Abstract
As there are no effective treatments for muscular dystrophy (MD), identifying systemically acting small-molecule therapeutics is desirable. Tyrosine phosphorylation of β-dystroglycan, which occurs via tyrosine kinase in dystrophin-deficient muscles, has been reported to induce muscle damage, and several tyrosine kinase inhibitors have been researched as potential therapeutic agents for MD. Nilotinib, a second-generation tyrosine kinase inhibitor, was potentially effective in MD by reducing muscle fibrosis. However, there was a problem that its direct effect on satellite cells inhibited muscle differentiation. Dasatinib, a third-generation tyrosine kinase inhibitor, is also expected to be effective in MD, but its effect on muscle regeneration is unknown.
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