3-(4-methoxyphenyl)quinolin-2-carbaldehyde | 1422526-44-0

• 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: 3-(4-methoxyphenyl)quinolin-2-carbaldehyde
• 英文别名: 3-(4-Methoxyphenyl)quinoline-2-carbaldehyde；3-(4-methoxyphenyl)quinoline-2-carbaldehyde
• CAS: 1422526-44-0
• 化学式: C₁₇H₁₃NO₂
• 分子量: 263.296
• InChiKey: FVUYCCLAHUCUIX-UHFFFAOYSA-N

计算性质

• 辛醇/水分配系数(LogP)：
  3.6
• 重原子数：
  20
• 可旋转键数：
  3
• 环数：
  3.0
• sp3杂化的碳原子比例：
  0.06
• 拓扑面积：
  39.2
• 氢给体数：
  0
• 氢受体数：
  3

反应信息

• 作为反应物：
  描述：

  3-(4-methoxyphenyl)quinolin-2-carbaldehyde 生成 (E)-3-[3-(4-methoxyphenyl)quinolin-2-yl]-1-(3,4,5-trimethoxyphenyl)prop-2-en-1-one
  参考文献：
  名称：

  Discovery of 3-phenylquinolinylchalcone derivatives as potent and selective anticancer agents against breast cancers

  摘要：

  A number of 3-phenylquinolinylchalcone derivatives were synthesized and evaluated in vitro for their antiproliferative activities against three breast cancer cell lines (MCF-7, MDA-MB-231, and SKBR-3), and a non-cancer normal epithelial cell line (H184B5F5/M10). Among them, (E)-3-[3-(4-methoxyphenyl)quinolin-2-yl]-1-(3,4,5-trimethoxyphenyl)prop-2-en-1-one (7) was active against the growth of MCF-7, MDA-MB-231, and SKBR-3 with IC50 values of 1.05, 0.75, and 0.78 mu M respectively without significant cytotoxicity to the normal H184B5F5/M10 cell line and therefore, was selected as a new lead for further mechanism studies. Results indicated that compound 7 inhibited the polymerization of tubulins, induced G2/M cell cycle arrest via modulation of the cyclin B1, cdk1 and CDC25. Compound 7 ultimately induced cell apoptosis by the increase of apoptotic protein Bax and the decrease of anti-apoptotic protein Bcl-2. In addition, PARP was cleaved while caspase-3 and -8 activities were induced after the treatment of compound 7 for 24 h in a concentration-dependent manner. Thus, compound 7 induces cell cycle arrest at G2/M phase via cleavage of PARP, induces caspase-3 and -8 activities and consequently to cause the cell death. Further study on the structure optimization of 7 is ongoing. (C) 2015 Elsevier Masson SAS. All rights reserved.

  DOI：

  10.1016/j.ejmech.2015.04.054
• 作为产物：
  描述：

  3-(4-methoxyphenyl)-2-methylquinoline-4-carboxylic acid 在 selenium(IV) oxide 作用下， 以 1,4-二氧六环 为溶剂， 反应 6.0h， 生成 3-(4-methoxyphenyl)quinolin-2-carbaldehyde
  参考文献：
  名称：

  Synthesis and antiproliferative evaluation of 3-phenylquinolinylchalcone derivatives against non-small cell lung cancers and breast cancers

  摘要：

  Certain 3-phenylquinolinylchalcone derivatives were synthesized and evaluated for their antiproliferative activities. Among them, (E)-3-(3-(4-methoxyphenyl)quinolin-2-yl)-1-phenylprop-2-en-1-one (6a) and (E)-1-(5-bromothiophen-2-yl)-3-(3-(4-methoxyphenyl)quinolin-2-yeprop-2-en-1-one (11) were identified as potential lead compounds for further development. Compound 6a was active against the growth of H1299 and SKBR-3 with IC50 values of 1.41 and 0.70 mu M respectively which was more active than the positive topotecan (IC50 values of 6.02 and 8.91 mu M respectively). Compound 11 exhibited an IC50 value of less than 0.10 mu M against the growth of MDA-MB231, and non-cytotoxic to the normal mammary epithelial cell (H184B5F5/M10). Mechanism studies indicated that compound 11 induced cell cycle arrest at G2/M phase followed by activation of caspase-3, cleavage of PARP, and consequently caused the cell death. (C) 2012 Elsevier Masson SAS. All rights reserved.

