4-(4-butoxyphenylamino)-6-methyl-2-phenylpyridazin-3(2H)-one | 1184304-23-1

• 分子结构分类: 有机化合物 - 苯类化合物 - 苯酚醚
• 英文名称: 4-(4-butoxyphenylamino)-6-methyl-2-phenylpyridazin-3(2H)-one
• 英文别名: 4-(4-Butoxyanilino)-6-methyl-2-phenylpyridazin-3-one
• CAS: 1184304-23-1
• 化学式: C₂₁H₂₃N₃O₂
• 分子量: 349.433
• InChiKey: PMSONHXBOYXKFR-UHFFFAOYSA-N

计算性质

• 辛醇/水分配系数(LogP)：
  4.3
• 重原子数：
  26
• 可旋转键数：
  7
• 环数：
  3.0
• sp3杂化的碳原子比例：
  0.24
• 拓扑面积：
  53.9
• 氢给体数：
  1
• 氢受体数：
  4

反应信息

• 作为产物：
  描述：

  美坦法宗 、 4-丁氧基苯硼酸 在 copper diacetate 、 三乙胺 作用下， 以 二氯甲烷 为溶剂， 反应 12.0h， 以16%的产率得到4-(4-butoxyphenylamino)-6-methyl-2-phenylpyridazin-3(2H)-one
  参考文献：
  名称：

  6-Methyl-2,4-Disubstituted Pyridazin-3(2H)-ones: A Novel Class of Small-Molecule Agonists for Formyl Peptide Receptors

  摘要：

  Following a ligand-based drug design approach, a potent mixed formyl peptide receptor I (FPR1) and formyl peptide receptor-like I (FPRL1) agonist (14a) and a potent and specific FPRL1 agonist (14x) were identified. These compounds belong to a large series of pyridazin-3(2H)-one derivatives substituted with methyl group at position 6 and a methoxy benzyl at position 4. At position 2, an acetamide side chain is essential for activity. Likewise, the presence of lipophilic and/or electronegative substituents in the position para to the aryl group at the end of the chain plays a critical role for activity. Affinity for FPR1 receptors was evaluated by measuring intracellular calcium flux in HL-60 cells transfected with FPR1, FPRL1, and FPRL2, Agonists were able to activate intracellular calcium mobilization and chemotaxis in human neutrophils. The most potent chemotactic agent (EC50 = 0.6 mu M) was the mixed FPR/FPRL1 agonist 14h.

  DOI：

  10.1021/jm900592h

文献信息

• Method of treatment and compounds for use therein
  申请人：Baker Heart and Diabetes Institute

  公开号：US10328075B2

  公开（公告）日：2019-06-25

  The present invention relates generally to a method of therapeutically or prophylactically treating ischaemia-induced myocardial tissue damage, in particular ischaemia-reperfusion-induced myocardial tissue damage. More particularly, the present invention relates to a method of reducing the extent of ischaemia-induced myocardial tissue damage in a mammal by selectively upregulating FPR1-mediated ERK signalling. The method of the present invention is useful, inter alia, in reducing the extent and/or severity of myocardial tissue damage associated with conditions characterized by myocardial ischaemia or myocardial ischaemia and reperfusion, such as acute myocardial infarction caused by atherosclerotic artery occlusion or blood clot-induced artery occlusion.

  本发明一般涉及一种治疗或预防缺血诱导的心肌组织损伤，特别是缺血再灌注诱导的心肌组织损伤的方法。更具体地说，本发明涉及一种通过选择性上调 FPR1 介导的 ERK 信号来降低哺乳动物缺血诱导的心肌组织损伤程度的方法。本发明的方法特别适用于减少与心肌缺血或心肌缺血和再灌注相关的心肌组织损伤的程度和/或严重性，如动脉粥样硬化性动脉闭塞或血凝块诱发的动脉闭塞引起的急性心肌梗塞。
• A Method Of Treatment And Compounds For Use Therein
  申请人：Baker Heart and Diabetes Institute

  公开号：US20180092917A1

  公开（公告）日：2018-04-05

  The present invention relates generally to a method of therapeutically or prophylactically treating ischaemia-induced myocardial tissue damage, in particular ischaemia-reperfusion-induced myocardial tissue damage. More particularly, the present invention relates to a method of reducing the extent of ischaemia-induced myocardial tissue damage in a mammal by selectively upregulating FPR1-mediated ERK signalling. The method of the present invention is useful, inter alia, in reducing the extent and/or severity of myocardial tissue damage associated with conditions characterised by myocardial ischaemia or myocardial ischaemia and reperfusion, such as acute myocardial infarction caused by atherosclerotic artery occlusion or blood clot-induced artery occlusion.
• [EN] A METHOD OF TREATMENT AND COMPOUNDS FOR USE THEREIN<br/>[FR] MÉTHODE DE TRAITEMENT ET COMPOSÉS DESTINÉS À ÊTRE UTILISÉS DANS CETTE MÉTHODE
  申请人：BAKER IDI HEART & DIABETES INST HOLDINGS LTD

  公开号：WO2016123672A1

  公开（公告）日：2016-08-11

  The present invention relates generally to a method of therapeutically or prophylactically treating ischaemia-induced myocardial tissue damage, in particular ischaemia-reperfusion-induced myocardial tissue damage. More particularly, the present invention relates to a method of reducing the extent of ischaemia-induced myocardial tissue damage in a mammal by selectively upregulating FPRl-mediated ERK signalling. The method of the present invention is useful, inter alia, in reducing the extent and/or severity of myocardial tissue damage associated with conditions characterised by myocardial ischaemia or myocardial ischaemia and reperfusion, such as acute myocardial infarction caused by atherosclerotic artery occlusion or blood clot-induced artery occlusion.