描述：

  (R)-2-[2',2'-dimethyl-N(3')-tert-butoxycarbonyl-1',3'-oxazolidin-5'-yl]ethanal 在 palladium 10% on activated carbon 、 氢气 作用下， 以 四氢呋喃 、 甲醇 为溶剂， 反应 1.5h， 生成 4-[(5R)-2,2-dimethyl-3-[(2-methylpropan-2-yl)oxycarbonyl]-1,3-oxazolidin-5-yl]butanoic acid
  参考文献：
  名称：

  Negamycin Analogue with Readthrough-Promoting Activity as a Potential Drug Candidate for Duchenne Muscular Dystrophy

  摘要：

  A series of (+)-negamycin 1 analogues were synthesized, and their readthrough-promoting activity was evaluated for nonsense mutations in Duchenne muscular dystrophy 3 (DMD). A structure activity relationship study indicated that 11b was the most potent drug 0 candidate. Immunohistochemical analyses suggested that treatment with 11b restored dystrophin expression in mdx mice, a DMD mouse model. Furthermore, lib decreased serum creatine kinase (CK) levels, an indicator of muscle fiber destruction. Most importantly, 11b demonstrated lower toxicity than 1, and thus, it could be a useful candidate for long-term treatment of DMD.

  DOI：

  10.1021/ml200245t