Cambridge id 6592111

• 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: Cambridge id 6592111
• 英文别名: 4-[2-[(4-methoxyphenyl)sulfonylamino]ethyl]benzenesulfonamide
• 化学式: C₁₅H₁₈N₂O₅S₂
• mdl: MFCD02861836
• 分子量: 370.45
• InChiKey: XVRQULFNTTVQCZ-UHFFFAOYSA-N

计算性质

• 辛醇/水分配系数(LogP)：
  1.4
• 重原子数：
  24
• 可旋转键数：
  7
• 环数：
  2.0
• sp3杂化的碳原子比例：
  0.2
• 拓扑面积：
  132
• 氢给体数：
  2
• 氢受体数：
  7

反应信息

• 作为反应物：
  描述：

  4-氯异硫氰酸苯酯 、 Cambridge id 6592111 在 potassium carbonate 作用下， 以 水 、 丙酮 为溶剂， 反应 18.0h， 生成 4-fluoro-N-(4-(N-(phenylcarbamothioyl)sulfamoyl)phenethyl)-benzenesulfonamide
  参考文献：
  名称：

  Novel sulfonyl(thio)urea derivatives act efficiently both as insulin secretagogues and as insulinomimetic compounds

  摘要：

  Glibenclamide is widely used in the management of non-insulin dependent diabetes mellitus, but numerous risks limit its use in therapy. In the search for novel structures that are safer and more efficient than glibenclamide, we obtained new chemical analogs based on bioisosterism, through the treatment of benzenesulfonamide derivatives with isothiocyanates and isocyanates, affording (thio)ureas with good yield. We also verified the hypoglycemic activity, through an in vivo approach. Most of these synthesized compounds improved glucose tolerance, and the mechanism of action of the best compound (7) suggests that its effect is mediated by insulin secretion, while its hypoglycemic action is triggered by glucose uptake involving GLUT4 expression and translocation through PI-3K and PKA activity and active de novo protein synthesis in skeletal muscle. Taking all these factors together, sulfonylthiourea 7 acts as an insulin secretagogue and insulinomimetic agent on glucose homeostasis, and does not exhibit toxicity in acute treatment.

  DOI：

  10.1016/j.ejmech.2014.09.007
• 作为产物：
  描述：

  对甲氧基苯磺酰氯 、 4-(2-氨乙基)苯磺酰胺 在 吡啶 作用下， 以 二氯甲烷 为溶剂， 生成 Cambridge id 6592111
  参考文献：
  名称：

  一种新型的磺酰胺衍生物，可作为抗血液恶性肿瘤的强效选择性凋亡剂

  摘要：

  当前可获得的针对血液系统恶性肿瘤的化学治疗药物具有多种不良反应，并且与高死亡率相关。因此，在这项研究中，我们评估了26种新的磺酰胺衍生物对急性白血病和多发性骨髓瘤细胞的细胞毒性作用，以试图发现一种可以用作新化学治疗剂原型的新的选择性和安全化合物。最具细胞毒性的化合物DFS16以浓度和时间依赖性方式降低K562，Jurkat和MM.1S细胞的细胞活力，并且对非肿瘤细胞的细胞毒性明显降低。在急性白血病细胞上，磺酰胺DFS16通过Bax / Bcl-2倒置激活FasR表达和ΔΨm丢失，从而激活内在和外在凋亡。在K562中DFS16通过激活caspase-3诱导凋亡，而在Jurkat中，它诱导AIF释放和caspase-3独立凋亡。在多发性骨髓瘤中，DFS16诱导细胞周期停滞在G2 / M期，并伴随ΔΨm丢失而凋亡。总之，结果表明，新的磺酰胺衍生物DFS16在急性白血病和多发性骨髓瘤细胞中诱导凋亡

  DOI：

  10.1007/s11696-019-00984-7

文献信息

• Carbonic anhydrase inhibitors. Part 61. Quantum chemical QSAR of a group of benzenedisulfonamides
  作者：Brian W. Clare、Claudiu T. Supuran

