甲基4-乙基-碘苯甲酸酯 | 51885-91-7

• 分子结构分类: 有机化合物 - 苯类化合物 - 苯和取代衍生物
• 中文名称: 甲基4-乙基-碘苯甲酸酯
• 英文名称: methyl 4-ethyl-3-iodobenzoate
• CAS: 51885-91-7
• 化学式: C₁₀H₁₁IO₂
• 分子量: 290.101
• InChiKey: JTKHZRNJWHCKFS-UHFFFAOYSA-N

计算性质

• 辛醇/水分配系数(LogP)：
  3.2
• 重原子数：
  13
• 可旋转键数：
  3
• 环数：
  1.0
• sp3杂化的碳原子比例：
  0.3
• 拓扑面积：
  26.3
• 氢给体数：
  0
• 氢受体数：
  2

安全信息

• 危险性防范说明：
  P261,P305+P351+P338
• 危险性描述：
  H227,H315,H319,H335,H412

反应信息

• 作为反应物：
  描述：

  甲基4-乙基-碘苯甲酸酯 在 氘氧化钠 、 重水 、 锌 作用下， 生成 4-Ethyl-3-d-benzoic acid
  参考文献：
  名称：

  Conformations of Bridged Diphenyls. V. A Nuclear Magnetic Resonance Comparative Study of the Conformations of Identically Substituted Diphenyl Ethers, Sulfides, Methanes, Ketones, Sulfoxides, and Sulfones

  摘要：

  使用在之前的论文中发展的核磁共振方法，比较了两个系列的构象，一个是双邻位取代的，另一个是三邻位取代的，这两个系列都是六个相同取代的桥联二苯基化合物。已经证明醚类化合物、硫醚和甲烷在构象上是相同的，其中二邻位取代的环垂直于中央桥平面，而另一个环位于该平面上，一个邻位氢原子占据“内部”或“近端”位置。苯甲酮和亚砜更倾向于采取一个构象，其中每个环与中央平面之间的二面角约为40-50°，一个邻位氢原子占据“外部”或“远端”位置。砜类化合物采取了两个环更接近垂直于中央平面的构象。

  DOI：

  10.1139/v74-093
• 作为产物：
  描述：

  4-乙基-3-硝基苯甲酸甲酯 在 镍 氢气 作用下， 以 乙醇 为溶剂， 生成 甲基4-乙基-碘苯甲酸酯
  参考文献：
  名称：

  Conformations of Bridged Diphenyls. V. A Nuclear Magnetic Resonance Comparative Study of the Conformations of Identically Substituted Diphenyl Ethers, Sulfides, Methanes, Ketones, Sulfoxides, and Sulfones

  摘要：

  使用在之前的论文中发展的核磁共振方法，比较了两个系列的构象，一个是双邻位取代的，另一个是三邻位取代的，这两个系列都是六个相同取代的桥联二苯基化合物。已经证明醚类化合物、硫醚和甲烷在构象上是相同的，其中二邻位取代的环垂直于中央桥平面，而另一个环位于该平面上，一个邻位氢原子占据“内部”或“近端”位置。苯甲酮和亚砜更倾向于采取一个构象，其中每个环与中央平面之间的二面角约为40-50°，一个邻位氢原子占据“外部”或“远端”位置。砜类化合物采取了两个环更接近垂直于中央平面的构象。

  DOI：

  10.1139/v74-093

文献信息

• Design and Optimization of 3′-(Imidazo[1,2-<i>a</i>]pyrazin-3-yl)-[1,1′-biphenyl]-3-carboxamides as Selective DDR1 Inhibitors
  作者：Cheng Mo、Zhang Zhang、Yupeng Li、Minhao Huang、Jian Zou、Jinfeng Luo、Zheng-Chao Tu、Yong Xu、Xiaomei Ren、Ke Ding、Xiaoyun Lu

  DOI：10.1021/acsmedchemlett.9b00495

  日期：2020.3.12

  DDR1 is considered as a promising target for cancer therapy, and selective inhibitors against DDR1 over other kinases may be considered as promising therapeutic agents. Herein, we have identified a series of 3'-(imidazo[1,2-alpha]pyrazin-3-yl)-[1,1'-biphenyl]-3-carboxamides as novel selective DDR1 inhibitors. Among these, compound 8v potently inhibited DDR1 with an IC50 of 23.8 nM, while it showed less inhibitory activity against DDR2 (IC50 = 1740 nM) and negligible activities against Bcr-Abl (IC50 > 10 mu M) and c-Kit (IC50 > 10 mu M). 8v also exhibited excellent selectivity in a KINOMEscan screening platform with 468 kinases. This compound dose-dependently suppressed NSCLC cell tumorigenicity, migration, and invasion. Collectively, these studies support its potential application for treatment of NSCLC.
• Design, Synthesis, and Biological Evaluation of 3-(Imidazo[1,2-<i>a</i>]pyrazin-3-ylethynyl)-4-isopropyl-<i>N</i>-(3-((4-methylpiperazin-1-yl)methyl)-5-(trifluoromethyl)phenyl)benzamide as a Dual Inhibitor of Discoidin Domain Receptors 1 and 2
  作者：Zhen Wang、Yali Zhang、Daniel M. Pinkas、Alice E. Fox、Jinfeng Luo、Huocong Huang、Shengyang Cui、Qiuping Xiang、Tingting Xu、Qiuju Xun、Dongsheng Zhu、Zhengchao Tu、Xiaomei Ren、Rolf A. Brekken、Alex N. Bullock、Guang Liang、Ke Ding、Xiaoyun Lu

