{4-[(4-甲基苯基)氨基磺酰基]苯基}硼酸 | 957062-88-3

• 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: {4-[(4-甲基苯基)氨基磺酰基]苯基}硼酸
• 中文别名: 4-(4-甲基苯基氨磺酰基)苯硼酸
• 英文名称: 4-(N-p-tolylsulfamoyl)phenylboronic acid
• 英文别名: N-p-Tolyl 4-boronobenzenesulfonamide；[4-[(4-methylphenyl)sulfamoyl]phenyl]boronic acid
• CAS: 957062-88-3
• 化学式: C₁₃H₁₄BNO₄S
• 分子量: 291.135
• InChiKey: RGJGYRYMFMLJEU-UHFFFAOYSA-N

物化性质

• 沸点：
  503.4±60.0 °C(Predicted)
• 密度：
  1.38±0.1 g/cm3(Predicted)

计算性质

• 辛醇/水分配系数(LogP)：
  0.48
• 重原子数：
  20
• 可旋转键数：
  4
• 环数：
  2.0
• sp3杂化的碳原子比例：
  0.08
• 拓扑面积：
  95
• 氢给体数：
  3
• 氢受体数：
  5

反应信息

• 作为反应物：
  描述：

  (6-chloro-3-methyl-4-trifluoromethanesulfonyloxy-naphthalen-2-yl)-acetic acid methyl ester 、 {4-[(4-甲基苯基)氨基磺酰基]苯基}硼酸 在 palladium diacetate 、 sodium carbonate 、 三苯基膦 作用下， 以 乙二醇二甲醚 、 水 为溶剂， 反应 2.0h， 以30%的产率得到[6-chloro-3-methyl-4-(4-p-tolylsulfamoyl-phenyl)-naphthalen-2-yl]-acetic acid methyl ester
  参考文献：
  名称：

  SUBSTITUTED NAPHTHYLACETIC ACIDS

  摘要：

  这项发明涉及式(I)的化合物： 及其药学上可接受的盐，其中R 1 ，R 2 ，R 3 和X在详细说明和权利要求中有定义。此外，本发明涉及制造和使用式I的化合物的方法，以及含有这种化合物的药物组合物。式I的化合物是CRTH2受体的拮抗剂或部分激动剂，可能在治疗与该受体相关的疾病和紊乱方面有用，如哮喘。

  公开号：

  US20130225588A1

文献信息

• PYRROLE TRICYCLIC COMPOUNDS AS A2A / A2B INHIBITORS
  申请人：Incyte Corporation

  公开号：US20190337957A1

  公开（公告）日：2019-11-07

  This application relates to compounds of Formula (I): or pharmaceutically acceptable salts or stereoisomers thereof, which modulate the activity of adenosine receptors, such as subtypes A2A and A2B receptors, and are useful in the treatment of diseases related to the activity of adenosine receptors including, for example, cancer, inflammatory diseases, cardiovascular diseases, and neurodegenerative diseases.

  这种应用与式（I）的化合物有关： 或其药用可接受的盐或立体异构体，其调节腺苷受体的活性，如A2A和A2B受体亚型，并且在治疗与腺苷受体活性相关的疾病方面具有用处，例如癌症、炎症性疾病、心血管疾病和神经退行性疾病。
• Inhibitory Kappa B Kinase α (IKKα) Inhibitors That Recapitulate Their Selectivity in Cells against Isoform-Related Biomarkers
  作者：Nahoum G. Anthony、Jessica Baiget、Giacomo Berretta、Marie Boyd、David Breen、Joanne Edwards、Carly Gamble、Alexander I. Gray、Alan L. Harvey、Sophia Hatziieremia、Ka Ho Ho、Judith K. Huggan、Stuart Lang、Sabin Llona-Minguez、Jia Lin Luo、Kathryn McIntosh、Andrew Paul、Robin J. Plevin、Murray N. Robertson、Rebecca Scott、Colin J. Suckling、Oliver B. Sutcliffe、Louise C. Young、Simon P. Mackay

  DOI：10.1021/acs.jmedchem.7b00484

  日期：2017.8.24

  IKK beta plays a central role in the canonical NF-kB pathway, which has been extensively characterized. The role of IKK alpha in the noncanonical NF-kB pathway, and indeed in the canonical pathway as a complex with IKK beta, is less well understood. One major reason for this is the absence of chemical tools designed as selective inhibitors for IKK alpha over IKK beta. Herein, we report for the first time a series of novel, potent, and selective inhibitors of IKK alpha. We demonstrate effective target engagement and selectivity with IKK alpha in U2OS cells through inhibition of IKK alpha-driven p100 phosphorylation in the noncanonical NF-kB pathway without affecting IKK beta-dependent IKapp-B alpha loss in the canonical pathway. These compounds represent the first chemical tools that can be used to further characterize the role of IKK alpha a in cellular signaling, to dissect this from IKK beta and to validate it in its own right as a target in inflammatory diseases.