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n-pentylphosphine | 10038-55-8

中文名称
——
中文别名
——
英文名称
n-pentylphosphine
英文别名
pentyl-phosphine;Pentyl-phosphin;n-Pentylphosphin;Pentylphosphin;Amylphosphin;Phosphine, pentyl-;pentylphosphane
n-pentylphosphine化学式
CAS
10038-55-8
化学式
C5H13P
mdl
——
分子量
104.132
InChiKey
WEYHWRWGAACKIL-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):
    1.7
  • 重原子数:
    6
  • 可旋转键数:
    3
  • 环数:
    0.0
  • sp3杂化的碳原子比例:
    1.0
  • 拓扑面积:
    0
  • 氢给体数:
    0
  • 氢受体数:
    0

反应信息

  • 作为反应物:
    描述:
    yttrium(pentamethylcyclopentadienyl)2CH(trimethylsilyl)2n-pentylphosphine 在 H2 作用下, 以 氘代甲苯 为溶剂, 生成 bis(pentamethylcyclopentadienyl)(n-pentylphosphine)(n-pentylphosphido)yttrium 、 [(pentamethylcyclopentadienyl)2yttrium]2(n-C5H11PH)2 、 ((pentamethylcyclopentadienyl)2yttrium)2(n-C5H11PH)(H)
    参考文献:
    名称:
    有机镧系元素催化的膦基烯烃和膦基炔烃的分子内氢膦化/环化:范围、选择性和机理
    摘要:
    Cp'(2)LnE(TMS)(2) (Cp' = eta(5)-Me(5)C(5); Ln = La, Sm, Y, Lu; E = CH, N;TMS = SiMe(3)) 作为膦烯烃和膦炔烃 RHP(CH(2))(n)()CH=CH(2) (R = Ph, H; n = 3, 4) 和 H(2)P(CH(2))(n)C 三键 C-Ph (n = 3, 4) 分别提供相应的杂环。这些过程的动力学和机械数据表现出与有机镧系元素介导的分子内加氢胺化/环化的相似之处以及明显的差异。本催化循环的周转限制步骤是将碳-碳不饱和键插入 Ln-P 键,然后快速质子化生成的 Ln-C 键。在大约一个半衰期内,速率定律在 [催化剂] 中是一级的,在 [底物] 中是零级的,杂环产物在更高的转化率下会侵入。催化剂的静止状态很可能是镧系膦-磷化物复合物,二聚体 [Cp'(2)YP(H)Ph](2) 被分离出来并具
    DOI:
    10.1021/ja010811i
  • 作为产物:
    描述:
    pentylphosphonic acid dibutyl ester 在 lithium aluminium tetrahydride 作用下, 生成 n-pentylphosphine
    参考文献:
    名称:
    Eotaxin Expression by Epithelial Cells and Plasma Cells in Chronic Asthma
    摘要:
    Chemoattractants such as eotaxin are believed to play an important role in the recruitment of eosinophils into the airways in asthma. We investigated expression of eotaxin in the airway wall in a model of chronic human asthma, in which systemically sensitized mice were exposed to low mass concentrations of aerosolized antigen for 6 weeks. In these animals, the number of intraepithelial eosinophils in the airways was significantly increased 3 hours after exposure and declined by 24 hours. In parallel, immunoreactivity for eotaxin was strikingly up-regulated in airway epithelial cells and in inflammatory cells in the lamina propria. The latter were identified as plasma cells by double immunofluorescent labeling. Increased expression of eotaxin by epithelial cells and plasma cells was also demonstrated in a case of fatal human asthma. In contrast, sensitized mice that received a single exposure to a high mass concentration of aerosolized antigen exhibited delayed eosinophil recruitment, which did not correlate with eotaxin expression. Furthermore, in sensitized chronically exposed interieukin-13-deficient mice there was virtually no recruitment of eosinophils into the airways, although eotaxin expression was greater than or equal to that in wild-type mice. These results indicate that there are striking differences between acute and chronic exposure models in the time course of eotaxin expression and eosinophil recruitment. Although high eotaxin levels alone are not sufficient to cause recruitment of eosinophils into the airways, recurrent exposure may generate or up-regulate additional signals required for eosinophil chemotaxis.
    DOI:
    10.1038/labinvest.3780442
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文献信息

