9-hydroxy-6-(4-hydroxyphenyl)-11H-indeno[1,2-c]quinolin-11-one | 1198747-72-6

• 分子结构分类: 有机化合物 - 有机杂环化合物 - 喹啉及其衍生物
• 英文名称: 9-hydroxy-6-(4-hydroxyphenyl)-11H-indeno[1,2-c]quinolin-11-one
• 英文别名: 9-Hydroxy-6-(4-hydroxyphenyl)indeno[1,2-c]quinolin-11-one；9-hydroxy-6-(4-hydroxyphenyl)indeno[1,2-c]quinolin-11-one
• CAS: 1198747-72-6
• 化学式: C₂₂H₁₃NO₃
• 分子量: 339.35
• InChiKey: DSHQDIQITCXNTO-UHFFFAOYSA-N

计算性质

• 辛醇/水分配系数(LogP)：
  4.3
• 重原子数：
  26
• 可旋转键数：
  1
• 环数：
  5.0
• sp3杂化的碳原子比例：
  0.0
• 拓扑面积：
  70.4
• 氢给体数：
  2
• 氢受体数：
  4

反应信息

• 作为反应物：
  描述：

  9-hydroxy-6-(4-hydroxyphenyl)-11H-indeno[1,2-c]quinolin-11-one 在 盐酸羟胺 作用下， 以 乙二醇乙醚 为溶剂， 反应 3.0h， 以61%的产率得到9-hydroxy-6-(4-hydroxyphenyl)-11H-indeno[1,2-c]quinolin-11-one oxime hydrochloride
  参考文献：
  名称：

  Synthesis and antiproliferative evaluation of 6-aryl-11-iminoindeno[1,2-c]quinoline derivatives

  摘要：

  A number of 6-aryl-11-iminoindeno[1,2-c]quinoline derivatives were synthesized and evaluated for their antiproliferative activities. Among them, (E)-6-{4-[3-(dimethylamino)propoxy]phenyl}-2-fluoro-9-hydroxy-11H-indeno[1,2-c]quinolin-11-one O-3-(dimethylamino)propyl oxime (23a) was the most active, exhibited GI(50) values of 0.64, 0.39, 0.55, 0.67, and 0.65 mu M against the growth of Hep G2, Hep 3B, A549, H1299, and MDA-MB-231, respectively. Compound 23a inhibited the growth of hepatoma cell lines in a dose-and time-dependent manner. The proportion of cells was decreased in the G1 and accumulated in G2/M phase after 12 h treatment of 23a, while the hypodiploid (sub-G0/G1 phase) cells increased. Further investigations have shown that 23a induced cell cycle arrest at G2/M phase and induce apoptosis via activation of p53, Bax, and caspase-8 which consequently cause cell death. (C) 2011 Elsevier Ltd. All rights reserved.

  DOI：

  10.1016/j.bmc.2011.10.014
• 作为产物：
  描述：

  9-methoxy-6-(4-methoxyphenyl)-11H-indeno[1,2-c]quinolin-11-one 在 氢溴酸 作用下， 反应 48.0h， 以78%的产率得到9-hydroxy-6-(4-hydroxyphenyl)-11H-indeno[1,2-c]quinolin-11-one
  参考文献：
  名称：

  Synthesis and antiproliferative evaluation of 6-arylindeno[1,2-c]quinoline derivatives

  摘要：

  A number of 6-arylindeno[1,2-c]quinoline derivatives were synthesized and evaluated for their antiproliferative activities against the growth of five cancer cell lines including human hepatocelluar carcinoma (Hep G2, Hep 3B and Hep2.2.1), non-small cell lung cancer (A549 and H1299), and normal diploid embryonic lung cell line (MRC-5). The preliminary results indicated that 9-(3-(dimethylamino) propoxy)-6-(4-(3-(dimethylamino)propoxy)phenyl)-2-fluoro-11H-indeno[1,2-c]quinolin-11-one (14c) was the most potent with GI(50) values of 0.61, 0.67, 0.59, and 0.72 mu M against the growth of Hep G2, Hep 3B, Hep 2.2.1, and H1299 cells, respectively. Results have also shown that 2,9-bis(3-(dimethylamino)propoxy)-6-(4-(3-(dimethylamino)propoxy)phenyl)-11H-indeno[1,2-c]quinolin-11-one (17), which exhibited GI(50) of 0.60 and 0.68 mu M against the growth of Hep G2 and A549, respectively, was more active than the positive topotecan and irinotecan. Compound 17 was less toxic than topotecan against the growth of normal cell (MRC-5) and therefore, was selected for further evaluation. Results indicated that compound 17 induce cell cycle arrest in G2/M phase, DNA fragmentation, and disrupt the microtubule network in A549 cells. The apoptotic induction may through the cleavage of PARP. (C) 2009 Elsevier Ltd. All rights reserved.

