1-hydroxy-3-[3-bromo-propoxy]-9,10-anthraquinone | 333407-07-1

• 分子结构分类: 有机化合物 - 苯类化合物 - 蒽
• 英文名称: 1-hydroxy-3-[3-bromo-propoxy]-9,10-anthraquinone
• 英文别名: 1-Hydroxy-3-(3-bromopropoxy)-9,10-anthraquinone；3-(3-bromopropoxy)-1-hydroxyanthracene-9,10-dione
• CAS: 333407-07-1
• 化学式: C₁₇H₁₃BrO₄
• 分子量: 361.192
• InChiKey: KHHYRDXZGUEGPM-UHFFFAOYSA-N

物化性质

• 沸点：
  564.0±50.0 °C(Predicted)
• 密度：
  1.586±0.06 g/cm3(Predicted)

计算性质

• 辛醇/水分配系数(LogP)：
  4.6
• 重原子数：
  22
• 可旋转键数：
  4
• 环数：
  3.0
• sp3杂化的碳原子比例：
  0.18
• 拓扑面积：
  63.6
• 氢给体数：
  1
• 氢受体数：
  4

反应信息

• 作为反应物：
  描述：

  异丙醇胺 、 1-hydroxy-3-[3-bromo-propoxy]-9,10-anthraquinone 以 乙醇 为溶剂， 反应 1.0h， 以28%的产率得到1-hydroxy-3-[3-(2-hydroxypropylamino)propoxy]-9,10-anthraquinone hydrochloride
  参考文献：
  名称：

  Anthraquinone derivatives induce G2/M cell cycle arrest and apoptosis in NTUB1 cells

  摘要：

  Thirteen anthraquinone derivatives 5-17 including two 3-(3-alkylaminopropoxy)-9,10-anthraquinone (NHA) derivatives 5 and 6, and 11 1-hydroxy-3-(3-alkylaminopropoxy)-9,10-anthraquinone (MHA) derivatives 7-17 were synthesized, evaluated for cytotoxicities against two cancer cell lines, and assayed the generation of reactive oxygen species (ROS) in NTUB1 cells (a human bladder carcinoma cell line). Compound 9 bearing a pyrrolidinyl group induced the stronger cytotoxic effect than those of other synthesized NHA and MHA derivatives. Exposure of NTUB1 cells to, 9, 13, and 17 for 24 h significantly increased the production of ROS, respectively. Flow cytometric analysis exhibited that the exposure of NTUB1 cells to the selective 9 led to the G2/M phase arrest accompanied by an increase of apoptotic cell death after the incubation for 24 h. Compound 9 induced up-regulation of cyclinB1 and p21 expressions. Biological results suggested that the induction of G2/M arrest, apoptosis, and cell death by 9 may associate with increased expression of p21 and cyclin B1, elevation of Bax and p53 levels, and generation of ROS in the cell. In conclusion, these series of compounds may be used as anticancer agents. (C) 2011 Elsevier Ltd. All rights reserved.

  DOI：

  10.1016/j.bmc.2011.07.021
• 作为产物：
  描述：

  1,3-二羥蒽醌 、 1,3-二溴丙烷 在 氢氧化钾 作用下， 以 甲醇 为溶剂， 以40%的产率得到1-hydroxy-3-[3-bromo-propoxy]-9,10-anthraquinone
  参考文献：
  名称：

  Synthesis and cytotoxic effect of 1,3-dihydroxy-9,10-anthraquinone derivatives

  摘要：

  1,3-Dihydroxy-9,10-anthraquinone (4) was reacted with epichlorohydrin or 1,omega -dibromo-alkane to yield 1-hydroxy-3-(2,3-epoxypropoxy)-9, 10-anthraquinone (5) and 1-hydroxy-3-(3-chloro-2-hydroxypropoxy) (6) or 1-hydroxy-3-(omega -bromoalkoxy)-9,10-anthraquinone. Ring-opening of the epoxide (5) or 1-hydroxy-3-(omega -bromoalkoxy)-9,10-anthraquinones with appropriate amines, afforded various 1-hydroxy-3-(3-alkylamino-2-hydroxypropoxy)-9,10-anthraquinones. The synthetic compounds were tested in vitro inhibition of human T-24, Hep 3B, Hep G2, SiHa, HT-3, PLC/PRF/5 and 212 cells. Almost all compounds showed significant inhibitory activity against several different cancer cell lines. Structure-activity analysis indicated epoxidation of the hydroxyanthraquinone increased cytotoxicity against tumour cells, but ring-opening of the epoxide group with amine did not enhance the cytotoxic activity. The phosphatidylserine (PS) externalization and DNA fragmentation in SiHa cells were significantly observed after 48 h incubation with selected compound 19. The results show that 19 cause cell death by apoptosis. (C) 2000 Editions scientifiques et medicales Elsevier SAS.

  DOI：

  10.1016/s0223-5234(00)01190-9

文献信息

• 1,3-Dihydroxyl-9,10-anthraquinone and 3-[(3-amino)-propoxy]- 9,10-anthraquinone derivatives and pharmaceutical compositions comprising the same
  申请人：Lin Chun-Nan

  公开号：US20080027141A1

  公开（公告）日：2008-01-31

  Disclosed herein are 1,3-dihydroxyl-9,10-anthraquinone and 3-[(3-amino)-propoxy]-9,10-anthraquinone derivatives, in particular 1,3-dihydroxy-4-prenyl-9,10-anthraquinone and 3-[3-(4-methylpiperazinyl)-propoxy]-9,10-anthraquinone, which are found to have inhibitory activities against several types of human tumor/cancer cells and thus can be used in the manufacture of pharmaceutical compositions for use in the treatment of tumors/cancers.

