4-(3-chloro-4-(dimethylamino)-2,5-dioxo-2,5-dihydro-1H-pyrrol-1-yl)-N-(2-methoxyphenyl)benzamide | 1355590-54-3

• 分子结构分类: 有机化合物 - 苯类化合物 - 苯和取代衍生物
• 英文名称: 4-(3-chloro-4-(dimethylamino)-2,5-dioxo-2,5-dihydro-1H-pyrrol-1-yl)-N-(2-methoxyphenyl)benzamide
• 英文别名: 4-[3-chloro-4-(dimethylamino)-2,5-dioxopyrrol-1-yl]-N-(2-methoxyphenyl)benzamide
• CAS: 1355590-54-3
• 化学式: C₂₀H₁₈ClN₃O₄
• 分子量: 399.834
• InChiKey: BLHZYPDJISQSJT-UHFFFAOYSA-N

计算性质

• 辛醇/水分配系数(LogP)：
  3
• 重原子数：
  28
• 可旋转键数：
  5
• 环数：
  3.0
• sp3杂化的碳原子比例：
  0.15
• 拓扑面积：
  79
• 氢给体数：
  1
• 氢受体数：
  5

反应信息

• 作为产物：
  描述：

  N-(2-methoxyphenyl)-4-nitrobenzamide 在 palladium on activated charcoal 、 氢气 作用下， 以 1,4-二氧六环 、 乙醇 为溶剂， 反应 18.5h， 生成 4-(3-chloro-4-(dimethylamino)-2,5-dioxo-2,5-dihydro-1H-pyrrol-1-yl)-N-(2-methoxyphenyl)benzamide
  参考文献：
  名称：

  Wnt Inhibition Correlates with Human Embryonic Stem Cell Cardiomyogenesis: A Structure–Activity Relationship Study Based on Inhibitors for the Wnt Response

  摘要：

  Human embryonic stem cell-based high-content screening of 550 known signal transduction modulators showed that one "lead" (1, a recently described inhibitor of the proteolytic degradation of Axin) stimulated cardiomyogenesis. Because Axin controls canonical Wnt signaling, we conducted an investigation to determine whether the cardiogenic activity of 1 is Wnt-dependent, and we developed a structure-activity relationship to optimize the cardiogenic properties of 1. We prepared analogues with a range of potencies (low nanomolar to inactive) for Wnt/beta-catenin inhibition and for cardiogenic induction. Both functional activities correlated positively (r(2) = 0.72). The optimal compounds induced cardiogenesis 1.5-fold greater than 1 at 30-fold lower concentrations. In contrast, no correlation was observed for cardiogenesis and modulation of transforming growth factor beta (TGF beta)/Smad signaling that prominently influences cardiogenesis. Taken together, these data show that Wnt signaling inhibition is essential for cardiogenic activity and that the pathway can be targeted for the design of druglike cardiogenic molecules.

  DOI：

  10.1021/jm2010223