N-acetyl-D-phenylalanyl-D-leucinamide | 438451-53-7

• 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: N-acetyl-D-phenylalanyl-D-leucinamide
• 英文别名: (2R)-2-[[(2R)-2-acetamido-3-phenylpropanoyl]amino]-4-methylpentanamide
• CAS: 438451-53-7
• 化学式: C₁₇H₂₅N₃O₃
• 分子量: 319.404
• InChiKey: MIBKYCHGORAHFL-HUUCEWRRSA-N

计算性质

• 辛醇/水分配系数(LogP)：
  0.7
• 重原子数：
  23
• 可旋转键数：
  8
• 环数：
  1.0
• sp3杂化的碳原子比例：
  0.47
• 拓扑面积：
  101
• 氢给体数：
  3
• 氢受体数：
  3

反应信息

• 作为反应物：
  描述：

  N-acetyl-D-phenylalanyl-D-leucinamide 、 N-A-(2,4-二硝基-5-氟苯基)-L-丙氨酸 在 盐酸 、 碳酸氢钠 作用下， 以 水 、 丙酮 为溶剂， 反应 1.0h， 生成 L-FDAA-D-leucine 、 (5-(((S)-1-amino-1-oxopropan-2-yl)amino)-2,4-dinitrophenyl)-D-phenylalanine
  参考文献：
  名称：

  Nobilamides A–H, Long-Acting Transient Receptor Potential Vanilloid-1 (TRPV1) Antagonists from Mollusk-Associated Bacteria

  摘要：

  New compounds nobilamides A-H and related known compounds A-3302-A and A-3302-B were isolated based upon their suppression of capsaicin-induced calcium uptake in a mouse dorsal root ganglion primary cell culture assay. Two of these compounds, nobilamide B and A-3302-A, were shown to be long-acting antagonists of mouse and human TRPV1 channels, abolishing activity for >1 h after removal of drug presumably via a covalent attachment. Other derivatives also inhibited the TRPV1 channel, albeit with low potency, affording a structure-activity profile to support the proposed mechanism of action. While the activities were modest, we propose a new mechanism of action and a new site of binding for these inhibitors that may spur development of related analogues for treatment of pain.

  DOI：

  10.1021/jm101621u

文献信息

• Nobilamides A–H, Long-Acting Transient Receptor Potential Vanilloid-1 (TRPV1) Antagonists from Mollusk-Associated Bacteria
  作者：Zhenjian Lin、Christopher A. Reilly、Rowena Antemano、Ronald W. Hughen、Lenny Marett、Gisela P. Concepcion、Margo G. Haygood、Baldomero M. Olivera、Alan Light、Eric W. Schmidt

  DOI：10.1021/jm101621u

  日期：2011.6.9

  New compounds nobilamides A-H and related known compounds A-3302-A and A-3302-B were isolated based upon their suppression of capsaicin-induced calcium uptake in a mouse dorsal root ganglion primary cell culture assay. Two of these compounds, nobilamide B and A-3302-A, were shown to be long-acting antagonists of mouse and human TRPV1 channels, abolishing activity for >1 h after removal of drug presumably via a covalent attachment. Other derivatives also inhibited the TRPV1 channel, albeit with low potency, affording a structure-activity profile to support the proposed mechanism of action. While the activities were modest, we propose a new mechanism of action and a new site of binding for these inhibitors that may spur development of related analogues for treatment of pain.