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N-(undec-10-enyl)hydroxylamine | 1560911-03-6

中文名称
——
中文别名
——
英文名称
N-(undec-10-enyl)hydroxylamine
英文别名
N-undec-10-enylhydroxylamine
N-(undec-10-enyl)hydroxylamine化学式
CAS
1560911-03-6
化学式
C11H23NO
mdl
——
分子量
185.31
InChiKey
FXGAROSFXLWDJD-UHFFFAOYSA-N
BEILSTEIN
——
EINECS
——
  • 物化性质
  • 计算性质
  • ADMET
  • 安全信息
  • SDS
  • 制备方法与用途
  • 上下游信息
  • 反应信息
  • 文献信息
  • 表征谱图
  • 同类化合物
  • 相关功能分类
  • 相关结构分类

计算性质

  • 辛醇/水分配系数(LogP):
    3.8
  • 重原子数:
    13
  • 可旋转键数:
    10
  • 环数:
    0.0
  • sp3杂化的碳原子比例:
    0.82
  • 拓扑面积:
    32.3
  • 氢给体数:
    2
  • 氢受体数:
    2

反应信息

  • 作为反应物:
    描述:
    N-(undec-10-enyl)hydroxylamine 在 sodium hydroxide 作用下, 以 1,4-二氧六环二氯甲烷 为溶剂, 反应 21.0h, 生成 2-undec-10-enyl-[1,2,4]oxadiazolidine-3,5-dione
    参考文献:
    名称:
    Inhibition of long chain fatty acyl-CoA synthetase (ACSL) and ischemia reperfusion injury
    摘要:
    Various triacsin C analogs, containing different alkenyl chains and carboxylic acid bioisoteres including 4-aminobenzoic acid, isothiazolidine dioxide, hydroxylamine, hydroxytriazene, and oxadiazolidine dione, were synthesized and their inhibitions of long chain fatty acyl-CoA synthetase (ACSL) were examined. Two methods, a cell-based assay of ACSL activity and an in situ [C-14]-palmitate incorporation into extractable lipids were used to study the inhibition. Using an in vivo leukocyte recruitment inhibition protocol, the translocation of one or more cell adhesion molecules from the cytoplasm to the plasma membrane on either the endothelium or leukocyte or both was inhibited by inhibitors 1, 9, and triacsin C. The results suggest that inhibition of ACSL may attenuate the vascular inflammatory component associated with ischemia reperfusion injury and lead to a decrease of infarct expansion. (C) 2014 Elsevier Ltd. All rights reserved.
    DOI:
    10.1016/j.bmcl.2014.01.016
  • 作为产物:
    描述:
    10-十一烯醛盐酸盐酸羟胺 、 sodium cyanoborohydride 、 sodium hydroxide 作用下, 以 甲醇乙醇 为溶剂, 反应 4.0h, 生成 N-(undec-10-enyl)hydroxylamine
    参考文献:
    名称:
    Inhibition of long chain fatty acyl-CoA synthetase (ACSL) and ischemia reperfusion injury
    摘要:
    Various triacsin C analogs, containing different alkenyl chains and carboxylic acid bioisoteres including 4-aminobenzoic acid, isothiazolidine dioxide, hydroxylamine, hydroxytriazene, and oxadiazolidine dione, were synthesized and their inhibitions of long chain fatty acyl-CoA synthetase (ACSL) were examined. Two methods, a cell-based assay of ACSL activity and an in situ [C-14]-palmitate incorporation into extractable lipids were used to study the inhibition. Using an in vivo leukocyte recruitment inhibition protocol, the translocation of one or more cell adhesion molecules from the cytoplasm to the plasma membrane on either the endothelium or leukocyte or both was inhibited by inhibitors 1, 9, and triacsin C. The results suggest that inhibition of ACSL may attenuate the vascular inflammatory component associated with ischemia reperfusion injury and lead to a decrease of infarct expansion. (C) 2014 Elsevier Ltd. All rights reserved.
    DOI:
    10.1016/j.bmcl.2014.01.016
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文献信息

  • POLYMERISIERBARE ZUSAMMENSETZUNG AUF THIOL-EN-BASIS
    申请人:Karl Leibinger Medizintechnik GmbH & Co. KG
    公开号:EP4091599A1
    公开(公告)日:2022-11-23
    Die vorliegende Erfindung betrifft die Verwendung von Verbindungen, die pro Molekül jeweils zumindest eine polymerisierbare C-C-Doppelbindung, zumindest eine haftungsvermittelnde Gruppierung und einen dazwischen liegenden zumindest zweiwertigen Spacer aufweisen, als Primer in einer polymerisierbaren Zusammensetzung auf Thiol-En-Basis, die weiters zumindest einen radikalischen Initiator, Monomere mit zumindest zwei polymerisierbaren C-C-Doppelbindungen pro Molekül und Polythiole mit zumindest zwei SH-Gruppen pro Molekül umfasst, mit dem Kennzeichen, dass die Primer als polymerisierbare Doppelbindungen 5-Norbornen-2-yl-Gruppen und aus Phosphonsäure-Gruppen und 3,4-Dihydroxyphenyl-Gruppen ausgewählte Gruppen als haftungsvermittelnde Gruppierungen umfassen; entsprechende Zusammensetzungen auf Thiol-En-Basis; entsprechende, für diesen Zweck geeignete Norbornen-Derivate; sowie konkrete, erstmalig synthetisierte Vertreter solcher Norbornen-Derivate.
    本发明涉及在可聚合硫醇烯基组合物中使用每分子至少有一个可聚合的 C-C 双键、 至少有一个促进粘附的基团和至少有一个二价间隔的化合物作为引物,该组合物还包 括至少一种自由基引发剂、每分子至少有两个可聚合 C-C 双键的单体和每分子至少有两个 SH 基团的聚硫醇,其特征是引物包括作为可聚合双键的 5-降冰片烯-2-基团和选自膦酸基团和 3,4-二羟基苯基基团的基团作为促粘基团;相应的以硫醇烯为基础的组合物;适用于这一目的的相应降冰片烯衍生物;以及首次合成的此类降冰片烯衍生物的具体代表。
  • Inhibition of long chain fatty acyl-CoA synthetase (ACSL) and ischemia reperfusion injury
    作者:Allan M. Prior、Man Zhang、Nina Blakeman、Palika Datta、Hung Pham、Qian Chen、Lindon H. Young、Margaret T. Weis、Duy H. Hua
    DOI:10.1016/j.bmcl.2014.01.016
    日期:2014.2
    Various triacsin C analogs, containing different alkenyl chains and carboxylic acid bioisoteres including 4-aminobenzoic acid, isothiazolidine dioxide, hydroxylamine, hydroxytriazene, and oxadiazolidine dione, were synthesized and their inhibitions of long chain fatty acyl-CoA synthetase (ACSL) were examined. Two methods, a cell-based assay of ACSL activity and an in situ [C-14]-palmitate incorporation into extractable lipids were used to study the inhibition. Using an in vivo leukocyte recruitment inhibition protocol, the translocation of one or more cell adhesion molecules from the cytoplasm to the plasma membrane on either the endothelium or leukocyte or both was inhibited by inhibitors 1, 9, and triacsin C. The results suggest that inhibition of ACSL may attenuate the vascular inflammatory component associated with ischemia reperfusion injury and lead to a decrease of infarct expansion. (C) 2014 Elsevier Ltd. All rights reserved.
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