  • Intramolecular Hydrophosphination/Cyclization of Phosphinoalkenes and Phosphinoalkynes Catalyzed by Organolanthanides:  Scope, Selectivity, and Mechanism
    作者:Michael R. Douglass、Charlotte L. Stern、Tobin J. Marks
    DOI:10.1021/ja010811i
    日期:2001.10.1
    Organolanthanide complexes of the general type Cp'(2)LnE(TMS)(2) (Cp' = eta(5)-Me(5)C(5); Ln = La, Sm, Y, Lu; E = CH, N; TMS = SiMe(3)) serve as effective precatalysts for the rapid intramolecular hydrophosphination/cyclization of the phosphinoalkenes and phosphinoalkynes RHP(CH(2))(n)()CH=CH(2) (R = Ph, H; n = 3, 4) and H(2)P(CH(2))(n)C triple bond C-Ph (n = 3, 4) to afford the corresponding heterocycles
    Cp'(2)LnE(TMS)(2) (Cp' = eta(5)-Me(5)C(5); Ln = La, Sm, Y, Lu; E = CH, N;TMS = SiMe(3)) 作为膦烯烃和膦炔烃 RHP(CH(2))(n)()CH=CH(2) (R = Ph, H; n = 3, 4) 和 H(2)P(CH(2))(n)C 三键 C-Ph (n = 3, 4) 分别提供相应的杂环。这些过程的动力学和机械数据表现出与有机镧系元素介导的分子内加氢胺化/环化的相似之处以及明显的差异。本催化循环的周转限制步骤是将碳-碳不饱和键插入 Ln-P 键,然后快速质子化生成的 Ln-C 键。在大约一个半衰期内,速率定律在 [催化剂] 中是一级的,在 [底物] 中是零级的,杂环产物在更高的转化率下会侵入。催化剂的静止状态很可能是镧系膦-磷化物复合物,二聚体 [Cp'(2)YP(H)Ph](2) 被分离出来并具
  • Eotaxin Expression by Epithelial Cells and Plasma Cells in Chronic Asthma
    作者:Rakesh K Kumar、Paul S Thomas、Da-Qiang Seetoo、Cristan Herbert、Andrew N J McKenzie、Paul S Foster、Andrew R Lloyd
    DOI:10.1038/labinvest.3780442
    日期:2002.4
    Chemoattractants such as eotaxin are believed to play an important role in the recruitment of eosinophils into the airways in asthma. We investigated expression of eotaxin in the airway wall in a model of chronic human asthma, in which systemically sensitized mice were exposed to low mass concentrations of aerosolized antigen for 6 weeks. In these animals, the number of intraepithelial eosinophils in the airways was significantly increased 3 hours after exposure and declined by 24 hours. In parallel, immunoreactivity for eotaxin was strikingly up-regulated in airway epithelial cells and in inflammatory cells in the lamina propria. The latter were identified as plasma cells by double immunofluorescent labeling. Increased expression of eotaxin by epithelial cells and plasma cells was also demonstrated in a case of fatal human asthma. In contrast, sensitized mice that received a single exposure to a high mass concentration of aerosolized antigen exhibited delayed eosinophil recruitment, which did not correlate with eotaxin expression. Furthermore, in sensitized chronically exposed interieukin-13-deficient mice there was virtually no recruitment of eosinophils into the airways, although eotaxin expression was greater than or equal to that in wild-type mice. These results indicate that there are striking differences between acute and chronic exposure models in the time course of eotaxin expression and eosinophil recruitment. Although high eotaxin levels alone are not sufficient to cause recruitment of eosinophils into the airways, recurrent exposure may generate or up-regulate additional signals required for eosinophil chemotaxis.
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