3-amino-N-(4-bromophenyl)propanamide hydrochloride salt | 1193388-90-7

• 分子结构分类: 有机化合物 - 有机酸及其衍生物 - 羧酸及其衍生物
• 英文名称: 3-amino-N-(4-bromophenyl)propanamide hydrochloride salt
• 英文别名: 3-amino-N-(4-bromophenyl)propanamide hydrochloride；3-amino-N-(4-bromophenyl)propanamide;hydrochloride
• CAS: 1193388-90-7
• 化学式: C₉H₁₁BrN₂O*ClH
• mdl: MFCD12912923
• 分子量: 279.564
• InChiKey: XNTHPUDCCNQKNU-UHFFFAOYSA-N

计算性质

• 辛醇/水分配系数(LogP)：
  1.29
• 重原子数：
  14
• 可旋转键数：
  3
• 环数：
  1.0
• sp3杂化的碳原子比例：
  0.222
• 拓扑面积：
  55.1
• 氢给体数：
  3
• 氢受体数：
  2

反应信息

• 作为反应物：
  描述：

  3-amino-N-(4-bromophenyl)propanamide hydrochloride salt 在 铁粉 、 氯化铵 、 N,N-二异丙基乙胺 作用下， 以 四氢呋喃 、 乙醇 、 水 为溶剂， 反应 2.0h， 生成 3-((5-amino-6-chloropyrimidin-4-yl)amino)-N-(4-bromophenyl)propanamide
  参考文献：
  名称：

  Discovery and Development of TMPRSS6 Inhibitors Modulating Hepcidin Levels in Human Hepatocytes

  摘要：

  Iron overload disorders are characterized by the body's inability to regulate iron absorption and its storage which can lead to organ failures. Accumulated evidence has revealed that hepcidin, the master regulator of iron homeostasis, is negatively modulated by TMPRSS6 (matriptase-2), a liver-specific type II transmembrane serine protease (TTSP). Here, we report that treatment with a pep-tidomimetic inhibitor affecting TMPRSS6 activity increases hepcidin production in hepatic cells. Moreover, similar effects were observed when using non-peptidic inhibitors obtained through optimization of hits from high-throughput screening. Using HepG2 cells and human primary hepato-cytes, we show that TMPRSS6 inhibitors block TMPRSS6- dependent hemojuvelin cleavage and increase HAMP expression and levels of secreted hepcidin.

  DOI：

  10.1016/j.chembiol.2019.09.004
• 作为产物：
  描述：

  tert-butyl (3-((4-bromophenyl)amino)-3-oxopropyl)carbamate 在 盐酸 作用下， 以 1,4-二氧六环 、 水 为溶剂， 以94%的产率得到3-amino-N-(4-bromophenyl)propanamide hydrochloride salt
  参考文献：
  名称：

  Discovery and Development of TMPRSS6 Inhibitors Modulating Hepcidin Levels in Human Hepatocytes

  摘要：

  Iron overload disorders are characterized by the body's inability to regulate iron absorption and its storage which can lead to organ failures. Accumulated evidence has revealed that hepcidin, the master regulator of iron homeostasis, is negatively modulated by TMPRSS6 (matriptase-2), a liver-specific type II transmembrane serine protease (TTSP). Here, we report that treatment with a pep-tidomimetic inhibitor affecting TMPRSS6 activity increases hepcidin production in hepatic cells. Moreover, similar effects were observed when using non-peptidic inhibitors obtained through optimization of hits from high-throughput screening. Using HepG2 cells and human primary hepato-cytes, we show that TMPRSS6 inhibitors block TMPRSS6- dependent hemojuvelin cleavage and increase HAMP expression and levels of secreted hepcidin.

  DOI：

  10.1016/j.chembiol.2019.09.004

文献信息

• Discovery and Development of TMPRSS6 Inhibitors Modulating Hepcidin Levels in Human Hepatocytes
  作者：François Béliveau、Aarti Tarkar、Sébastien P. Dion、Antoine Désilets、Mariana Gabriela Ghinet、Pierre-Luc Boudreault、Catherine St-Georges、Éric Marsault、Daniel Paone、Jon Collins、Colin H. Macphee、Nino Campobasso、Arthur Groy、Josh Cottom、Michael Ouellette、Andrew J. Pope、Richard Leduc

  DOI：10.1016/j.chembiol.2019.09.004

  日期：2019.11

  Iron overload disorders are characterized by the body's inability to regulate iron absorption and its storage which can lead to organ failures. Accumulated evidence has revealed that hepcidin, the master regulator of iron homeostasis, is negatively modulated by TMPRSS6 (matriptase-2), a liver-specific type II transmembrane serine protease (TTSP). Here, we report that treatment with a pep-tidomimetic inhibitor affecting TMPRSS6 activity increases hepcidin production in hepatic cells. Moreover, similar effects were observed when using non-peptidic inhibitors obtained through optimization of hits from high-throughput screening. Using HepG2 cells and human primary hepato-cytes, we show that TMPRSS6 inhibitors block TMPRSS6- dependent hemojuvelin cleavage and increase HAMP expression and levels of secreted hepcidin.