Why the study?
Do allosteric modulators of GSK-3β improve delayed myogenesis and provide neuroprotection in cells derived from CDM1 and SMA patients?
Do allosteric modulators of GSK-3β improve delayed myogenesis and provide neuroprotection in cells derived from CDM1 and SMA patients?
Allosteric modulators of GSK-3β show potential for treating chronic diseases like DM1 and SMA by improving cellular phenotypes while potentially avoiding side effects of strong GSK-3β inhibition.
These preclinical results suggest allosteric GSK-3β modulation may offer a safer therapeutic pathway for neuromuscular.
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.
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Pérez et al. (2017) studied this question.
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