2-hydroxy-4-(methoxymethoxy)-5-(3-methylbut-2-enyl)benzaldehyde | 151359-13-6

• 分子结构分类: 有机化合物 - 有机氧化合物
• 英文名称: 2-hydroxy-4-(methoxymethoxy)-5-(3-methylbut-2-enyl)benzaldehyde
• CAS: 151359-13-6
• 化学式: C₁₄H₁₈O₄
• 分子量: 250.295
• InChiKey: IQTSUCMOPUITAT-UHFFFAOYSA-N

计算性质

• 辛醇/水分配系数(LogP)：
  2.7
• 重原子数：
  18.0
• 可旋转键数：
  6.0
• 环数：
  1.0
• sp3杂化的碳原子比例：
  0.36
• 拓扑面积：
  55.76
• 氢给体数：
  1.0
• 氢受体数：
  4.0

反应信息

• 作为反应物：
  描述：

  2-hydroxy-4-(methoxymethoxy)-5-(3-methylbut-2-enyl)benzaldehyde 、 碘甲烷 在 sodium hydride 作用下， 以 N,N-二甲基甲酰胺 为溶剂， 反应 0.5h， 以92%的产率得到
  参考文献：
  名称：

  Concise synthesis of licochalcone C and its regioisomer, licochalcone H

  摘要：

  Licochalone C (7a) 是一种从膨胀甘草中分离出来的逆查尔酮，具有有效的抗氧化特性并能抑制细菌生长和细胞呼吸。生物学研究表明甘草查尔酮 C 通过降低诱导型一氧化氮合酶的表达和活性以及调节超氧化物歧化酶、过氧化氢酶和谷胱甘肽过氧化物酶活性的抗氧化网络活性来减轻脂多糖和干扰素 γ 诱导的炎症反应。 Licochalcone C 还抑制藤黄微球菌膜部分中的 NADH-细胞色素 C 还原酶。由于甘草查尔酮 C 的药理活性研究正在进行中，并且该化合物的天然产物产率很低，因此我们报告了甘草查尔酮 C (7a) 及其区域异构体（暂称为甘草查尔酮 H (7b)）的简明四步合成，通过使用酸-介导的克莱森-施密特缩合作为关键步骤，总产率分别为 6% 和 20%。

  DOI：

  10.1007/s12272-013-0222-3
• 作为产物：
  描述：

  2-甲基-3-丁烯-2-醇 在 三氟化硼乙醚 、 potassium carbonate 作用下， 以 1,4-二氧六环 、 丙酮 为溶剂， 反应 5.0h， 生成 2-hydroxy-4-(methoxymethoxy)-5-(3-methylbut-2-enyl)benzaldehyde
  参考文献：
  名称：

  Concise synthesis of licochalcone C and its regioisomer, licochalcone H

  摘要：

  Licochalone C (7a) 是一种从膨胀甘草中分离出来的逆查尔酮，具有有效的抗氧化特性并能抑制细菌生长和细胞呼吸。生物学研究表明甘草查尔酮 C 通过降低诱导型一氧化氮合酶的表达和活性以及调节超氧化物歧化酶、过氧化氢酶和谷胱甘肽过氧化物酶活性的抗氧化网络活性来减轻脂多糖和干扰素 γ 诱导的炎症反应。 Licochalcone C 还抑制藤黄微球菌膜部分中的 NADH-细胞色素 C 还原酶。由于甘草查尔酮 C 的药理活性研究正在进行中，并且该化合物的天然产物产率很低，因此我们报告了甘草查尔酮 C (7a) 及其区域异构体（暂称为甘草查尔酮 H (7b)）的简明四步合成，通过使用酸-介导的克莱森-施密特缩合作为关键步骤，总产率分别为 6% 和 20%。

  DOI：

  10.1007/s12272-013-0222-3

文献信息

• JAK2 regulation by licochalcone H inhibits the cell growth and induces apoptosis in oral squamous cell carcinoma
  作者：Ha-Na Oh、Keon Bong Oh、Mee-Hyun Lee、Ji-Hye Seo、Eunae Kim、Goo Yoon、Seung-Sik Cho、Young Sik Cho、Hyun Woo Choi、Jung-II Chae、Jung-Hyun Shim

  DOI：10.1016/j.phymed.2018.09.180

  日期：2019.1

  Background: Licochalconce (LC) H is an artificial compound in the course of synthesizing LCC in 2013. So far, few studies on the effects of LCH have been found in the literature. Despite progress in treatment modalities for oral cancer, the cure from cancer has still limitations.Purpose: The effects of LCH were investigated on human oral squamous cell carcinoma (OSCC) cells to elucidate its mechanisms.Study Design: We explored the mechanism of action of LCH by which it could have effects on JAK2/STAT3 signaling pathway.Methods: To confirm LCH anti-cancer effect, analyzed were MTT assay, DAPI staining, soft agar, kinase assay, molecular docking simulation, flow cytometry and Western blotting analysis.Results: According to docking and molecular dynamics simulations, the predicted pose of the complex LCH and JAK2 seems reasonable and LCH is strongly bound to active JAK2 with opened activation loop. The LCH inhibitor is surrounded by specific ATP-binding pocket in which it is stabilized by forming hydrogen bonds and hydrophobic interactions. It is shown that LCH plays as a competitive inhibitor in an active state of JAK2. LCH caused a dose-dependent decrease in phosphorylation of JAK2 and STAT3. More interestingly, LCH suppressed JAK2 kinase activity in vitro by its direct binding to the JAK2. LCH significantly inhibited the JAK2/STAT3 signaling pathway, causing the down-regulation of target genes such as Bcl-2, survivin, cyclin D1, p21 and p27. In addition, LCH inhibited cell proliferation and colony formation of OSCC cells in a dose- and time-dependent manner, as well as induction of cell apoptosis through extrinsic and intrinsic pathway. The induction of apoptosis in OSCC cells by LCH was evident in the increased production of ROS, loss of mitochondrial membrane potential, release of cyto c, variation of apoptotic proteins and activation of caspase cascade.Conclusion: LCH not only induces apoptosis in OSCC cells through the JAK/STAT3 signaling pathway but also inhibits cell growth. It is proposed that LCH has a promising use for the chemotherapeutic agent of oral cancer.