  DOI：

  10.1016/j.bmc.2009.09.021

文献信息

• Synthesis and antiproliferative evaluation of 6-arylindeno[1,2-c]quinoline derivatives
  作者：Chih-Hua Tseng、Yeh-Long Chen、Kuin-Yu Chung、Chih-Mei Cheng、Chi-Huei Wang、Cherng-Chyi Tzeng

  DOI：10.1016/j.bmc.2009.09.021

  日期：2009.11

  A number of 6-arylindeno[1,2-c]quinoline derivatives were synthesized and evaluated for their antiproliferative activities against the growth of five cancer cell lines including human hepatocelluar carcinoma (Hep G2, Hep 3B and Hep2.2.1), non-small cell lung cancer (A549 and H1299), and normal diploid embryonic lung cell line (MRC-5). The preliminary results indicated that 9-(3-(dimethylamino) propoxy)-6-(4-(3-(dimethylamino)propoxy)phenyl)-2-fluoro-11H-indeno[1,2-c]quinolin-11-one (14c) was the most potent with GI(50) values of 0.61, 0.67, 0.59, and 0.72 mu M against the growth of Hep G2, Hep 3B, Hep 2.2.1, and H1299 cells, respectively. Results have also shown that 2,9-bis(3-(dimethylamino)propoxy)-6-(4-(3-(dimethylamino)propoxy)phenyl)-11H-indeno[1,2-c]quinolin-11-one (17), which exhibited GI(50) of 0.60 and 0.68 mu M against the growth of Hep G2 and A549, respectively, was more active than the positive topotecan and irinotecan. Compound 17 was less toxic than topotecan against the growth of normal cell (MRC-5) and therefore, was selected for further evaluation. Results indicated that compound 17 induce cell cycle arrest in G2/M phase, DNA fragmentation, and disrupt the microtubule network in A549 cells. The apoptotic induction may through the cleavage of PARP. (C) 2009 Elsevier Ltd. All rights reserved.
• Synthesis and antiproliferative evaluation of 6-aryl-11-iminoindeno[1,2-c]quinoline derivatives
  作者：Chih-Hua Tseng、Cherng-Chyi Tzeng、Kuin-Yu Chung、Chai-Lin Kao、Chih-Yao Hsu、Chih-Mei Cheng、Keng-Shiang Huang、Yeh-Long Chen

  DOI：10.1016/j.bmc.2011.10.014

  日期：2011.12

  A number of 6-aryl-11-iminoindeno[1,2-c]quinoline derivatives were synthesized and evaluated for their antiproliferative activities. Among them, (E)-6-4-[3-(dimethylamino)propoxy]phenyl}-2-fluoro-9-hydroxy-11H-indeno[1,2-c]quinolin-11-one O-3-(dimethylamino)propyl oxime (23a) was the most active, exhibited GI(50) values of 0.64, 0.39, 0.55, 0.67, and 0.65 mu M against the growth of Hep G2, Hep 3B, A549, H1299, and MDA-MB-231, respectively. Compound 23a inhibited the growth of hepatoma cell lines in a dose-and time-dependent manner. The proportion of cells was decreased in the G1 and accumulated in G2/M phase after 12 h treatment of 23a, while the hypodiploid (sub-G0/G1 phase) cells increased. Further investigations have shown that 23a induced cell cycle arrest at G2/M phase and induce apoptosis via activation of p53, Bax, and caspase-8 which consequently cause cell death. (C) 2011 Elsevier Ltd. All rights reserved.