3-(2-chloropyridin-4-yl)isochromen-1-one | 1094019-40-5

• 分子结构分类: 有机化合物 - 苯丙烷和聚酮 - 异香豆素及其衍生物
• 英文名称: 3-(2-chloropyridin-4-yl)isochromen-1-one
• CAS: 1094019-40-5
• 化学式: C₁₄H₈ClNO₂
• 分子量: 257.676
• InChiKey: FQHMRJCRYOEWDD-UHFFFAOYSA-N

计算性质

• 辛醇/水分配系数(LogP)：
  3.51
• 重原子数：
  18.0
• 可旋转键数：
  1.0
• 环数：
  3.0
• sp3杂化的碳原子比例：
  0.0
• 拓扑面积：
  43.1
• 氢给体数：
  0.0
• 氢受体数：
  3.0

反应信息

• 作为反应物：
  描述：

  3-(2-chloropyridin-4-yl)isochromen-1-one 在 氨 、 盐酸 作用下， 以 甲醇 、 水 为溶剂， 反应 1.0h， 以93%的产率得到3-(2-chloropyridin-4-yl)isoquinolin-1-ol
  参考文献：
  名称：

  Identification of Orally Available Naphthyridine Protein Kinase D Inhibitors

  摘要：

  A novel 2,6-naphthyridine was identified by high throughput screen (HTS) as a dual protein kinase C/D (PKC/PKD) inhibitor. PKD inhibition in the heart was proposed as a potential antihypertrophic mechanism with application as a heart failure therapy. As PKC was previously identified as the immediate upstream activator of PKD, PKD vs PKC selectivity was essential to understand the effect of PKD inhibition in models of cardiac hypertrophy and heart failure. The present study describes the modification of the HTS hit to a series of prototype pan-PKD inhibitors with routine 1000-fold PKD vs PKC selectivity. Example compounds inhibited PKD activity in vitro, in cells, and in vivo following oral administration. Their effects on heart morphology and function are discussed herein.

  DOI：

  10.1021/jm100075z
• 作为产物：
  描述：

  N-tert-butyl-2-[2-(2-chloropyridin-4-yl)-2-oxoethyl]benzamide 在 溶剂黄146 作用下， 生成 3-(2-chloropyridin-4-yl)isochromen-1-one
  参考文献：
  名称：

  Identification of Orally Available Naphthyridine Protein Kinase D Inhibitors

  摘要：

  A novel 2,6-naphthyridine was identified by high throughput screen (HTS) as a dual protein kinase C/D (PKC/PKD) inhibitor. PKD inhibition in the heart was proposed as a potential antihypertrophic mechanism with application as a heart failure therapy. As PKC was previously identified as the immediate upstream activator of PKD, PKD vs PKC selectivity was essential to understand the effect of PKD inhibition in models of cardiac hypertrophy and heart failure. The present study describes the modification of the HTS hit to a series of prototype pan-PKD inhibitors with routine 1000-fold PKD vs PKC selectivity. Example compounds inhibited PKD activity in vitro, in cells, and in vivo following oral administration. Their effects on heart morphology and function are discussed herein.

  DOI：

  10.1021/jm100075z