Centro de Investigaciones Biológicas-CSIC , Ramiro de Maeztu 9, 28040 Madrid, Spain.
Department of Pediatrics, Division of Neurology, Cincinnati Children's Hospital , Cincinnati, Ohio 45219, United States.
J Med Chem. 2017 Jun 22;60(12):4983-5001. doi: 10.1021/acs.jmedchem.7b00395. Epub 2017 Jun 6.
Glycogen synthase kinase 3 β (GSK-3β) is a central target in several unmet diseases. To increase the specificity of GSK-3β inhibitors in chronic treatments, we developed small molecules allowing subtle modulation of GSK-3β activity. Design synthesis, structure-activity relationships, and binding mode of quinoline-3-carbohydrazide derivatives as allosteric modulators of GSK-3β are presented here. Furthermore, we show how allosteric binders may overcome the β-catenin side effects associated with strong GSK-3β inhibition. The therapeutic potential of some of these modulators has been tested in human samples from patients with congenital myotonic dystrophy type 1 (CDM1) and spinal muscular atrophy (SMA) patients. We found that compound 53 improves delayed myogenesis in CDM1 myoblasts, while compounds 1 and 53 have neuroprotective properties in SMA-derived cells. These findings suggest that the allosteric modulators of GSK-3β may be used for future development of drugs for DM1, SMA, and other chronic diseases where GSK-3β inhibition exhibits therapeutic effects.
糖原合酶激酶 3β(GSK-3β)是几种未满足需求疾病的重要靶点。为了提高慢性治疗中 GSK-3β 抑制剂的特异性,我们开发了能够细微调节 GSK-3β 活性的小分子。本文介绍了作为 GSK-3β 别构调节剂的喹啉-3-甲酰肼衍生物的设计、合成、构效关系和结合模式。此外,我们还展示了别构配体如何克服与强烈 GSK-3β 抑制相关的β-连环蛋白副作用。一些调节剂的治疗潜力已在患有先天性肌强直性营养不良 1 型(CDM1)和脊髓性肌萎缩症(SMA)患者的人类样本中进行了测试。我们发现,化合物 53 可改善 CDM1 成肌细胞的延迟肌发生,而化合物 1 和 53 在 SMA 衍生细胞中具有神经保护作用。这些发现表明,GSK-3β 的别构调节剂可能用于开发用于 DM1、SMA 和其他 GSK-3β 抑制具有治疗效果的慢性疾病的药物。