  DOI：

  10.1016/j.ejmech.2012.11.027

文献信息

• Synthesis, antiproliferative and anti-dengue virus evaluations of 2-aroyl-3-arylquinoline derivatives
  作者：Chih-Hua Tseng、Chun-Kuang Lin、Yeh-Long Chen、Chih-Yao Hsu、Huey-Nan Wu、Chin-Kai Tseng、Jin-Ching Lee

  DOI：10.1016/j.ejmech.2014.03.074

  日期：2014.5

  A number of 2-aroy1-3-arylquinoline derivatives was synthesized and evaluated for their anti-Dengue virus activity. Both 2-(hydroxyphenylmethyl)-3-(4-methoxyphenyl)quinoline (13a) and 2-(4-hydroxybenzoyl)-3-(4-hydroxyphenyl)quinoline (17) were found to significantly inhibit the DENV2 RNA expression in Huh-7-DV-Fluc cells with a potency approximately equal to that of ribavirin and the inhibition is in a dose-dependent manner. Compounds 13a and 17 reduced DENV replication in both viral protein and mRNA levels, and no significant cell cytotoxicity was detected, with greater than 50% viability of Huh-7-DV-Fluc cells at a concentration of 100 mu M. However, significant cytotoxicity was detected for the positive ribavirin. In addition, we performed infectious assay to further verify the inhibitory activity of 13a and 17 on DENV replication in protein and RNA levels. On the other hand, compounds 19a-19c exhibited IC50 values ranged from 4.47 to 8.68 1iM against A549, H1299, MCF-7, and Huh-7 which were approximately equal potent to the positive topotecan. Structural optimization of lead compounds, 13a and 17, and their detailed molecular mechanism of action are ongoing. (C) 2014 Elsevier Masson SAS. All rights reserved.
• Synthesis and antiproliferative evaluation of 3-phenylquinolinylchalcone derivatives against non-small cell lung cancers and breast cancers
  作者：Chih-Hua Tseng、Yeh-Long Chen、Chih-Yao Hsu、Tzu-Chiang Chen、Chih-Mei Cheng、Hsien-Cheng Tso、Yan-Jia Lu、Cherng-Chyi Tzeng

  DOI：10.1016/j.ejmech.2012.11.027

  日期：2013.1

  Certain 3-phenylquinolinylchalcone derivatives were synthesized and evaluated for their antiproliferative activities. Among them, (E)-3-(3-(4-methoxyphenyl)quinolin-2-yl)-1-phenylprop-2-en-1-one (6a) and (E)-1-(5-bromothiophen-2-yl)-3-(3-(4-methoxyphenyl)quinolin-2-yeprop-2-en-1-one (11) were identified as potential lead compounds for further development. Compound 6a was active against the growth of H1299 and SKBR-3 with IC50 values of 1.41 and 0.70 mu M respectively which was more active than the positive topotecan (IC50 values of 6.02 and 8.91 mu M respectively). Compound 11 exhibited an IC50 value of less than 0.10 mu M against the growth of MDA-MB231, and non-cytotoxic to the normal mammary epithelial cell (H184B5F5/M10). Mechanism studies indicated that compound 11 induced cell cycle arrest at G2/M phase followed by activation of caspase-3, cleavage of PARP, and consequently caused the cell death. (C) 2012 Elsevier Masson SAS. All rights reserved.
• Discovery of 3-phenylquinolinylchalcone derivatives as potent and selective anticancer agents against breast cancers
  作者：Chih-Hua Tseng、Cherng-Chyi Tzeng、Chih-Yao Hsu、Chih-Mei Cheng、Chia-Ning Yang、Yeh-Long Chen

  DOI：10.1016/j.ejmech.2015.04.054

  日期：2015.6

  A number of 3-phenylquinolinylchalcone derivatives were synthesized and evaluated in vitro for their antiproliferative activities against three breast cancer cell lines (MCF-7, MDA-MB-231, and SKBR-3), and a non-cancer normal epithelial cell line (H184B5F5/M10). Among them, (E)-3-[3-(4-methoxyphenyl)quinolin-2-yl]-1-(3,4,5-trimethoxyphenyl)prop-2-en-1-one (7) was active against the growth of MCF-7, MDA-MB-231, and SKBR-3 with IC50 values of 1.05, 0.75, and 0.78 mu M respectively without significant cytotoxicity to the normal H184B5F5/M10 cell line and therefore, was selected as a new lead for further mechanism studies. Results indicated that compound 7 inhibited the polymerization of tubulins, induced G2/M cell cycle arrest via modulation of the cyclin B1, cdk1 and CDC25. Compound 7 ultimately induced cell apoptosis by the increase of apoptotic protein Bax and the decrease of anti-apoptotic protein Bcl-2. In addition, PARP was cleaved while caspase-3 and -8 activities were induced after the treatment of compound 7 for 24 h in a concentration-dependent manner. Thus, compound 7 induces cell cycle arrest at G2/M phase via cleavage of PARP, induces caspase-3 and -8 activities and consequently to cause the cell death. Further study on the structure optimization of 7 is ongoing. (C) 2015 Elsevier Masson SAS. All rights reserved.