rac-Balanol

• 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: rac-Balanol
• 英文别名: 2-[2,6-dihydroxy-4-[3-[(4-hydroxybenzoyl)amino]azepan-4-yl]oxycarbonylbenzoyl]-3-hydroxybenzoic acid
• 化学式: C₂₈H₂₆N₂O₁₀
• 分子量: 550.5
• InChiKey: XYUFCXJZFZPEJD-UHFFFAOYSA-N

计算性质

• 辛醇/水分配系数(LogP)：
  0.7
• 重原子数：
  40
• 可旋转键数：
  8
• 环数：
  4.0
• sp3杂化的碳原子比例：
  0.21
• 拓扑面积：
  203
• 氢给体数：
  7
• 氢受体数：
  11

文献信息

• Neuronal Pain Pathway Modulators
  申请人：Ambron Richard

  公开号：US20080176920A1

  公开（公告）日：2008-07-24

  The present invention relates to compounds that may be used to inhibit activation of protein kinase G (“PKG”). It is based, at least in part, on the discovery of the tertiary structure of PKG and the identification of molecules that either bind to the active site of PKG and/or are analogs of balanol.

  本发明涉及可用于抑制蛋白激酶G（PKG）激活的化合物。至少部分基于对PKG的三级结构的发现以及发现绑定于PKG活性位点和/或是巴洛酮类似物的分子的识别。
• NEURONAL PAIN PATHWAY MODULATORS
  申请人：The Trustees of Columbia University in the City of New York

  公开号：US20150126576A1

  公开（公告）日：2015-05-07

  The present invention relates to compounds that may be used to inhibit activation of protein kinase G (“PKG”). It is based, at least in part, on the discovery of the tertiary structure of PKG and the identification of molecules that either bind to the active site of PKG and/or are analogs of balanol.

  本发明涉及可用于抑制蛋白激酶G（“PKG”）激活的化合物。它至少部分地基于发现PK G的三级结构以及识别既能够与PKG的活性位点结合，又是巴洛诺（balanol）的类似物的分子。
• Neuronal pain pathway
  申请人：THE TRUSTEES OF COLUMBIA UNIVERSITY IN THE CITY OF NEW YORK

  公开号：US10485845B2

  公开（公告）日：2019-11-26

  The present invention relates to the discovery of a novel molecular pathway involved in long-term hyperexcitability of sensory neurons, which, in higher animals, is associated with persistent pain. It is based on the discovery that, following injury to an axon of a neuron, an increase in nitric oxide synthase activity results in increased nitric oxide production, which, in turn, activates guanylyl cyclase, thereby increasing levels of cGMP. Increased cGMP results in activation of protein kinase G (“PKG”), which then is retrogradely transported along the axon to the neuron cell body, where it phosphorylates MAPKerk.

  本发明涉及一种新型分子通路的发现，这种通路参与了感觉神经元的长期过度兴奋，在高等动物中，这种兴奋与持续性疼痛有关。它基于以下发现：神经元轴突受伤后，一氧化氮合酶活性的增加会导致一氧化氮产量的增加，而一氧化氮合酶又会激活鸟苷酸环化酶，从而提高 cGMP 的水平。增加的 cGMP 会激活蛋白激酶 G（"PKG"），然后沿着轴突逆向运输到神经元细胞体，在那里使 MAPKerk 磷酸化。
• NEURONAL PAIN PATHWAY
  申请人：Ambron Richard

  公开号：US20120295853A1

  公开（公告）日：2012-11-22

  The present invention relates to the discovery of a novel molecular pathway involved in long-term hyperexcitability of sensory neurons, which, in higher animals, is associated with persistent pain. It is based on the discovery that, following injury to an axon of a neuron, an increase in nitric oxide synthase activity results in increased nitric oxide production, which, in turn, activates guanylyl cyclase, thereby increasing levels of cGMP. Increased cGMP results in activation of protein kinase G (“PKG”), which then is retrogradely transported along the axon to the neuron cell body, where it phosphorylates MAPKerk.
• US8252754B2
  申请人：——

  公开号：US8252754B2

  公开（公告）日：2012-08-28