N-(2-氨基甲酰基苯基)-1H-吲哚-2-甲酰胺 | 1052179-94-8

• 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: N-(2-氨基甲酰基苯基)-1H-吲哚-2-甲酰胺
• 英文名称: N-(2-carbamoylphenyl)-1H-indole-2-carboxamide
• CAS: 1052179-94-8
• 化学式: C₁₆H₁₃N₃O₂
• 分子量: 279.298
• InChiKey: DTSAWLRNXRKYOZ-UHFFFAOYSA-N

物化性质

• 沸点：
  466.5±25.0 °C(Predicted)
• 密度：
  1.400±0.06 g/cm3(Temp: 20 °C; Press: 760 Torr)(Predicted)

计算性质

• 辛醇/水分配系数(LogP)：
  2.6
• 重原子数：
  21
• 可旋转键数：
  3
• 环数：
  3.0
• sp3杂化的碳原子比例：
  0.0
• 拓扑面积：
  88
• 氢给体数：
  3
• 氢受体数：
  2

反应信息

• 作为反应物：
  描述：

  N-(2-氨基甲酰基苯基)-1H-吲哚-2-甲酰胺 在 potassium tert-butylate 作用下， 以 乙醇 、 甲苯 为溶剂， 反应 6.5h， 生成 2-(4-chloroquinazolin-2-yl)-1H-indole-3-carbaldehyde
  参考文献：
  名称：

  一种吲哚甲醛的制备方法

  摘要：

  本发明公开了一种吲哚甲醛的制备方法,即2‑[4‑[[2‑(1‑吡咯基)乙基]氨基]喹唑啉‑2‑基]‑1H‑吲哚‑3‑甲醛（Ⅰ）的制备方法，属于化学药物中间体制备方法技术领域，利用1H‑吲哚‑2‑甲酸、2‑氨基苯甲酰胺和2‑吡咯烷基乙胺为原料，经酰化、环合、Vilsmeier反应和缩合反应制备吲哚甲醛（Ⅰ）。本发明方法采用相对廉价易得的原料，操作安全便捷，条件温和，收率较高。

  公开号：

  CN109456310A
• 作为产物：
  描述：

  吲哚-2-羧酸 、 2-氨基苯甲酰胺 在 N,N'-二环己基碳二亚胺 作用下， 以 四氢呋喃 为溶剂， 反应 12.0h， 以78%的产率得到N-(2-氨基甲酰基苯基)-1H-吲哚-2-甲酰胺
  参考文献：
  名称：

  芸苔碱和生物碱A，B的杂种的合成

  摘要：

  7,12-二氢吲哚的合成[2'，3'：3,4]吡咯并[2,1- b ]喹唑啉-5-酮，含有天然生物碱的共同的结构特征的混合化合物吴茱萸次碱（吴茱萸）和褪黑素A（Peganum nigellastrum）是通过脱氧维西酮的活性亚甲基转化而进行的。7-羟基-8-去甲rutacarcarpine的合成是通过第一次全合成布查达汀（bouchardatia neurococca）及其酸催化的闭环反应。合成的生物碱类似物是新的杂环系统的第一个代表。对合成化合物的初步测试显示，在与对照药物依托泊苷相当的浓度下，其对HeLa细胞具有细胞毒活性，并诱导了凋亡。

  DOI：

  10.1016/j.tetlet.2008.05.141

文献信息

• 芳基取代的酰胺类化合物及其制备方法、包含 其的药物组合物及其应用
  申请人：中国医学科学院医药生物技术研究所

  公开号：CN105198786B

  公开（公告）日：2018-06-29

  本发明涉及式(I)的芳基取代的酰胺类化合物及其制备方法、包含其的药物组合物以及它们在制药中的应用，其中Arl、L1、M1、M2、L2和Ar2如本文中所定义。本发明的芳基取代的酰胺类化合物可以激动TRPV1、激动核受体(LXRs、PPARs、RXR)、调节胆固醇外排相关蛋白ABCA1/G1、SR‑BI的表达、调节炎症相关蛋白TNF‑α等的表达，从而发挥促进胆固醇和脂质外排、降糖、调节血脂、抗炎、降低血压等作用，用于治疗和/或预防和/或缓解心脑血管疾病、调节血脂、抗动脉粥样硬化、糖尿病、抗炎、疼痛以及抗高血压等疾病。
• [EN] STREPTOCOCCUS MUTANS GLUCOSYL TRANSFERASE INHIBITORS FOR DENTAL CARIES THERAPY<br/>[FR] INHIBITEURS DE GLUCOSYLE TRANSFÉRASE DE STREPTOCOCCUS MUTANS POUR LA THÉRAPIE DES CARIES DENTAIRES
  申请人：UAB RESEARCH FOUNDATION

  公开号：WO2019195430A1

  公开（公告）日：2019-10-10

  The present invention is related to the inhibition of the formation of Streptococci biofilms through the inhibition of glucosyl transferase (Gtf). Compounds, compositions and methods for inhibiting Streptococcus biofilm formation, as well as for preventing, inhibiting and/or treating the formation of dental caries, and methods of identifying compounds that prevent, inhibit and/or treat the formation of dental caries are provided.

