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N-(4-ethoxy-phenyl)-[1,3,5]triazine-2,4-diamine | 91333-18-5

中文名称
——
中文别名
——
英文名称
N-(4-ethoxy-phenyl)-[1,3,5]triazine-2,4-diamine
英文别名
N2-(4-ethoxy-phenyl)-[1,3,5]triazine-2,4-diyldiamine;N2-(4-Aethoxy-phenyl)-[1,3,5]triazin-2,4-diyldiamin;6-(4-Aethoxy-anilino)-4-amino-1.3.5-triazin;N-(4-ethoxyphenyl)-1,3,5-triazine-2,4-diamine;2-N-(4-ethoxyphenyl)-1,3,5-triazine-2,4-diamine
<i>N</i>-(4-ethoxy-phenyl)-[1,3,5]triazine-2,4-diamine化学式
CAS
91333-18-5
化学式
C11H13N5O
mdl
MFCD07157546
分子量
231.257
InChiKey
ZWXHFGCPMUAGGL-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

物化性质

  • 熔点:
    209-210 °C
  • 沸点:
    468.1±47.0 °C(Predicted)
  • 密度:
    1.299±0.06 g/cm3(Predicted)

计算性质

  • 辛醇/水分配系数(LogP):
    1.8
  • 重原子数:
    17
  • 可旋转键数:
    4
  • 环数:
    2.0
  • sp3杂化的碳原子比例:
    0.18
  • 拓扑面积:
    86
  • 氢给体数:
    2
  • 氢受体数:
    6

安全信息

  • 危险等级:
    IRRITANT

反应信息

  • 作为产物:
    描述:
    amino-p-phenetidino-[1,3,5]triazine-2-carboxylic acid ethyl ester 在 盐酸氢氧化钾 作用下, 生成 N-(4-ethoxy-phenyl)-[1,3,5]triazine-2,4-diamine
    参考文献:
    名称:
    Age-Related Increase of Brain Cyclooxygenase Activity and Dietary Modulation of Oxidative Status
    摘要:
    Several studies have demonstrated that inhibitors of cyclooxygenase (COX) attenuate various neuronal injuries and age-dependent demented conditions. From these findings, we proposed to test the effect of age on COX activity and its. possible suppression by the antiaging action of dietary restriction in the rat brain. The status of reactive oxygen species (ROS) was also assessed to correlate with COX activity to delineate the underlying mechanism of the altered COX activity during aging. These results showed that COX activity significantly increased in 24-month-old rats compared with 6-month-old rats in an ad libitum group. Interestingly, mRNA and protein levels of COX-2 showed little corresponding age-related change. The formation of ROS was found to increase gradually with age in ad libitum fed rats. However, dietary restriction suppressed the increase at the age of 24 months. To substantiate the relationship between ROS and COX activity when the rats were 24 months of age, we conducted in vitro experiments with a C6 glioma cell line. Together, it is concluded that increased COX activity with age is due to the activation of COX catalytic reaction by ROS without increased gene expression of COX-2 and that it is related to the increased pro-oxidant status in aged rats.
    DOI:
    10.1093/gerona/56.10.b426
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文献信息

  • Papini, Gazzetta Chimica Italiana, 1950, vol. 80, p. 844,848
    作者:Papini
    DOI:——
    日期:——
  • Clauder; Bulcsu, Magyar Kemiai Folyoirat, 1951, vol. 57, p. 68,71
    作者:Clauder、Bulcsu
    DOI:——
    日期:——
  • Age-Related Increase of Brain Cyclooxygenase Activity and Dietary Modulation of Oxidative Status
    作者:B. S. Baek、J. W. Kim、J. H. Lee、H. J. Kwon、N. D. Kim、H. S. Kang、M. A. Yoo、B. P. Yu、H. Y. Chung
    DOI:10.1093/gerona/56.10.b426
    日期:2001.10.1
    Several studies have demonstrated that inhibitors of cyclooxygenase (COX) attenuate various neuronal injuries and age-dependent demented conditions. From these findings, we proposed to test the effect of age on COX activity and its. possible suppression by the antiaging action of dietary restriction in the rat brain. The status of reactive oxygen species (ROS) was also assessed to correlate with COX activity to delineate the underlying mechanism of the altered COX activity during aging. These results showed that COX activity significantly increased in 24-month-old rats compared with 6-month-old rats in an ad libitum group. Interestingly, mRNA and protein levels of COX-2 showed little corresponding age-related change. The formation of ROS was found to increase gradually with age in ad libitum fed rats. However, dietary restriction suppressed the increase at the age of 24 months. To substantiate the relationship between ROS and COX activity when the rats were 24 months of age, we conducted in vitro experiments with a C6 glioma cell line. Together, it is concluded that increased COX activity with age is due to the activation of COX catalytic reaction by ROS without increased gene expression of COX-2 and that it is related to the increased pro-oxidant status in aged rats.
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