2-(甲基氨基)苯甲酸乙酯 | 35472-56-1

• 物质功能分类: 化学试剂 - 有机试剂 - 酯类
• 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: 2-(甲基氨基)苯甲酸乙酯
• 英文名称: N-methyl-anthranilic acid ethyl ester
• 英文别名: ethyl N-methylanthranilate；ethyl 2-(methylamino)benzoate
• CAS: 35472-56-1
• 化学式: C₁₀H₁₃NO₂
• mdl: MFCD11174593
• 分子量: 179.219
• InChiKey: WBSWYVBUGLBCOV-UHFFFAOYSA-N

物化性质

• 熔点：
  39°C
• 沸点：
  311.75°C (rough estimate)
• 密度：
  1.1248 (rough estimate)
• LogP：
  3.22
• 物理描述：
  Solid
• 溶解度：
  Very slightly soluble in water

计算性质

• 辛醇/水分配系数(LogP)：
  3.3
• 重原子数：
  13
• 可旋转键数：
  4
• 环数：
  1.0
• sp3杂化的碳原子比例：
  0.3
• 拓扑面积：
  38.3
• 氢给体数：
  1
• 氢受体数：
  3

安全信息

• 海关编码：
  2922499990
• 危险性防范说明：
  P261,P280,P305+P351+P338
• 危险性描述：
  H302,H315,H319,H332,H335

反应信息

• 作为反应物：
  描述：

  2-(甲基氨基)苯甲酸乙酯 在 铁粉 、 sodium hydride 、 溶剂黄146 、 N,N-二异丙基乙胺 作用下， 以 1,4-二氧六环 、 N,N-二甲基乙酰胺 、 mineral oil 为溶剂， 反应 15.0h， 生成 2-氯-5,11-二甲基-5H-苯并[E]嘧啶并[5,4-B][1,4]二氮杂-6(11H)-
  参考文献：
  名称：

  基于5,11-二氢-6H-苯并[e]嘧啶基[5,4-b] [1,4]二氮杂-6-6支架的DCLK1激酶抑制剂的合成与结构-活性关系。

  摘要：

  Doublecortin样激酶1（DCLK1）是一种丝氨酸/苏氨酸激酶，在胃肠道癌（包括食道癌，胃癌，结肠直肠癌和胰腺癌）中过表达。DCLK1还用作簇状细胞的标志物，簇状细胞可调节肠道中的II型免疫力。但是，DCLK1的基板和功能尚未得到充分研究。我们最近描述了第一个选择性DCLK1 / 2抑制剂DCLK1-IN-1，该抑制剂的开发是为了辅助这一重要激酶的功能表征。在这里，我们描述了5,11-二氢-6 H-苯并[ e ]嘧啶基[5,4- b ] [1,4]二氮杂-6-1 DCLK1抑制剂的合成与构效关系，从而鉴定了DCLK1-IN-1。

  DOI：

  10.1021/acs.jmedchem.0c00596
• 作为产物：
  描述：

  N-methyl-N-carbethoxyanthranilic acid 在 sodium 作用下， 以 乙醚 、 xylene 为溶剂， 反应 6.0h， 生成 2-(甲基氨基)苯甲酸乙酯
  参考文献：
  名称：

  Sodium metal-promoted condensations of carbamates

  摘要：

  DOI：

  10.1021/jo00392a042

文献信息

• The p38-MK2-HuR pathway potentiates EGFRvIII–IL-1β-driven IL-6 secretion in glioblastoma cells
  作者：F M S Gurgis、Y T Yeung、M X M Tang、B Heng、M Buckland、A J Ammit、J Haapasalo、H Haapasalo、G J Guillemin、T Grewal、L Munoz