  DOI：10.1016/s0223-5234(99)80096-8

  日期：1999.6

  The synthesis of a large group of benzenesulfonamides containing both a primary and secondary sulfonamide moiety is described. These compounds are powerful inhibitors of several isozymes of the enzyme carbonic anhydrase. Separate QSAR's are given for inhibition of three of these isozymes, using descriptors mainly derived from molecular orbital calculations by the semiempirical AM1 method. Activity was found to depend on electrostatic potential-based charges on the atoms of both sulfonamide groups, HOMO and LUMO energies, dipole moments, and lipophilicities. These results are compared with those from other studies. (C) Elsevier, Paris.
• Design and synthesis of procollagen C-proteinase inhibitors
  作者：Eric Turtle、Nicholas Chow、Charles Yang、Sergio Sosa、Udo Bauer、Mitch Brenner、David Solow-Cordero、Wen-Bin Ho

  DOI：10.1016/j.bmcl.2012.10.067

  日期：2012.12

  Non-peptidic inhibitors of procollagen C-proteinase (PCP) were designed from substrate leads. Compounds were optimized for potency and selectivity, with N-substituted aryl sulfonamide hydroxamates having the best combination of these properties. Compounds 89 and 60 have IC50 values of 10 and 80 nM, respectively, against PCP; excellent selectivity over MMP's 1, 2, and 9; and activity in cell-based collagen deposition assays. (C) 2012 Elsevier Ltd. All rights reserved.
• A novel sulfonamide derivative as a strong and selective apototic agent against hematological malignancies
  作者：Álisson Bigolin、Mariana F. Maioral、Natália M. Stefanes、Alessandra Mascarello、Louise D. Chiaradia-Delatorre、Ricardo J. Nunes、Rosendo A. Yunes、Maria Cláudia Santos-Silva

  DOI：10.1007/s11696-019-00984-7

  日期：2020.9

  it was significantly less cytotoxic to non-tumor cells. On acute leukemia cells, sulfonamide DFS16 activated intrinsic and extrinsic apoptosis with Bax/Bcl-2 inversion, increased FasR expression and ΔΨm loss. In K562, DFS16 induced apoptosis by caspase-3 activation, while in Jurkat, it induced AIF release and caspase-3 independent apoptosis. In multiple myeloma, DFS16 induced cell cycle arrest at the

  当前可获得的针对血液系统恶性肿瘤的化学治疗药物具有多种不良反应，并且与高死亡率相关。因此，在这项研究中，我们评估了26种新的磺酰胺衍生物对急性白血病和多发性骨髓瘤细胞的细胞毒性作用，以试图发现一种可以用作新化学治疗剂原型的新的选择性和安全化合物。最具细胞毒性的化合物DFS16以浓度和时间依赖性方式降低K562，Jurkat和MM.1S细胞的细胞活力，并且对非肿瘤细胞的细胞毒性明显降低。在急性白血病细胞上，磺酰胺DFS16通过Bax / Bcl-2倒置激活FasR表达和ΔΨm丢失，从而激活内在和外在凋亡。在K562中DFS16通过激活caspase-3诱导凋亡，而在Jurkat中，它诱导AIF释放和caspase-3独立凋亡。在多发性骨髓瘤中，DFS16诱导细胞周期停滞在G2 / M期，并伴随ΔΨm丢失而凋亡。总之，结果表明，新的磺酰胺衍生物DFS16在急性白血病和多发性骨髓瘤细胞中诱导凋亡
• Novel sulfonyl(thio)urea derivatives act efficiently both as insulin secretagogues and as insulinomimetic compounds
  作者：Alessandra Mascarello、Marisa Jádna Silva Frederico、Alisson Jhonathan Gomes Castro、Camila P. Mendes、Márcio Ferreira Dutra、Viviane Mara Woehl、Rosendo Augusto Yunes、Fátima Regina Mena Barreto Silva、Ricardo José Nunes

  DOI：10.1016/j.ejmech.2014.09.007

  日期：2014.10

  Glibenclamide is widely used in the management of non-insulin dependent diabetes mellitus, but numerous risks limit its use in therapy. In the search for novel structures that are safer and more efficient than glibenclamide, we obtained new chemical analogs based on bioisosterism, through the treatment of benzenesulfonamide derivatives with isothiocyanates and isocyanates, affording (thio)ureas with good yield. We also verified the hypoglycemic activity, through an in vivo approach. Most of these synthesized compounds improved glucose tolerance, and the mechanism of action of the best compound (7) suggests that its effect is mediated by insulin secretion, while its hypoglycemic action is triggered by glucose uptake involving GLUT4 expression and translocation through PI-3K and PKA activity and active de novo protein synthesis in skeletal muscle. Taking all these factors together, sulfonylthiourea 7 acts as an insulin secretagogue and insulinomimetic agent on glucose homeostasis, and does not exhibit toxicity in acute treatment.