N-(2-羟基乙基)-二十烷酰胺 | 94421-69-9

• 分子结构分类: 有机化合物 - 有机氮化合物
• 中文名称: N-(2-羟基乙基)-二十烷酰胺
• 英文名称: N-(2-hydroxyethyl)icosanamide
• 英文别名: N-Arachidoylethanolamine
• CAS: 94421-69-9
• 化学式: C₂₂H₄₅NO₂
• mdl: MFCD00717688
• 分子量: 355.605
• InChiKey: AUJVQJHODMISJP-UHFFFAOYSA-N

物化性质

• 溶解度：
  DMF：10mg/mL； DMSO：20mg/mL；乙醇：2.5mg/mL； PBS（pH 7.2）：0.15 mg/mL

计算性质

• 辛醇/水分配系数(LogP)：
  8.3
• 重原子数：
  25
• 可旋转键数：
  20
• 环数：
  0.0
• sp3杂化的碳原子比例：
  0.954
• 拓扑面积：
  49.3
• 氢给体数：
  2
• 氢受体数：
  2

反应信息

• 作为产物：
  描述：

  、 C.I.酸性橙108 以 二氯甲烷 为溶剂， 生成 N-(2-羟基乙基)-二十烷酰胺
  参考文献：
  名称：

  N-(2-羟基-乙基)酰胺衍生物的合成及抗惊厥活性

  摘要：

  合成了一系列新型 N-(2-羟乙基)酰胺衍生物，并通过最大电休克 (MES) 试验筛选其抗惊厥活性，并通过旋转棒试验 (Tox) 评估其神经毒性。最大电休克试验表明，N-（2-羟乙基）癸酰胺 1g、N-（2-羟乙基）棕榈酰胺 1l 和 N-（2-羟乙基）硬脂酰胺 1n 显示出更好的抗惊厥活性，并且具有更低的抗惊厥活性。毒性比标记的抗癫痫药丙戊酸盐要低。在抗 MES 效力测试中，这些化合物的中位有效剂量 (ED50) 分别为 22.0、23.3、20.5 mg/kg，中位毒性剂量 (TD50) 分别为 599.8、>1000、>1000 mg/kg，导致保护指数 (PI) 分别为 27.5、>42.9、>48.8。这是比标记的抗癫痫药物丙戊酸盐（PI = 1.6）更好的保护指数。为了进一步研究几种不同模型中抗惊厥活性的影响，测试了化合物 1g、1l 和 1n 引起的惊厥，这些化学物质包括戊四

  DOI：

  10.1002/ardp.200800153

文献信息

• METHODS AND COMPOSITIONS FOR TREATING INFLAMMATION
  申请人：UNIVERSITY OF MASSACHUSETTS

  公开号：US20200138756A1

  公开（公告）日：2020-05-07

  Disclosed herein are methods and compositions for treating neutrophil-mediated inflammation by targeting, in any combination, the pro-inflammatory MRP2/HXA3 pathway and/or the anti-inflammatory P-gp/endocannabinoid pathway and/or the anti-inflammatory MRP 1/L-AMEND pathway, comprising administering to the subject a therapeutically effective amount of (a) one or more first compound that inhibits the activity and/or level of one or more of multidrug resistance protein 2 (MRP2) and hepoxilin A3 (HXA3) synthase, and/or (b) one or more second compound that increases the level and/or activity of one or more N-acylethanolamines (NAEs), and/or (c) one or more third compound that increases the level and/or activity of multidrug resistance protein 1 (MRP1), wherein the therapeutic amount of the first, second, and third compounds reduces migration of neutrophils into the target tissue.

  本文披露了一种治疗中性粒细胞介导炎症的方法和组合物，通过以任何组合方式靶向抗炎 MRP2/HXA3 途径和/或抗炎 P-gp/内源性大麻素途径和/或抗炎 MRP 1/L-AMEND 途径，包括向受试者施用治疗有效量的（a）抑制一种或多种多药耐药蛋白2（MRP2）和肝过氧化脂酸A3（HXA3）合酶的活性和/或水平的一种或多种第一化合物，和/或（b）增加一种或多种N-乙酰基乙醇胺（NAEs）的水平和/或活性的一种或多种第二化合物，和/或（c）增加一种或多种多药耐药蛋白1（MRP1）的水平和/或活性的一种或多种第三化合物，其中第一、第二和第三化合物的治疗量减少中性粒细胞向目标组织的迁移。
• Organic Compounds
  申请人：GIVAUDAN S.A.

