DMD – ANIMAL MODELS & PRECLINICAL TREATMENT

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The overexpression and the increased activity of redox-sensitive protein Src-Tyrosine Kinase (TK) in dystrophin-deficient muscles can contribute to β-dystroglycan (β-DG) degradation and in reinforcing proinflammatory damaging signalling. According to the hypothesis that Src-TK is a feasible drug target for ameliorating Duchenne Muscular Dystrophy (DMD), we have recently focused on preclinical studies for repurposing dasatinib, a Src-TK’s competitive inhibitor. We have shown that a 4-week subcutaneous treatment with dasatinib (5mg/kg, 3 times/week) induced an increment in β-DG at muscle level, although a parallel limited efficacy on pathology-related functional, structural and biochemical indices was observed.

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