  DOI：10.1038/onc.2014.225

  日期：2015.5.28

  The microenvironment of glioblastoma (GBM) contains high levels of inflammatory cytokine interleukin 6 (IL-6), which contributes to promote tumour progression and invasion. The common epidermal growth factor receptor variant III (EGFRvIII) mutation in GBM is associated with significantly higher levels of IL-6. Furthermore, elevated IL-1β levels in GBM tumours are also believed to activate GBM cells and enhance IL-6 production. However, the crosstalk between these intrinsic and extrinsic factors within the oncogene-microenvironment of GBM causing overproduction of IL-6 is poorly understood. Here, we show that EGFRvIII potentiates IL-1β-induced IL-6 secretion from GBM cells. Importantly, exacerbation of IL-6 production is most effectively attenuated in EGFRvIII-expressing GBM cells with inhibitors of p38 mitogen-activated protein kinase (p38 MAPK) and MAPK-activated protein kinase 2 (MK2). Enhanced IL-6 production and increased sensitivity toward pharmacological p38 MAPK and MK2 inhibitors in EGFRvIII-expressing GBM cells is associated with increased MK2-dependent nuclear–cytoplasmic shuttling and accumulation of human antigen R (HuR), an IL-6 mRNA-stabilising protein, in the cytosol. IL-1β-stimulated activation of the p38 MAPK–MK2-HuR pathway significantly enhances IL-6 mRNA stability in GBM cells carrying EGFRvIII. Further supporting a role for the p38 MAPK–MK2-HuR pathway in the development of inflammatory environment in GBM, activated MK2 is found in more than 50% of investigated GBM tissues and correlates with lower grade and secondary GBMs. Taken together, p38 MAPK–MK2-HuR signalling may enhance the potential of intrinsic (EGFRvIII) and extrinsic (IL-1β) factors to develop an inflammatory GBM environment. Hence, further improvement of brain-permeable and anti-inflammatory inhibitors targeting p38 MAPK, MK2 and HuR may combat progression of lower grade gliomas into aggressive GBMs.

  胶质母细胞瘤(GBM)的微环境中含有高水平的炎症细胞因子白细胞介素6(IL-6),这有助于促进肿瘤进展和侵袭。GBM中常见的表皮生长因子受体变异体III(EGFRvIII)突变与更高的IL-6水平显著相关。此外,GBM肿瘤中升高的IL-1β水平也被认为能激活GBM细胞并增强IL-6的产生。然而,导致IL-6过度产生GBM中的致癌基因-微环境中的这些内在和外在因素之间的相互作用在很大程度上仍未得到理解。在这里,我们展示了EGFRvIII增强了IL-1β诱导的GBM细胞中的IL-6分泌。重要的是,在表达EGFRvIII的GBM细胞中,p38促分裂原活化蛋白激酶(p38 MAPK)和MAPK活化蛋白激酶2(MK2)的抑制剂最有效地减弱了IL-6的产生。在表达EGFRvIII的GBM细胞中,增强的IL-6产生和对药物p38 MAPK和MK2抑制剂的增加的敏感性与增加的依赖MK2的核质穿梭和IL-6 mRNA稳定蛋白——人抗原R(HuR)在胞质的积累相关。IL-1β刺激的p38 MAPK-MK2-HuR途径的激活在携带EGFRvIII的GBM细胞中显著增强了IL-6 mRNA的稳定性。进一步支持p38 MAPK-MK2-HuR途径在GBM炎症环境发展中的作用,在超过50%的被调查的GBM组织中发现了激活的MK2,并且与较低级别和继发性GBM相关。总的来说,p38 MAPK-MK2-HuR信号可能增强内在(EGFRvIII)和外在(IL-1β)因素发展GBM炎症环境的潜力。因此,进一步改进针对p38 MAPK、MK2和HuR的脑渗透和抗炎抑制剂可能有助于阻止低级别胶质瘤进展为侵袭性GBM。
• Acetic Acid Accelerated Visible-Light Photoredox Catalyzed<i>N</i>-Demethylation of<i>N,N</i>-Dimethylaminophenyl Derivatives
  作者：Guolin Wu、Yazhen Li、Xuemei Yu、Yu Gao、Haijun Chen

  DOI：10.1002/adsc.201601108

  日期：2017.2.20

  N,N‐Dimethylaminophenyl moiety is a common fragment in medicinal chemistry as several pharmaceuticals bearing this privileged motif are on the market and under clinical evaluation. Oxidative N‐demethylation is generally regarded as the major metabolic pathway. However, pharmacokinetics, metabolites studies as well as the further structural modification are precluded by the impracticality of chemical