  本文披露了1,3-二羟基-9,10-蒽醌和3-[(3-氨基)-丙氧基]-9,10-蒽醌衍生物，特别是1,3-二羟基-4-异戊烯基-9,10-蒽醌和3-[3-(4-甲基哌嗪基)-丙氧基]-9,10-蒽醌，发现它们具有对几种人类肿瘤/癌细胞的抑制活性，因此可用于制造用于治疗肿瘤/癌症的药物组合物。
• Design, synthesis and cytotoxic effect of hydroxy- and 3-alkylaminopropoxy-9,10-anthraquinone derivatives
  作者：Chi-Huang Teng、Shen-Jeu Won、Chun-Nan Lin

  DOI：10.1016/j.bmc.2005.03.001

  日期：2005.5

  In previous paper, we have reported the synthesis and the cytotoxic effect of 1,3-dihydroxy-9,10-anthraquinone derivatives. For further design of more potent compounds, a new series of 1-hydroxy-3-(3-alkylaminopropoxy)-9,10-anthraquinones and 3-(3-alkylaminopropoxy)-9,10-anthraquinones have been synthesized. The cytotoxicity of synthetic compounds were evaluated against human Hep G2, Hep 3B and HT-29

  在以前的论文中，我们已经报道了1,3-二羟基-9,10-蒽醌衍生物的合成和细胞毒性作用。为了进一步设计更有效的化合物，已经合成了一系列新的1-羟基-3-（3-烷基氨基丙氧基）-9,10-蒽醌和3-（3-烷基氨基丙氧基）-9,10-蒽醌。评估了合成化合物对人类Hep G2，Hep 3B和HT-29细胞的细胞毒性。几乎所有化合物在体外均显示出对Hep G2，Hep 3B和HT-29细胞系的显着抑制活性。化合物5以浓度依赖的方式表现出针对Hep G2的选择性细胞毒性，ED50值为1.23 +/- 0.05 microM。结构活性分析表明，大多数1-羟基-3-（3-烷基氨基-2-羟基丙氧基）-9 10-蒽醌在体外对Hep 3B细胞系显示出比1-羟基-3-或3-（3-烷基氨基丙氧基）-9,10-蒽醌更强的细胞毒性作用。与选择性化合物16孵育72小时后，显着观察到亚G1细胞阶段和MCF-7细胞DNA片
• Anthraquinone derivatives induce G2/M cell cycle arrest and apoptosis in NTUB1 cells
  作者：Huang-Yao Tu、A-Mei Huang、Chi-Huang Teng、Tzyh-Chyuan Hour、Shyh-Chyun Yang、Yeong-Shiau Pu、Chun-Nan Lin

  DOI：10.1016/j.bmc.2011.07.021

  日期：2011.9

  Thirteen anthraquinone derivatives 5-17 including two 3-(3-alkylaminopropoxy)-9,10-anthraquinone (NHA) derivatives 5 and 6, and 11 1-hydroxy-3-(3-alkylaminopropoxy)-9,10-anthraquinone (MHA) derivatives 7-17 were synthesized, evaluated for cytotoxicities against two cancer cell lines, and assayed the generation of reactive oxygen species (ROS) in NTUB1 cells (a human bladder carcinoma cell line). Compound 9 bearing a pyrrolidinyl group induced the stronger cytotoxic effect than those of other synthesized NHA and MHA derivatives. Exposure of NTUB1 cells to, 9, 13, and 17 for 24 h significantly increased the production of ROS, respectively. Flow cytometric analysis exhibited that the exposure of NTUB1 cells to the selective 9 led to the G2/M phase arrest accompanied by an increase of apoptotic cell death after the incubation for 24 h. Compound 9 induced up-regulation of cyclinB1 and p21 expressions. Biological results suggested that the induction of G2/M arrest, apoptosis, and cell death by 9 may associate with increased expression of p21 and cyclin B1, elevation of Bax and p53 levels, and generation of ROS in the cell. In conclusion, these series of compounds may be used as anticancer agents. (C) 2011 Elsevier Ltd. All rights reserved.
• Synthesis and cytotoxic effect of 1,3-dihydroxy-9,10-anthraquinone derivatives
  作者：Bai-Luh Wei、Szu-Huei Wu、Mei-Ing Chung、Shen-Jeu Won、Chun-Nan Lin

  DOI：10.1016/s0223-5234(00)01190-9

  日期：2000.12

  1,3-Dihydroxy-9,10-anthraquinone (4) was reacted with epichlorohydrin or 1,omega -dibromo-alkane to yield 1-hydroxy-3-(2,3-epoxypropoxy)-9, 10-anthraquinone (5) and 1-hydroxy-3-(3-chloro-2-hydroxypropoxy) (6) or 1-hydroxy-3-(omega -bromoalkoxy)-9,10-anthraquinone. Ring-opening of the epoxide (5) or 1-hydroxy-3-(omega -bromoalkoxy)-9,10-anthraquinones with appropriate amines, afforded various 1-hydroxy-3-(3-alkylamino-2-hydroxypropoxy)-9,10-anthraquinones. The synthetic compounds were tested in vitro inhibition of human T-24, Hep 3B, Hep G2, SiHa, HT-3, PLC/PRF/5 and 212 cells. Almost all compounds showed significant inhibitory activity against several different cancer cell lines. Structure-activity analysis indicated epoxidation of the hydroxyanthraquinone increased cytotoxicity against tumour cells, but ring-opening of the epoxide group with amine did not enhance the cytotoxic activity. The phosphatidylserine (PS) externalization and DNA fragmentation in SiHa cells were significantly observed after 48 h incubation with selected compound 19. The results show that 19 cause cell death by apoptosis. (C) 2000 Editions scientifiques et medicales Elsevier SAS.