We used two different dystrophin-deficient models—classic mdx mice with moderate symptoms and D2.DMDel8-34 mice (D2.DMD) with severe progression similar to DMD—and found that intraperitoneal administration of VBIT-4 (20 mg/kg) delayed the development of pathology in D2.DMDel8-34 mice but had no effect on the mdx phenotype with mild symptoms. The gene discussed is DMD; the disease is Duchenne muscular dystrophy.