[(3S)-1-fluoro-3-hydroxy-4-octadec-9-enoyloxybutyl]phosphonic acid

• 分子结构分类: 有机化合物 - 脂质和类脂质分子 - 脂肪酰基
• 英文名称: [(3S)-1-fluoro-3-hydroxy-4-octadec-9-enoyloxybutyl]phosphonic acid
• 化学式: C₂₂H₄₂FO₆P
• 分子量: 452.5
• InChiKey: YRZFDGAGYVFBGZ-BGERDNNASA-N

计算性质

• 辛醇/水分配系数(LogP)：
  6
• 重原子数：
  30
• 可旋转键数：
  21
• 环数：
  0.0
• sp3杂化的碳原子比例：
  0.86
• 拓扑面积：
  104
• 氢给体数：
  3
• 氢受体数：
  7

文献信息

• Lysophosphatidic acid analogs and inhibition of neointima formation
  申请人：——

  公开号：US20040204383A1

  公开（公告）日：2004-10-14

  The phospholipid growth factor lysophosphatidic acids (LPAs) containing unsaturated fatty acids (18:1, 18:2 and 20:4) and fatty alcohols containing hydrocarbon chains with more than 4 carbons were capable of inducing a rapid formation of neointima, an initial step in the development of atherosclerotic plaque. LPAs with saturated fatty acids did not induce neointima formation. A Peroxisome Proliferator-Activated Receptors gamma (PPAR&ggr;)-specific agonist Rosiglitasone also induced a profound formation of neointima. GW9662, a selective and irreversible antagonist of PPAR&ggr;, abolished LPA- and Rosiglitazone-induced neointima formation, indicating that LPA-induced neointima formation requires the activation of PPAR&ggr;. These data suggest that LPA analogs that bind to but do not activate downstream signaling of PPAR&ggr; or antagonists of PPAR&ggr; that inhibit PPAR&ggr; signaling would be useful in the prevention and/or treatment of neointima formation and atherosclerosis.

  磷脂生长因子溶血磷脂酸（LPAs）含有不饱和脂肪酸（18:1、18:2 和 20:4）和碳氢链超过 4 个碳原子的脂肪醇，能够诱导新内膜的快速形成，这是动脉粥样硬化斑块发展的第一步。含有饱和脂肪酸的 LPA 不会诱导新生内膜的形成。一种过氧化物酶体增殖激活受体γ（PPAR&ggr;）特异性激动剂Rosiglitasone也能诱导新生内膜的快速形成。GW9662是一种选择性和不可逆的PPAR&ggr;拮抗剂，它能消除LPA和罗格列酮诱导的新生血管形成，表明LPA诱导的新生血管形成需要PPAR&ggr;的激活。这些数据表明，与 PPAR&ggr; 结合但不激活 PPAR&ggr; 下游信号传导的 LPA 类似物或抑制 PPAR&ggr; 信号传导的 PPAR&ggr; 拮抗剂将有助于预防和/或治疗新内膜形成和动脉粥样硬化。
• EP1613298A2
  申请人：——

  公开号：EP1613298A2

  公开（公告）日：2006-01-11
• EP1613298A4
  申请人：——

  公开号：EP1613298A4

  公开（公告）日：2007-10-03
• [EN] LYSOPHOSPHATIDIC ACID ANALOGS AND INHIBITION OF NEOINTIMA FORMATION<br/>[FR] ANALOGUES D'ACIDES LYSOPHOSPHATIDIQUES ET INHIBITION DE FORMATION DE NEOINTIMA
  申请人：UNIV TENNESSEE RES FOUNDATION

  公开号：WO2004091496A2

  公开（公告）日：2004-10-28

  The phospholipid growth factor lysophosphatidic acids (LPAs) containing unsaturated fatty acids (18:1, 18:2 and 20:4) and fatty alcohols containing hydrocarbon chains with more than 4 carbons were capable of inducing a rapid formation of neointima, an initial step in the development of atherosclerotic plaque. LPAs with saturated fatty acids did not induce neointima formation. A Peroxisome Proliferator-Activated Receptors gamma (PPARϜ)-specific agonist Rosiglitasone also induced a profound formation of neointima. GW9662, a selective and irreversible antagonist of PPARϜ, abolished LPA- and Rosiglitazone-induced neointima formation, indicating that LPA-induced neointima formation requires the activation of PPARϜ. These data suggest that LPA analogs that bind to but do not activate downstream signaling of PPARϜ or antagonists of PPARϜ that inhibit PPARy signaling would be useful in the prevention and/or treatment of neointima formation and atherosclerosis.