  本发明涉及通过抑制葡萄糖基转移酶(Gtf)来抑制链球菌生物膜形成的方法。提供了用于抑制链球菌生物膜形成的化合物、组合物和方法，以及用于预防、抑制和/或治疗龋齿形成的方法，以及用于识别能够预防、抑制和/或治疗龋齿形成的化合物的方法。
• A novel HSF1 activator ameliorates non‐alcoholic steatohepatitis by stimulating mitochondrial adaptive oxidation
  作者：Yong Rao、Chan Li、Yu‐Tao Hu、Yao‐Hao Xu、Bing‐Bing Song、Shi‐Yao Guo、Zhi Jiang、Dan‐Dan Zhao、Shuo‐Bin Chen、Jia‐Heng Tan、Shi‐Liang Huang、Qing‐Jiang Li、Xiao‐Jun Wang、Ying‐Jun Zhang、Ji‐Ming Ye、Zhi‐Shu Huang

  DOI：10.1111/bph.15727

  日期：2022.4

  Background and PurposeNon‐alcoholic steatohepatitis (NASH) is the more severe form of metabolic associated fatty liver disease (MAFLD) and no pharmacological treatment as yet been approved. Identification of novel therapeutic targets and their agents is critical to overcome the current inadequacy of drug treatment for NASH.Experimental ApproachThe correlation between heat shock factor 1 (HSF1) levels and the development of NASH and the target genes of HSF1 in hepatocyte were investigated by chromatin‐immunoprecipitation sequencing. The effects and mechanisms of SYSU‐3d in alleviating NASH were examined in relevant cell models and mouse models (the Ob/Ob mice, high‐fat and high‐cholesterol diet and the methionine‐choline deficient diet‐fed mice). The actions of SYSU‐3d in vivo were evaluated.Key ResultsHSF1 is progressively reduced with mitochondrial dysfunction in NASH pathogenesis and activation of this transcription factor by its newly identified activator SYSU‐3d effectively inhibited all manifestations of NASH in mice. When activated, the phosphorylated HSF1 (Ser326) translocated to nucleus and bound to the promoter of PPARγ coactivator‐1α (PGC‐1α) to induce mitochondrial biogenesis. Thus, increasing mitochondrial adaptive oxidation and inhibiting oxidative stress. The deletion of HSF1 and PGC‐1α or recovery of HSF1 in HSF1‐deficiency cells showed the HSF1/PGC‐1α pathway was mainly responsible for the anti‐NASH effects of SYSU‐3d independent of AMP‐activated protein kinase (AMPK).Conclusion and ImplicationsActivation of HSF1 is a practical therapeutic approach for NASH treatment via the HSF1/PGC‐1α/mitochondrial pathway and SYSU‐3d can be considered as a potential candidate for the treatment of NASH.
• STREPTOCOCCUS MUTANS GLUCOSYL TRANSFERASE INHIBITORS FOR DENTAL CARIES THERAPY
  申请人：UAB Research Foundation

  公开号：US20210115007A1

  公开（公告）日：2021-04-22

  The present invention is related to the inhibition of the formation of Streptococci biofilms through the inhibition of glucosyl transferase (Gtf). Compounds, compositions and methods for inhibiting Streptococcus biofilm formation, as well as for preventing, inhibiting and/or treating the formation of dental caries, and methods of identifying compounds that prevent, inhibit and/or treat the formation of dental caries are provided.
• Synthesis of hybrids between the alkaloids rutaecarpine and luotonins A, B
  作者：Máté Bubenyák、Melinda Pálfi、Mária Takács、Szabolcs Béni、Éva Szökő、Béla Noszál、József Kökösi

  DOI：10.1016/j.tetlet.2008.05.141

  日期：2008.8

  The synthesis of 7,12-dihydroindolo[2′,3′:3,4]pyrrolo[2,1-b]quinazolin-5-one, a hybrid compound containing common structural features of the natural alkaloids rutaecarpine (Evodia rutaecarpa) and luotonin A (Peganum nigellastrum), was performed by active methylene group transformations of deoxyvasicinone. The synthesis of 7-hydroxy-8-norrutaecarpine was accomplished via the first total synthesis of

  7,12-二氢吲哚的合成[2'，3'：3,4]吡咯并[2,1- b ]喹唑啉-5-酮，含有天然生物碱的共同的结构特征的混合化合物吴茱萸次碱（吴茱萸）和褪黑素A（Peganum nigellastrum）是通过脱氧维西酮的活性亚甲基转化而进行的。7-羟基-8-去甲rutacarcarpine的合成是通过第一次全合成布查达汀（bouchardatia neurococca）及其酸催化的闭环反应。合成的生物碱类似物是新的杂环系统的第一个代表。对合成化合物的初步测试显示，在与对照药物依托泊苷相当的浓度下，其对HeLa细胞具有细胞毒活性，并诱导了凋亡。