N-benzyl-N-isopentyl-3-nitrobenzamide | 945714-72-7

• 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: N-benzyl-N-isopentyl-3-nitrobenzamide
• 英文别名: NTR-N2A2B4；N-benzyl-N-(3-methylbutyl)-3-nitrobenzamide
• CAS: 945714-72-7
• 化学式: C₁₉H₂₂N₂O₃
• 分子量: 326.395
• InChiKey: MXMIDYYINUXBIU-UHFFFAOYSA-N

计算性质

• 辛醇/水分配系数(LogP)：
  4.4
• 重原子数：
  24
• 可旋转键数：
  6
• 环数：
  2.0
• sp3杂化的碳原子比例：
  0.32
• 拓扑面积：
  66.1
• 氢给体数：
  0
• 氢受体数：
  3

反应信息

• 作为产物：
  描述：

  异戊胺 在 4-二甲氨基吡啶 、 N,N-二异丙基乙胺 作用下， 以 甲醇 、 二氯甲烷 为溶剂， 反应 8.0h， 生成 N-benzyl-N-isopentyl-3-nitrobenzamide
  参考文献：
  名称：

  Structure–activity relationships of small molecule inhibitors of RAGE-Aβ binding

  摘要：

  The Receptor for Advanced Glycation Endproducts ('RAGE') mediates transport of amyloid-beta peptide (A beta) into the brain, and is therefore an important target for the development of therapeutic agents for Alzheimer's disease. We describe structure activity relationships for inhibition of RAGE-A beta binding, derived from the analysis of a library of tertiary amides. (C) 2013 Elsevier Ltd. All rights reserved.

  DOI：

  10.1016/j.tet.2013.05.079

文献信息

• INHIBITING AMYLOID-BETA PEPTIDE/RAGE INTERACTION AT THE BLOOD-BRAIN BARRIER
  申请人：THE UNIVERSITY OF ROCHESTER

  公开号：EP1993527A2

  公开（公告）日：2008-11-26
• EP1993527A4
  申请人：——

  公开号：EP1993527A4

  公开（公告）日：2009-08-05
• Inhibiting Amyloid-Beta Peptide/Rage Interaction At The Blood-Brain Barrier
  申请人：Zlokovic Berislav V.

  公开号：US20110039908A1

  公开（公告）日：2011-02-17

  Small molecules are used to inhibit specific receptor-ligand interaction between Alzheimer's amyloid-β peptide (Aβ) and Receptor for Advanced Gly-cation Endproducts (RAGE). Objectives include treating Alzheimer's disease and other pathologies involving cerebral amyloid angiopathy; improving blood flow to or within the brain; decreasing the level of Aβ in the brain; reducing neuropathology associated with Alzheimer's disease; reducing inflammation and/or oxidant stress in the brain; improving memory and/or learning; treating other conditions involving Aβ/RAGE interaction at the blood-brain barrier, RAGE-mediated transport of Aβ into the brain, or RAGE activation in brain vasculature and/or brain parenchyma (e.g., diabetic complications); or any combination thereof.
• US8778985B2
  申请人：——

  公开号：US8778985B2

  公开（公告）日：2014-07-15
• [EN] INHIBITING AMYLOID-BETA PEPTIDE/RAGE INTERACTION AT THE BLOOD-BRAIN BARRIER<br/>[FR] INHIBITION DE L'INTERACTION PEPTIDE AMYLOÏDE BÊTA/RAGE AU NIVEAU DE LA BARRIÈRE HÉMATO-ENCÉPHALIQUE
  申请人：UNIV ROCHESTER

  公开号：WO2007089616A2

  公开（公告）日：2007-08-09

  [EN] Small molecules are used to inhibit specific receptor-ligand interaction between Alzheimer's amyloid-ß peptide (Aß) and Receptor for Advanced GIy- cation Endproducts (RAGE). Objectives include treating Alzheimer's disease and other pathologies involving cerebral amyloid angiopathy; improving blood flow to or within the brain; decreasing the level of Aß in the brain; reducing neuropathology associated with Alzheimer's disease; reducing inflammation and/or oxidant stress in the brain; improving memory and/or learning; treating other conditions involving Aß/RAGE interaction at the blood-brain barrier, RAGE-mediated transport of Aß into the brain, or RAGE activation in brain vasculature and/or brain parenchyma (e.g., diabetic complications); or any combination thereof.
  [FR] L'invention concerne de petites molécules qui sont utilisées pour inhiber une interaction récepteur/ligand spécifique entre le peptide amyloïde ß de la maladie d'Alzheimer (Aß) et le récepteur RAGE (Receptor for Advanced Glycation Endproducts). Les cibles comprennent le traitement de la maladie d'Alzheimer et d'autres pathologies impliquant une angiopathie amyloïde cérébrale ; l'amélioration de la circulation sanguine de ou vers le cerveau ; la diminution du taux d'Aß dans le cerveau ; la réduction de la neuropathologie associée à la maladie d'Alzheimer ; la réduction de l'inflammation et/ou du stress oxydatif dans le cerveau ; l'amélioration de la mémoire et/ou de la cognition ; le traitement d'autres conditions impliquant l'interaction Aß/RAGE au niveau de la barrière hémato-encéphalique, le transport d'Aß médié par RAGE dans le cerveau, ou l'activation de RAGE dans la vasculature cérébrale et/ou le parenchyme cérébral (par exemple les complications diabétiques) ; ou une combinaison quelconque des précédents.