  DOI：10.1021/acs.jmedchem.8b01045

  日期：2018.9.13

  Discoidin-domain receptors 1 and 2 (DDR1 and DDR2) are new potential targets for anti-inflammatory-drug discovery. A series of heterocycloalkynylbenzimides were designed and optimized to coinhibit DDR1 and DDR2. One of the most promising compounds, Sn, tightly bound to DDR1 and DDR2 proteins with K-d values of 7.9 and 8.0 nM; potently inhibited the kinases with IC50 values of 9.4 and 20.4 nM, respectively; and was significantly less potent for a panel of 403 wild-type kinases at 1.0 mu M. DDR1- and DDR2-kinase inhibition by 5n was validated by Western-blotting analysis in primary human lung fibroblasts. The compound also dose-dependently inhibited lipopolysaccharide (LPS)-induced interleukin 6 (IL-6) release in vitro and exhibited promising in vivo anti-inflammatory effects in an LPS-induced-acute-lung-injury (ALI) mouse model. Compound 5n may serve as a lead compound for new anti-inflammatory drug discovery.
• Discovery and Optimization of 3-(2-(Pyrazolo[1,5-<i>a</i>]pyrimidin-6-yl)ethynyl)benzamides as Novel Selective and Orally Bioavailable Discoidin Domain Receptor 1 (DDR1) Inhibitors
  作者：Mingshan Gao、Lei Duan、Jinfeng Luo、Lianwen Zhang、Xiaoyun Lu、Yan Zhang、Zhang Zhang、Zhengchao Tu、Yong Xu、Xiaomei Ren、Ke Ding

  DOI：10.1021/jm301824k

  日期：2013.4.25

  Discoidin domain receptor 1 (DDR1) is an emerging potential molecular target for new anticancer drug discovery. We have discovered a series of 3-(2-(pyrazolo[1,5-a]pyrimidin-6-yl) ethynyl)-benzamides that are selective and orally bioavailable DDR1 inhibitors. The two most promising compounds (7rh and 7rj) inhibited the enzymatic activity of DDR1, with IC50 values of 6.8 and 7.0 nM, respectively, but were significantly less potent in suppressing the kinase activities of DDR2, Bcr-Abl, and c-Kit. Further study revealed that 7rh bound with DDR1 with a K-d value of 0.6 nM, while it was significantly less potent to the other 455 kinases tested. The S(35) and S(10) selectivity scores of 7rh were 0.035 and 0.008, respectively. The compounds also potently inhibited the proliferation of cancer cells expressing high levels of DDR1 and strongly suppressed cancer cell invasion, adhesion, and tumorigenicity. Preliminary pharmacokinetic studies suggested that they possessed good PK profiles, with oral bioavailabilities of 67.4% and 56.2%, respectively.
• Identification of GZD824 as an Orally Bioavailable Inhibitor That Targets Phosphorylated and Nonphosphorylated Breakpoint Cluster Region–Abelson (Bcr-Abl) Kinase and Overcomes Clinically Acquired Mutation-Induced Resistance against Imatinib
  作者：Xiaomei Ren、Xiaofen Pan、Zhang Zhang、Deping Wang、Xiaoyun Lu、Yupeng Li、Donghai Wen、Huoyou Long、Jinfeng Luo、Yubing Feng、Xiaoxi Zhuang、Fengxiang Zhang、Jianqi Liu、Fang Leng、Xingfen Lang、Yang Bai、Miaoqin She、Zhengchao Tu、Jingxuan Pan、Ke Ding

  DOI：10.1021/jm301581y

  日期：2013.2.14

  Bcr-Abl(T315)I mutation-induced imatinib resistance remains a major challenge for clinical management of chronic myelogenous leukemia (CML). Herein, we report GZD824 (10a) as a novel orally bioavailable inhibitor against a broad spectrum of Bcr-Abl mutants including T315I. It tightly bound to Bcr-Abl(WT) and Bcr-Abl(T315I) with K-d values of 0.32 and 0.71 nM, respectively, and strongly inhibited the kinase functions with nanomolar IC50 values. The compound potently suppressed proliferation of Bcr-Abl-positive K562 and Ku812 human CML cells with IC50 values of 0.2 and 0.13 nM, respectively. It also displayed good oral bioavailability (48.7%), a reasonable half-life (10.6 h), and promising in vivo antitumor efficacy. It induced tumor regression in mouse xenograft tumor models driven by Bcr-Abl(WT) or the mutants and significantly improved the survival of mice bearing an allograft leukemia model with Ba/F3 cells harboring Bcr-Abl(T315I). GZD824 represents a promising lead candidate for development of Bcr-Abl inhibitors to overcome acquired imatinib resistance.
• 10.1021/acs.jmedchem.4c00162
  作者：Liu, Lianchao、Zhao, Lijie、Yang, Lujun、Chai, Minxue、Liu, Zhengyong、Ma, Nan、Wang, Yongxing、Wu, Qinxue、Guo, Jing、Zhou, Fengtao、Huang, Weixue、Ren, Xiaomei、Wang, Jian、Ding, Ming、Wang, Zhen、Ding, Ke

  DOI：10.1021/acs.jmedchem.4c00162

  日期：——