(E)-N-methyl-N-(tert-butoxycarbonyl)-4-[3-(5-ethoxypyridin)yl]-3-buten-1-amine | 326918-60-9

• 分子结构分类: 有机化合物 - 有机氧化合物
• 英文名称: (E)-N-methyl-N-(tert-butoxycarbonyl)-4-[3-(5-ethoxypyridin)yl]-3-buten-1-amine
• CAS: 326918-60-9
• 化学式: C₁₇H₂₆N₂O₃
• 分子量: 306.405
• InChiKey: DRCYRHCXIBVVNZ-VQHVLOKHSA-N

计算性质

• 辛醇/水分配系数(LogP)：
  3.75
• 重原子数：
  22.0
• 可旋转键数：
  6.0
• 环数：
  1.0
• sp3杂化的碳原子比例：
  0.53
• 拓扑面积：
  51.66
• 氢给体数：
  0.0
• 氢受体数：
  4.0

反应信息

• 作为反应物：
  描述：

  (E)-N-methyl-N-(tert-butoxycarbonyl)-4-[3-(5-ethoxypyridin)yl]-3-buten-1-amine 在 盐酸 作用下， 以 四氢呋喃 为溶剂， 以86.4%的产率得到TC-2559
  参考文献：
  名称：

  TC-2559: A novel orally active ligand selective at neuronal acetylcholine receptors

  摘要：

  TC-2559 [(E)-N-Methyl-4-[3-(5-ethoxypyridin)yl]-3-buten-1-amine] is a novel nicotinic agonist markedly more selective than recently reported novel nicotinic receptor Ligands (selectivity ratio for central nervous system (CNS) to peripheral nervous system (PNS)> 4000). TC-2559 competes effectively with [H-3]-nicotine binding (K-i = 5 nM) but not with [I-125]-bungarotoxin( > 50,000 nM). Dopamine release from striatal synaptosomes and ion flux from thalamic synaptosomes indicate that TC-2559 is potent and efficacious in the activation of CNS receptors and significantly reduced glutamate-induced neurotoxicity in vitro. TC-2559 has no detectable effects on muscle and ganglion-type nicotinic acetylcholine receptors at concentrations up to 1 mM. TC-2559 significantly attenuates scopolamine-induced cognitive deficits in a step-through passive avoidance task. Acute and repeated oral dosing of TC-2559 enhances performance in a radial arm maze task. Ln contrast to the effects of equimolar concentrations of (-) nicotine, TC-2559 does not induce hypothermia and locomotor activity is not enhanced following repeated daily administration of 14 days. TC-2559 has a markedly enhanced CNS-PNS selectivity ratio and an intra-CNS selectivity as evidenced by the improved cognition without increased locomotor activity. The in vitro and in vivo studies in the present study suggest that TC-2559 has the desired profile to be further evaluated as a potential therapeutic agent for neurodegenerative diseases. (C) 2000 Elsevier Science B.V. All rights reserved.

  DOI：

  10.1016/s0014-2999(00)00807-4
• 作为产物：
  描述：

  N-methyl-3-butenylamine 在 palladium diacetate 三乙胺 、 三(邻甲基苯基)磷 作用下， 以 四氢呋喃 、 乙腈 为溶剂， 生成 (E)-N-methyl-N-(tert-butoxycarbonyl)-4-[3-(5-ethoxypyridin)yl]-3-buten-1-amine
  参考文献：
  名称：

  TC-2559: A novel orally active ligand selective at neuronal acetylcholine receptors

  摘要：

  TC-2559 [(E)-N-Methyl-4-[3-(5-ethoxypyridin)yl]-3-buten-1-amine] is a novel nicotinic agonist markedly more selective than recently reported novel nicotinic receptor Ligands (selectivity ratio for central nervous system (CNS) to peripheral nervous system (PNS)> 4000). TC-2559 competes effectively with [H-3]-nicotine binding (K-i = 5 nM) but not with [I-125]-bungarotoxin( > 50,000 nM). Dopamine release from striatal synaptosomes and ion flux from thalamic synaptosomes indicate that TC-2559 is potent and efficacious in the activation of CNS receptors and significantly reduced glutamate-induced neurotoxicity in vitro. TC-2559 has no detectable effects on muscle and ganglion-type nicotinic acetylcholine receptors at concentrations up to 1 mM. TC-2559 significantly attenuates scopolamine-induced cognitive deficits in a step-through passive avoidance task. Acute and repeated oral dosing of TC-2559 enhances performance in a radial arm maze task. Ln contrast to the effects of equimolar concentrations of (-) nicotine, TC-2559 does not induce hypothermia and locomotor activity is not enhanced following repeated daily administration of 14 days. TC-2559 has a markedly enhanced CNS-PNS selectivity ratio and an intra-CNS selectivity as evidenced by the improved cognition without increased locomotor activity. The in vitro and in vivo studies in the present study suggest that TC-2559 has the desired profile to be further evaluated as a potential therapeutic agent for neurodegenerative diseases. (C) 2000 Elsevier Science B.V. All rights reserved.

  DOI：

  10.1016/s0014-2999(00)00807-4