5-benzylthiomethyl-4-hydroxy-3-methoxybenzaldehyde | 150900-45-1

• 分子结构分类: 有机化合物 - 苯类化合物 - 酚类
• 英文名称: 5-benzylthiomethyl-4-hydroxy-3-methoxybenzaldehyde
• 英文别名: 3-(Benzylsulfanylmethyl)-4-hydroxy-5-methoxybenzaldehyde；3-(benzylsulfanylmethyl)-4-hydroxy-5-methoxybenzaldehyde
• CAS: 150900-45-1
• 化学式: C₁₆H₁₆O₃S
• 分子量: 288.367
• InChiKey: QVYMASYZEOKVCC-UHFFFAOYSA-N

计算性质

• 辛醇/水分配系数(LogP)：
  2.9
• 重原子数：
  20
• 可旋转键数：
  6
• 环数：
  2.0
• sp3杂化的碳原子比例：
  0.19
• 拓扑面积：
  71.8
• 氢给体数：
  1
• 氢受体数：
  4

反应信息

• 作为反应物：
  描述：

  5-benzylthiomethyl-4-hydroxy-3-methoxybenzaldehyde 在 哌啶 、 三溴化硼 作用下， 以 乙醇 、 二氯甲烷 为溶剂， 反应 5.5h， 生成 3,4-dihydroxy-5-<(benzylthio)methyl>-α-carboxamidocinnamonitrile
  参考文献：
  名称：

  Tyrphostins. 3. Structure-activity relationship studies of .alpha.-substituted benzylidenemalononitrile 5-S-aryltyrphostins

  摘要：

  In this study we describe an extension of our previous studies on cis-benzylidenemalononitrile tyrphostins. We have introduced S-aryl substituents in the 5 position (meta vis-a-vis the malononitrile moiety). We find that these compounds are potent blockers of EGFR kinase and its homolog HER-2 kinase. Interestingly, we find that certain S-aryltyrphostins discriminate between EGFR and HER-2 kinase in favor of the HER-2 kinase domain by almost 2 orders of magnitude. When examined in intact cells it was found that these selective S-aryltyrphostins are equipotent in inhibiting EGF dependent proliferation of NIH 3T3 harboring either the EGF receptor or the chimera EGF/neu (HER1-2). These findings suggest that the antiproliferative activity of these tyrphostins is mainly due to the inhibition of a mitogenic signaling element downstream to the growth receptor kinase.

  DOI：

  10.1021/jm00075a010
• 作为产物：
  描述：

  3-(氯甲基)-4-羟基-5-甲氧基苯甲醛 、 苄硫醇 在 三乙胺 作用下， 以 二氯甲烷 为溶剂， 反应 3.0h， 以37%的产率得到5-benzylthiomethyl-4-hydroxy-3-methoxybenzaldehyde
  参考文献：
  名称：

  Tyrphostins. 3. Structure-activity relationship studies of .alpha.-substituted benzylidenemalononitrile 5-S-aryltyrphostins

  摘要：

  In this study we describe an extension of our previous studies on cis-benzylidenemalononitrile tyrphostins. We have introduced S-aryl substituents in the 5 position (meta vis-a-vis the malononitrile moiety). We find that these compounds are potent blockers of EGFR kinase and its homolog HER-2 kinase. Interestingly, we find that certain S-aryltyrphostins discriminate between EGFR and HER-2 kinase in favor of the HER-2 kinase domain by almost 2 orders of magnitude. When examined in intact cells it was found that these selective S-aryltyrphostins are equipotent in inhibiting EGF dependent proliferation of NIH 3T3 harboring either the EGF receptor or the chimera EGF/neu (HER1-2). These findings suggest that the antiproliferative activity of these tyrphostins is mainly due to the inhibition of a mitogenic signaling element downstream to the growth receptor kinase.

  DOI：

  10.1021/jm00075a010

文献信息

• METHODS AND COMPOSITIONS FOR TREATING LEUKEMIA
  申请人：HSC Research and Development Limited Partnership

  公开号：EP1161417B1

  公开（公告）日：2003-12-03
• Tyrphostins. 3. Structure-activity relationship studies of .alpha.-substituted benzylidenemalononitrile 5-S-aryltyrphostins
  作者：Aviv Gazit、Nir Osherov、Israel Posner、Allan Bar-Sinai、Chaim Gilon、Alexander Levitzki

  DOI：10.1021/jm00075a010

  日期：1993.11

  In this study we describe an extension of our previous studies on cis-benzylidenemalononitrile tyrphostins. We have introduced S-aryl substituents in the 5 position (meta vis-a-vis the malononitrile moiety). We find that these compounds are potent blockers of EGFR kinase and its homolog HER-2 kinase. Interestingly, we find that certain S-aryltyrphostins discriminate between EGFR and HER-2 kinase in favor of the HER-2 kinase domain by almost 2 orders of magnitude. When examined in intact cells it was found that these selective S-aryltyrphostins are equipotent in inhibiting EGF dependent proliferation of NIH 3T3 harboring either the EGF receptor or the chimera EGF/neu (HER1-2). These findings suggest that the antiproliferative activity of these tyrphostins is mainly due to the inhibition of a mitogenic signaling element downstream to the growth receptor kinase.