4-amino-N-(1,3-dihydrobenzoimidazol-2-ylidene)benzenesulfonamide | 52715-11-4

• 分子结构分类: 有机化合物 - 苯类化合物 - 苯和取代衍生物
• 英文名称: 4-amino-N-(1,3-dihydrobenzoimidazol-2-ylidene)benzenesulfonamide
• 英文别名: 4-Amino-N-1H-benzimidazol-2-yl-benzenesulfonamide；4-amino-N-(1H-benzimidazol-2-yl)benzenesulfonamide
• CAS: 52715-11-4
• 化学式: C₁₃H₁₂N₄O₂S
• 分子量: 288.33
• InChiKey: BBTWRHLPPWUHHQ-UHFFFAOYSA-N

计算性质

• 辛醇/水分配系数(LogP)：
  1.7
• 重原子数：
  20
• 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：
  109
• 氢给体数：
  3
• 氢受体数：
  5

反应信息

• 作为反应物：
  描述：

  4-amino-N-(1,3-dihydrobenzoimidazol-2-ylidene)benzenesulfonamide 在 sodium tetrahydroborate 作用下， 以 乙醇 为溶剂， 反应 18.0h， 生成 N-(1H-benzo[d]imidazol-2-yl)-4-((2-hydroxy-3-methoxybenzyl)amino)benzenesulfonamide
  参考文献：
  名称：

  4-（（2-羟基-3-甲氧基苄基）氨基）苯磺酰胺衍生物作为 12-脂氧化酶的强效和选择性抑制剂的合成和构效关系研究

  摘要：

  人类脂肪氧化酶 (LOX) 是一类含铁酶，可催化多不饱和脂肪酸氧化以提供相应的生物活性羟基二十碳四烯酸 (HETE) 代谢物。这些类二十烷酸信号分子参与了许多生理反应，例如血小板聚集、炎症和细胞增殖。我们小组对血小板型 12-( S )-LOX (12-LOX)产生了特别的兴趣，因为它在皮肤病、糖尿病、血小板止血、血栓形成和癌症中发挥了重要作用。在此，我们报告了基于 4-（（2-羟基-3-甲氧基苄基）氨基）苯磺酰胺的支架的鉴定和药物化学优化。顶级化合物，以35和36为例, 显示对 12-LOX 的 nM 效力，对相关脂肪氧化酶和环氧化酶具有出色的选择性，并具有良好的 ADME 特性。此外，这两种化合物均抑制 PAR-4 诱导的人血小板聚集和钙动员，并减少 β 细胞中的 12-HETE。

  DOI：

  10.1021/jm4016476
• 作为产物：
  描述：

  对乙酰胺基苯磺酰胺 在 sodium hydroxide 、 硫酸 作用下， 以 乙醇 为溶剂， 反应 14.0h， 生成 4-amino-N-(1,3-dihydrobenzoimidazol-2-ylidene)benzenesulfonamide
  参考文献：
  名称：

  Seshadri, S; Sanghavi, N M; Tawate, S R, Indian Journal of Chemistry - Section B Organic and Medicinal Chemistry, 1992, vol. 31, # 11, p. 748 - 752

  摘要：

  DOI：

文献信息

• The Interrelationship Among Muscle Mass, Strength, and the Ability to Perform Physical Tasks of Daily Living in Younger and Older Women
  作者：K. A. Landers、G. R. Hunter、C. J. Wetzstein、M. M. Bamman、R. L. Weinsier