  N，N-二甲基氨基苯基部分是药物化学中的常见片段，因为带有这种特权基序的几种药物已在市场上出售并正在临床评估中。氧化性N-去甲基化通常被认为是主要的代谢途径。但是，化学合成的不切实际性排除了药代动力学，代谢产物的研究以及进一步的结构修饰。这里，我们报告，乙酸可以加速显著可见光photoredox催化Ñ的-demethylation N，N- -dimethylaminophenyl衍生物。这种方法很容易进行大规模反应，甚至可能用于潜在的工业生产。
• Synthesis of mono-N-substituted functionalized anilines
  申请人：CONSORZIO INTERUNIVERSITARIO NAZIONALE "LA CHIMICA PER L'AMBIENTE"

  公开号：US20040127747A1

  公开（公告）日：2004-07-01

  The present invention relates to a process for direct and selective synthesis of mono-N-substituted functionalized anilines by using alkylating agents selected from the class of organic carbonates, preferably of the dialkyl, dibenzyl and diallyl types, in the presence of suitable catalysts that are chemically related to the class of aluminosilicates.

  本发明涉及一种利用来自有机碳酸酯类的烷基化剂，优选为二烷基、二苄基和二烯丙基类型，在与与硅铝酸盐类相关的适当催化剂存在的情况下，直接和选择性合成单-N-取代官能化苯胺的方法。
• BITTER TASTE MODIFIERS INCLUDING SUBSTITUTED 1-BENZYL-3-(1-(ISOXAZOL-4-YLMETHYL)-1H-PYRAZOL-4-YL)IMIDAZOLIDINE-2,4-DIONES AND COMPOSITIONS THEREOF
  申请人：SENOMYX, INC.

  公开号：US20160376263A1

  公开（公告）日：2016-12-29

  The present invention includes compounds and compositions known to modify the perception of bitter taste, and combinations of said compositions and compounds with additional compositions, compounds, and products. Exemplary compositions comprise one or more of the following: cooling agents; inactive drug ingredients; active pharmaceutical ingredients; food additives or foodstuffs; flavorants, or flavor enhancers; food or beverage products; bitter compounds; sweeteners; bitterants; sour flavorants; salty flavorants; umami flavorants; plant or animal products; compounds known to be used in pet care products; compounds known to be used in personal care products; compounds known to be used in home products; pharmaceutical preparations; topical preparations; cannabis-derived or cannabis-related products; compounds known to be used in oral care products; beverages; scents, perfumes, or odorants; compounds known to be used in consumer products; silicone compounds; abrasives; surfactants; warming agents; smoking articles; fats, oils, or emulsions; and/or probiotic bacteria or supplements.

  本发明涵盖已知用于改变苦味感知的化合物和组合物，以及所述组合物和化合物与额外的组合物、化合物和产品的组合。示例组合物包括以下一种或多种：冷却剂；无活性药物成分；活性药用成分；食品添加剂或食品；调味剂或调味增强剂；食品或饮料产品；苦味化合物；甜味剂；苦味剂；酸味调味剂；咸味调味剂；鲜味调味剂；植物或动物产品；已知用于宠物护理产品中的化合物；已知用于个人护理产品中的化合物；已知用于家用产品中的化合物；制药制剂；局部制剂；大麻衍生或与大麻相关的产品；已知用于口腔护理产品中的化合物；饮料；香味、香水或除臭剂；已知用于消费品中的化合物；硅化合物；磨料；表面活性剂；发热剂；吸烟物品；脂肪、油脂或乳化剂；和/或益生菌或补充剂。
• Bicyclic substituted hexahydrobenz[e]isoindole .alpha.-1 adrenergic
  申请人：Abbott Laboratories

  公开号：US05521181A1

  公开（公告）日：1996-05-28

  The present invention relates to a compound of the formula ##STR1## and the pharmaceutically acceptable salts thereof wherein W is a bicyclic heterocyclic ring system. The compounds are .alpha.-1 adrenergic antagonists and are useful in the treatment of BPH; also disclosed are .alpha.-1 antagonist compositions and a method for antagonizing .alpha.-1 receptors and treating BPH.

  本发明涉及一种具有以下结构的化合物##STR1##及其药学上可接受的盐，其中W是一个双环杂环环系统。这些化合物是α-1肾上腺能拮抗剂，可用于治疗前列腺增生症；还公开了α-1拮抗剂组合物以及拮抗α-1受体和治疗前列腺增生症的方法。

表征谱图