5-(4-硝基苯氧基)萘-1-胺 | 26196-60-1

• 分子结构分类: 有机化合物 - 有机氧化合物
• 中文名称: 5-(4-硝基苯氧基)萘-1-胺
• 英文名称: 5-(4-nitrophenoxy)naphthalen-1-amine
• 英文别名: 5-Aminonaphthyl-4-nitrophenyl-ether
• CAS: 26196-60-1
• 化学式: C₁₆H₁₂N₂O₃
• 分子量: 280.283
• InChiKey: QIUQPKIEPMEXNR-UHFFFAOYSA-N

物化性质

• 熔点：
  116-117 °C
• 沸点：
  479.7±25.0 °C(Predicted)
• 密度：
  1.345±0.06 g/cm3(Predicted)

计算性质

• 辛醇/水分配系数(LogP)：
  3.8
• 重原子数：
  21
• 可旋转键数：
  2
• 环数：
  3.0
• sp3杂化的碳原子比例：
  0.0
• 拓扑面积：
  81.1
• 氢给体数：
  1
• 氢受体数：
  4

反应信息

• 作为反应物：
  描述：

  5-(4-硝基苯氧基)萘-1-胺 在 tin(II) chloride dihdyrate 作用下， 以 2-甲基四氢呋喃 、 二氯甲烷 为溶剂， 反应 28.0h， 生成 1-(5-(4-aminophenoxy)naphthalen-1-yl)-3-phenylurea
  参考文献：
  名称：

  Discovery of VEGFR-2 inhibitors exerting significant anticancer activity against CD44+ and CD133+ cancer stem cells (CSCs): Reversal of TGF-β induced epithelial-mesenchymal transition (EMT) in hepatocellular carcinoma

  摘要：

  Hepatocellular carcinoma (HCC) is a malignancy characterized by neoangiogenesis, which is an augmented production of proangiogenic factors by the tumor and its adjacent infected cells. These dysregulated angiogenic factors are the therapeutic targets in anti-angiogenic drug development. The signaling pathway of vascular endothelial growth factor (VEGF)/VEGFR-2 is crucial for controlling the angiogenic responses in endothelial cells (ECs). In this study, we carried out a rational drug design approach wherein we have identified the novel orally bioavailable compound VS 8 as a potent VEGFR-2 inhibitor, which remarkably suppresses hVEGF and hVEGFR-2 expression in HUVECs and exhibits significant anti-angiogenic effects in CAM assay. Besides, VS 8 significantly induces apoptosis in HCC cell line (Hep G2). Later we examined its effectiveness against CD44+ and CD133+ CSCs. Here, VS 8 was found to be active against CSCs, and adequate for the cessation of the cell cycle at 'G₀/G₁' and 'S' phase in CD44+ and CD133+ CSCs respectively. Factually, transforming growth factor-β (TGF-β) stimulated epithelial-mesenchymal transition (EMT) induces invasion and migration of HCC cells, which results in the metastasis. Therefore, we studied the effect of VS 8 on EMT markers using flow cytometry, which suggested that VS 8 significantly upregulates E-cadherin (epithelial biomarker) and downregulates vimentin (mesenchymal biomarker). Further, VS 8 downregulates the expression of EMT-inducing transcription factors (EMT-TFs), i.e., SNAIL. Altogether, our findings indicate that VS 8 could be a promising drug candidate for cancer therapy.

  DOI：

  10.1016/j.ejmech.2020.112851
• 作为产物：
  描述：

  1-氨基-5-萘酚 、 对氟硝基苯 在 N-甲基吡咯烷酮 、 potassium carbonate 作用下， 以 甲苯 为溶剂， 反应 12.0h， 以82.01%的产率得到5-(4-硝基苯氧基)萘-1-胺
  参考文献：
  名称：

  Discovery of VEGFR-2 inhibitors exerting significant anticancer activity against CD44+ and CD133+ cancer stem cells (CSCs): Reversal of TGF-β induced epithelial-mesenchymal transition (EMT) in hepatocellular carcinoma

  摘要：

  Hepatocellular carcinoma (HCC) is a malignancy characterized by neoangiogenesis, which is an augmented production of proangiogenic factors by the tumor and its adjacent infected cells. These dysregulated angiogenic factors are the therapeutic targets in anti-angiogenic drug development. The signaling pathway of vascular endothelial growth factor (VEGF)/VEGFR-2 is crucial for controlling the angiogenic responses in endothelial cells (ECs). In this study, we carried out a rational drug design approach wherein we have identified the novel orally bioavailable compound VS 8 as a potent VEGFR-2 inhibitor, which remarkably suppresses hVEGF and hVEGFR-2 expression in HUVECs and exhibits significant anti-angiogenic effects in CAM assay. Besides, VS 8 significantly induces apoptosis in HCC cell line (Hep G2). Later we examined its effectiveness against CD44+ and CD133+ CSCs. Here, VS 8 was found to be active against CSCs, and adequate for the cessation of the cell cycle at 'G₀/G₁' and 'S' phase in CD44+ and CD133+ CSCs respectively. Factually, transforming growth factor-β (TGF-β) stimulated epithelial-mesenchymal transition (EMT) induces invasion and migration of HCC cells, which results in the metastasis. Therefore, we studied the effect of VS 8 on EMT markers using flow cytometry, which suggested that VS 8 significantly upregulates E-cadherin (epithelial biomarker) and downregulates vimentin (mesenchymal biomarker). Further, VS 8 downregulates the expression of EMT-inducing transcription factors (EMT-TFs), i.e., SNAIL. Altogether, our findings indicate that VS 8 could be a promising drug candidate for cancer therapy.

  DOI：

  10.1016/j.ejmech.2020.112851

文献信息

• US4008326A
  申请人：——

  公开号：US4008326A

  公开（公告）日：1977-02-15