  DOI：10.1093/gerona/56.10.b443

  日期：2001.10.1

  The purpose of this study was to objectively compare the difficulty and determine the contribution of strength and muscle mass to the performance of physical tasks of daily living in a group of younger and older women. A cross-sectional design was used. Volunteer participants were from the community of Birmingham, AL; there were 21 older (aged 60-75 years) and 20 younger (23-34 years) healthy women in the study. Subjects were matched for height and weight. Their testing included total and regional body composition evaluation by use of dual-energy x-ray absorptiometry, isometric strength tests of elbow flexors and knee extensors, and integrated electromyography (IEMG) evaluation while the subjects were standing from and sitting into a chair, and while they were carrying a small load (weight relative to strength). A two-way analysis of variance and a two-way analysis of covariance with repeated measures, Pearson product correlation, and first-order partial correlations were used to analyze the data. A significant inverse correlation was observed between age and isometric strength of both the knee extensors and elbow flexors. Adjusting for upper leg lean tissue did not change the significant inverse correlation between age and knee extensor strength. However, after an adjustment for arm lean tissue, there was no significant correlation between elbow flexor strength and age. Older women experienced significantly greater difficulty in standing than younger women as measured by quadriceps normalized IEMG (i.e., IEMG during task/IEMG during maximum isometric strength test). This difference persisted even after the covariate upper leg lean tissue was added to the model. No significant difference was observed between younger and older women for difficulty (biceps normalized IEMG) during the carry task after the covariate arm lean tissue was added to the model. The older women in this study had less strength in the knee extensors and experienced greater difficulty standing from a chair than the younger women, even after the covariate, upper leg lean tissue was added to the model. This suggests that other factors, in addition to loss of lean tissue, contribute to the age-related decline of muscular strength and the ability to perform tasks with the legs. In contrast, although elbow flexor strength declined, this appeared to be largely due to decreased arm lean tissue mass.
• Functionalized azoles and triazolo[1,5-a]pyrimidines as latent leishmanicides
  作者：Vishnu Ji Ram、Srivastava Pratibha、Sunil K. Singh、Mamta Kandpal、B.L. Tekwani

  DOI：10.1016/s0960-894x(97)00166-2

  日期：1997.4

  Triazolo[1,5-a]pyrimidine (3-6), benzoxazole (7a,b) and benzimidazole (7c) derivatives have been synthesized and evaluated for their in vitro leishmanicidal activity against L. donovani promastigotes. (C) 1997 Elsevier Science Ltd.
• Benvenuti; Severi; Sacchetti, Il Farmaco, 1997, vol. 52, # 4, p. 231 - 235
  作者：Benvenuti、Severi、Sacchetti、Melegari、Vampa、Zani、Mazza、Antolini

  DOI：——

  日期：——
• SOME SULFONAMIDE DERIVATIVES OF 2-AMINOBENZIMIDAZOLE¹
  作者：CHARLES C. PRICE、ROBERT H. REITSEMA

  DOI：10.1021/jo01166a010

  日期：1947.3
• Synthesis and Structure–Activity Relationship Studies of 4-((2-Hydroxy-3-methoxybenzyl)amino)benzenesulfonamide Derivatives as Potent and Selective Inhibitors of 12-Lipoxygenase
  作者：Diane K. Luci、J. Brian Jameson、Adam Yasgar、Giovanni Diaz、Netra Joshi、Auric Kantz、Kate Markham、Steve Perry、Norine Kuhn、Jennifer Yeung、Edward H. Kerns、Lena Schultz、Michael Holinstat、Jerry L. Nadler、David A. Taylor-Fishwick、Ajit Jadhav、Anton Simeonov、Theodore R. Holman、David J. Maloney

  DOI：10.1021/jm4016476

  日期：2014.1.23

  demonstrated role in skin diseases, diabetes, platelet hemostasis, thrombosis, and cancer. Herein, we report the identification and medicinal chemistry optimization of a 4-((2-hydroxy-3-methoxybenzyl)amino)benzenesulfonamide-based scaffold. Top compounds, exemplified by 35 and 36, display nM potency against 12-LOX, excellent selectivity over related lipoxygenases and cyclooxygenases, and possess favorable

  人类脂肪氧化酶 (LOX) 是一类含铁酶，可催化多不饱和脂肪酸氧化以提供相应的生物活性羟基二十碳四烯酸 (HETE) 代谢物。这些类二十烷酸信号分子参与了许多生理反应，例如血小板聚集、炎症和细胞增殖。我们小组对血小板型 12-( S )-LOX (12-LOX)产生了特别的兴趣，因为它在皮肤病、糖尿病、血小板止血、血栓形成和癌症中发挥了重要作用。在此，我们报告了基于 4-（（2-羟基-3-甲氧基苄基）氨基）苯磺酰胺的支架的鉴定和药物化学优化。顶级化合物，以35和36为例, 显示对 12-LOX 的 nM 效力，对相关脂肪氧化酶和环氧化酶具有出色的选择性，并具有良好的 ADME 特性。此外，这两种化合物均抑制 PAR-4 诱导的人血小板聚集和钙动员，并减少 β 细胞中的 12-HETE。