Src Tyrosine Kinase (TK), a redox-sensitive protein, is overexpressed in dystrophin-deficient muscles and can be overactive due to excessive production of reactive oxygen species, contributing to β-dystroglycan degradation and reinforcing damaging signaling. Thus, the pharmacological inhibition of Src TK seems a feasible strategy to ameliorate Duchenne muscular dystrophy (DMD). We focused on two Src TK inhibitors, PP2 and dasatinib. We performed a proof-of-concept preclinical study in treadmill exercised mdx mice by in vivo administration of PP2 and dasatinib at the same doses of 5 mg/kg, three times a week s.c..

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