(2,3-dimethoxy-benzylsulfanyl)-acetic acid | 100059-50-5

• 分子结构分类: 有机化合物 - 苯类化合物 - 苯和取代衍生物
• 英文名称: (2,3-dimethoxy-benzylsulfanyl)-acetic acid
• 英文别名: (2,3-Dimethoxy-benzylmercapto)-essigsaeure；2-[(2,3-Dimethoxyphenyl)methylsulfanyl]acetic acid
• CAS: 100059-50-5
• 化学式: C₁₁H₁₄O₄S
• 分子量: 242.296
• InChiKey: KJJGMBIDYLZXIJ-UHFFFAOYSA-N

计算性质

• 辛醇/水分配系数(LogP)：
  1.9
• 重原子数：
  16
• 可旋转键数：
  6
• 环数：
  1.0
• sp3杂化的碳原子比例：
  0.36
• 拓扑面积：
  81.1
• 氢给体数：
  1
• 氢受体数：
  5

反应信息

• 作为反应物：
  描述：

  (2,3-dimethoxy-benzylsulfanyl)-acetic acid 在 草酰氯 、 N,N-二甲基甲酰胺 作用下， 以 二氯甲烷 为溶剂， 反应 1.0h， 生成
  参考文献：
  名称：

  Discovery of Novel 4-Arylisochromenes as Anticancer Agents Inhibiting Tubulin Polymerization

  摘要：

  XJP-L (8), a derivative of the natural product (+/-)-7,8-dihydroxy-3-methylisochroman-4-one isolated from the peel of Musa sapien turn L., was found to exhibit weak inhibitory activity of tubulin polymerization (IC50 = 10.6 mu M) in our previous studies. Thus, a series of 4-arylisochromene derivatives were prepared by incorporating the trimethoxyphenyl moiety into 8, among which compound (+/-)-19b was identified as the most potent compound with IC50 values ranging from 10 to 25 nM against a panel of cancer cell lines. Further mechanism studies demonstrated that (+/-)-19b disrupted the intracellular microtubule network, caused G2/M phase arrest, induced cell apoptosis, and depolarized mitochondria of K562 cells. Moreover, ()-19b exhibited potent in vitro antivascular and in vivo antitumor activities. Notably, the R-configured enantiomer of (+/-)-19b, which was prepared by chiral separation, was slightly more potent than (+/-)-19b and was much more potent than the S-configured enantiomer in both antiproliferative and antitubulin assays. Our findings suggest that (+/-)-19b deserves further research as a potential antitubulin agent for the treatment of cancers.

  DOI：

  10.1021/acsmedchemlett.8b00217
• 作为产物：
  描述：

  2,3-二甲氧基苄基溴 在 水 、 potassium carbonate 、 sodium hydroxide 作用下， 以 甲醇 、 乙腈 为溶剂， 反应 1.0h， 生成 (2,3-dimethoxy-benzylsulfanyl)-acetic acid
  参考文献：
  名称：

  Discovery of Novel 4-Arylisochromenes as Anticancer Agents Inhibiting Tubulin Polymerization

  摘要：

  XJP-L (8), a derivative of the natural product (+/-)-7,8-dihydroxy-3-methylisochroman-4-one isolated from the peel of Musa sapien turn L., was found to exhibit weak inhibitory activity of tubulin polymerization (IC50 = 10.6 mu M) in our previous studies. Thus, a series of 4-arylisochromene derivatives were prepared by incorporating the trimethoxyphenyl moiety into 8, among which compound (+/-)-19b was identified as the most potent compound with IC50 values ranging from 10 to 25 nM against a panel of cancer cell lines. Further mechanism studies demonstrated that (+/-)-19b disrupted the intracellular microtubule network, caused G2/M phase arrest, induced cell apoptosis, and depolarized mitochondria of K562 cells. Moreover, ()-19b exhibited potent in vitro antivascular and in vivo antitumor activities. Notably, the R-configured enantiomer of (+/-)-19b, which was prepared by chiral separation, was slightly more potent than (+/-)-19b and was much more potent than the S-configured enantiomer in both antiproliferative and antitubulin assays. Our findings suggest that (+/-)-19b deserves further research as a potential antitubulin agent for the treatment of cancers.

  DOI：

  10.1021/acsmedchemlett.8b00217

文献信息

• Freudenberg et al., Chemische Berichte, 1959, vol. 92, p. 807,817
  作者：Freudenberg et al.

  DOI：——

  日期：——
• Discovery of Novel 4-Arylisochromenes as Anticancer Agents Inhibiting Tubulin Polymerization
  作者：Wenlong Li、Wen Shuai、Feijie Xu、Honghao Sun、Shengtao Xu、Hong Yao、Jie Liu、Hequan Yao、Zheying Zhu、Jinyi Xu

  DOI：10.1021/acsmedchemlett.8b00217

  日期：2018.10.11

  XJP-L (8), a derivative of the natural product (+/-)-7,8-dihydroxy-3-methylisochroman-4-one isolated from the peel of Musa sapien turn L., was found to exhibit weak inhibitory activity of tubulin polymerization (IC50 = 10.6 mu M) in our previous studies. Thus, a series of 4-arylisochromene derivatives were prepared by incorporating the trimethoxyphenyl moiety into 8, among which compound (+/-)-19b was identified as the most potent compound with IC50 values ranging from 10 to 25 nM against a panel of cancer cell lines. Further mechanism studies demonstrated that (+/-)-19b disrupted the intracellular microtubule network, caused G2/M phase arrest, induced cell apoptosis, and depolarized mitochondria of K562 cells. Moreover, ()-19b exhibited potent in vitro antivascular and in vivo antitumor activities. Notably, the R-configured enantiomer of (+/-)-19b, which was prepared by chiral separation, was slightly more potent than (+/-)-19b and was much more potent than the S-configured enantiomer in both antiproliferative and antitubulin assays. Our findings suggest that (+/-)-19b deserves further research as a potential antitubulin agent for the treatment of cancers.