3,5-bis-(3-hydroxy-4-methoxybenzylidene)tetrahydrothiopyran-4-one | 1088178-54-4

• 分子结构分类: 有机化合物 - 苯类化合物 - 酚类
• 英文名称: 3,5-bis-(3-hydroxy-4-methoxybenzylidene)tetrahydrothiopyran-4-one
• 英文别名: 3,5-Bis[(3-hydroxy-4-methoxyphenyl)methylidene]thian-4-one；3,5-bis[(3-hydroxy-4-methoxyphenyl)methylidene]thian-4-one
• CAS: 1088178-54-4
• 化学式: C₂₁H₂₀O₅S
• 分子量: 384.453
• InChiKey: WRNUUUREXVLBJO-UHFFFAOYSA-N

计算性质

• 辛醇/水分配系数(LogP)：
  3.5
• 重原子数：
  27
• 可旋转键数：
  4
• 环数：
  3.0
• sp3杂化的碳原子比例：
  0.19
• 拓扑面积：
  101
• 氢给体数：
  2
• 氢受体数：
  6

反应信息

• 作为反应物：
  描述：

  3,5-bis-(3-hydroxy-4-methoxybenzylidene)tetrahydrothiopyran-4-one 在 双氧水 、 溶剂黄146 作用下， 以32.4%的产率得到3,5-bis-(3-hydroxy-4-methoxybenzylidene)-1,1-dioxotetrahydro-1λ⁶-thiopyran-4-one
  参考文献：
  名称：

  Synthesis and Evaluation of Bisbenzylidenedioxotetrahydrothiopranones as Activators of Endoplasmic Reticulum (ER) Stress Signaling Pathways and Apoptotic Cell Death in Acute Promyelocytic Leukemic Cells

  摘要：

  Curcumin is known to trigger ER-stress induced cell death of acute promyelocytic leukemic (APL) cells by intercepting the degradation of nuclear co-repressor (N-CoR) protein which has a key role in the pathogenesis of APL. Replacing the heptadienedione moiety of curcumin with a monocarbonyl cross-conjugated dienone embedded in a tetrahydrothiopyranone dioxide ring resulted in thiopyranone dioxides that were more resilient to hydrolysis and had greater growth inhibitory activities than curcumin on APL cells. Several members intercepted the degradation of misfolded N-CoR and triggered the signaling cascade in the unfolded protein response (UPR) which led to apoptotic cell death. Microarray analysis showed that genes involved in protein processing pathways that were germane to the activation of the UPR were preferentially up-regulated in treated APL cells, supporting the notion that the UPR was a consequential mechanistic pathway affected by thiopyranone dioxides. The Michael acceptor reactivity of the scaffold may have a role in exacerbating ER stress in APL cells.

  DOI：

  10.1021/jm401352a
• 作为产物：
  描述：

  四氢噻喃-4-酮 、 异香兰素 在 盐酸 作用下， 以 乙醇 为溶剂， 以24.2%的产率得到3,5-bis-(3-hydroxy-4-methoxybenzylidene)tetrahydrothiopyran-4-one
  参考文献：
  名称：

  Synthesis and Evaluation of Bisbenzylidenedioxotetrahydrothiopranones as Activators of Endoplasmic Reticulum (ER) Stress Signaling Pathways and Apoptotic Cell Death in Acute Promyelocytic Leukemic Cells

  摘要：

  Curcumin is known to trigger ER-stress induced cell death of acute promyelocytic leukemic (APL) cells by intercepting the degradation of nuclear co-repressor (N-CoR) protein which has a key role in the pathogenesis of APL. Replacing the heptadienedione moiety of curcumin with a monocarbonyl cross-conjugated dienone embedded in a tetrahydrothiopyranone dioxide ring resulted in thiopyranone dioxides that were more resilient to hydrolysis and had greater growth inhibitory activities than curcumin on APL cells. Several members intercepted the degradation of misfolded N-CoR and triggered the signaling cascade in the unfolded protein response (UPR) which led to apoptotic cell death. Microarray analysis showed that genes involved in protein processing pathways that were germane to the activation of the UPR were preferentially up-regulated in treated APL cells, supporting the notion that the UPR was a consequential mechanistic pathway affected by thiopyranone dioxides. The Michael acceptor reactivity of the scaffold may have a role in exacerbating ER stress in APL cells.

  DOI：

  10.1021/jm401352a

文献信息

• Synthesis and Evaluation of Bisbenzylidenedioxotetrahydrothiopranones as Activators of Endoplasmic Reticulum (ER) Stress Signaling Pathways and Apoptotic Cell Death in Acute Promyelocytic Leukemic Cells
  作者：Kheng-Lin Tan、Azhar Ali、Yuhong Du、Haian Fu、Hai-Xiao Jin、Tan-Min Chin、Matiullah Khan、Mei-Lin Go

  DOI：10.1021/jm401352a

  日期：2014.7.24

  Curcumin is known to trigger ER-stress induced cell death of acute promyelocytic leukemic (APL) cells by intercepting the degradation of nuclear co-repressor (N-CoR) protein which has a key role in the pathogenesis of APL. Replacing the heptadienedione moiety of curcumin with a monocarbonyl cross-conjugated dienone embedded in a tetrahydrothiopyranone dioxide ring resulted in thiopyranone dioxides that were more resilient to hydrolysis and had greater growth inhibitory activities than curcumin on APL cells. Several members intercepted the degradation of misfolded N-CoR and triggered the signaling cascade in the unfolded protein response (UPR) which led to apoptotic cell death. Microarray analysis showed that genes involved in protein processing pathways that were germane to the activation of the UPR were preferentially up-regulated in treated APL cells, supporting the notion that the UPR was a consequential mechanistic pathway affected by thiopyranone dioxides. The Michael acceptor reactivity of the scaffold may have a role in exacerbating ER stress in APL cells.