  公开号：US20160242443A1

  公开（公告）日：2016-08-25

  This disclosure relates to flavour modification and to compounds of formula (I) wherein R 1 is selected from C 6 -C 20 alkyl, and C 9 -C 25 alkenyl, and i) R 3 and R 4 are hydrogen and R 2 the residue of a proteinogenic amino acid; ii) R 2 and R 3 are methyl and R 4 is hydrogen; or R 4 is hydrogen and R 2 and R 3 form together with the carbon atom to which they are attached cyclopropyl; iii) R 2 is hydrogen, and R 3 and R 4 together are —CH 2 —CH 2 —CH 2 —, useful in modifying flavours.

  本公开涉及味道改良和式(I)化合物，其中R1选自C6-C20烷基和C9-C25烯基，且i) R3和R4为氢，R2为蛋白质原性氨基酸的残基；ii) R2和R3为甲基，R4为氢；或R4为氢，R2和R3与它们所连接的碳原子一起形成环丙基；iii) R2为氢，R3和R4一起为—CH2—CH2—CH2—，有助于改良味道。
• LUBRICATING OIL COMPOSITION, AND SLIDING MECHANISM USING LUBRICATING OIL COMPOSITION
  申请人：Idemitsu Kosan Co., Ltd

  公开号：EP2826844A1

  公开（公告）日：2015-01-21

  Disclosed is a lubricating oil composition for low-friction sliding materials, which is used in a sliding mechanism where a DLC film containing hydrogen in an amount of from 5 atom% to 50 atom% is formed on at least one sliding surface. The lubricating oil composition contains, in the lubricant base oil therein and based on the total amount of the composition, (A) an organic zinc dithiophosphate in an amount of from 0.005% by mass to 0.12% by mass in terms of the phosphorus concentration therein, (B) an amide-based friction-reducing agent in an amount of from 0.05% by mass to 5.0% by mass, and (C) an alkaline earth metal salicylate-based detergent and/or an alkaline earth metal sulfonate-based detergent in an amount of from 0.05% by mass to 0.5o by mass in terms of the alkaline earth metal concentration therein.

  本发明公开了一种用于低摩擦滑动材料的润滑油组合物，该组合物用于在至少一个滑动表面上形成含氢量为 5 原子％至 50 原子％的 DLC 膜的滑动机构中。 该润滑油组合物在其中的润滑油基础油中，根据组合物的总量，含有 (A) 有机二硫代磷酸锌，以其中的磷浓度计，含量为 0.005% （质量分数）至 0.12% （质量分数）；(B) 酰胺基减摩剂，含量为 0.05% (质量)至 5.0% (质量)，以及 (C) 碱土金属水杨酸酯类洗涤剂和/或碱土金属磺酸盐类洗涤剂，以其中碱土金属浓度计，用量为 0.05% (质量)至 0.5o (质量)。
• ALDIMINES ET LEURS UTILISATIONS
  申请人：BOSTIK SA

  公开号：EP3838891A1

  公开（公告）日：2021-06-23

  La présente invention concerne des composé ayant l'une des formules (I) ou (II) suivantes : ainsi que leurs utilisations.

  本发明涉及具有下式（I）或（II）之一的化合物： 的化合物及其用途。
• Anandamide Biosynthesis Catalyzed by the Phosphodiesterase GDE1 and Detection of Glycerophospho-N-acyl Ethanolamine Precursors in Mouse Brain
  作者：Gabriel M. Simon、Benjamin F. Cravatt

  DOI：10.1074/jbc.m707807200

  日期：2008.4

  Anandamide (AEA) is an endogenous ligand of cannabinoid receptors and a well characterized mediator of many physiological processes including inflammation, pain, and appetite. The biosynthetic pathway(s) for anandamide and its N-acyl ethanolamine (NAE) congeners remain enigmatic. Previously, we proposed an enzymatic route for producing NAEs that involves the double-O-deacylation of N-acyl phosphatidylethanolamines (NAPEs) by alpha/beta-hydrolase 4 (ABDH4 or Abh4) to form glycerophospho (GP)-NAEs, followed by conversion of these intermediates to NAEs by an unidentified phosphodiesterase. Here, we report the detection and measurement of GP-NAEs, including the anandamide precursor glycerophospho-N-arachidonoylethanolamine (GP-NArE), as endogenous constituents of mouse brain tissue. Inhibition of the phosphodiesterase-mediated degradation of GP-NAEs ex vivo resulted in a striking accumulation of these lipids in brain extracts, suggesting a rapid endogenous flux through this pathway. Furthermore, we identify the glycerophosphodiesterase GDE1, also known as MIR16, as a broadly expressed membrane enzyme with robust GP-NAE phosphodiesterase activity. Together, these data provide evidence for a multistep pathway for the production of anandamide in the nervous system by the sequential actions of Abh4 and GDE1.