3-hydroxy-1-naphthalen-2-ylbut-2-en-1-one

• 分子结构分类: 有机化合物 - 苯类化合物 - 萘
• 英文名称: 3-hydroxy-1-naphthalen-2-ylbut-2-en-1-one
• 化学式: C₁₄H₁₂O₂
• 分子量: 212.248
• InChiKey: RPXMDPFQHCCMND-UHFFFAOYSA-N

计算性质

• 辛醇/水分配系数(LogP)：
  3.48
• 重原子数：
  16.0
• 可旋转键数：
  2.0
• 环数：
  2.0
• sp3杂化的碳原子比例：
  0.07
• 拓扑面积：
  37.3
• 氢给体数：
  1.0
• 氢受体数：
  2.0

反应信息

• 作为反应物：
  描述：

  3-hydroxy-1-naphthalen-2-ylbut-2-en-1-one 、 苯胺 在 盐酸 作用下， 以 水 、 甲苯 为溶剂， 以0.65 g的产率得到
  参考文献：
  名称：

  Hypoxia-Sensitive Metal β-Ketoiminato Complexes Showing Induced Single-Strand DNA Breaks and Cancer Cell Death by Apoptosis

  摘要：

  A series of ruthenium and iridium complexes have been synthesized and characterized with 20 novel crystal structures discussed. The library of beta-ketoiminato complexes has been shown to be active against MCF-7 (human breast carcinoma); HT-29 (human colon carcinoma), A2780 (hint-tan ovarian carcinoma), and A2780cis (cisplatin-resistant human ovarian carcinoma) cell lines, with selected complexes' being more than three tithes, as active as cisplatin against the A2780cis cell line. Selected complexes were also tested against the noncancerous ARPE-19 (retinal pigment epithelial cells) cell line, in Order to evaluate the complexes selectivity for cancer cells. Complexes have also been shown to be highly active under hypoxic,conditions, with the activities of some complexes increasing with a decrease in O-2 concentration. The enzyme thioredoxin reductase is overexpressed in cancer cells, and complexes reported herein have the advantage of inhibiting this enzyme, with IC50 values measured. in the nanomolar range. The anticancer activity of these complexes was further investigated to determine whether activity is due to effects on cellular growth or cell survival. The complexes were flail-id to induce significant levels of cancer cell,death by apoptosis with levels induced correlating closely with activity in chemosensitivity studies, As a possible cause of,cell death, the ability of the complexes to induce damage to cellular DNA was also assessed. The complexes failed to induce double-strand DNA breaks or DNA cross-linking but induced significant levels of single-strand DNA breaks, indicating a mechanism of action different from that of cisplatin.

  DOI：

  10.1021/acs.jmedchem.5b00455
• 作为产物：
  描述：

  乙酸乙酯 、 2-萘乙酮 在 sodium ethanolate 、 硫酸 作用下， 生成 3-hydroxy-1-naphthalen-2-ylbut-2-en-1-one
  参考文献：
  名称：

  Hypoxia-Sensitive Metal β-Ketoiminato Complexes Showing Induced Single-Strand DNA Breaks and Cancer Cell Death by Apoptosis

  摘要：

  A series of ruthenium and iridium complexes have been synthesized and characterized with 20 novel crystal structures discussed. The library of beta-ketoiminato complexes has been shown to be active against MCF-7 (human breast carcinoma); HT-29 (human colon carcinoma), A2780 (hint-tan ovarian carcinoma), and A2780cis (cisplatin-resistant human ovarian carcinoma) cell lines, with selected complexes' being more than three tithes, as active as cisplatin against the A2780cis cell line. Selected complexes were also tested against the noncancerous ARPE-19 (retinal pigment epithelial cells) cell line, in Order to evaluate the complexes selectivity for cancer cells. Complexes have also been shown to be highly active under hypoxic,conditions, with the activities of some complexes increasing with a decrease in O-2 concentration. The enzyme thioredoxin reductase is overexpressed in cancer cells, and complexes reported herein have the advantage of inhibiting this enzyme, with IC50 values measured. in the nanomolar range. The anticancer activity of these complexes was further investigated to determine whether activity is due to effects on cellular growth or cell survival. The complexes were flail-id to induce significant levels of cancer cell,death by apoptosis with levels induced correlating closely with activity in chemosensitivity studies, As a possible cause of,cell death, the ability of the complexes to induce damage to cellular DNA was also assessed. The complexes failed to induce double-strand DNA breaks or DNA cross-linking but induced significant levels of single-strand DNA breaks, indicating a mechanism of action different from that of cisplatin.

  DOI：

  10.1021/acs.jmedchem.5b00455