Keeping muscle strength and quality is important for maintaining healthy life expectancy. We previously reported that a pathological interaction between transient receptor potential canonical (TRPC) 3 protein and NADPH oxidase 2 (Nox2) protein promotes Nox2-dependent reactive oxygen species (ROS) production, leading to myocardial atrophy in rodents. We also reported that ibudilast, an anti-inflammatory drug used in the treatment of asthma and stroke, potently inhibits TRPC3-Nox2 complex formation and muscle atrophy in anthracycline-treated mice. Here, we investigated whether ibudilast attenuates skeletal muscle atrophy in Duchenne muscular dystrophy model (mdx) mice. Muscle strength was measured using hanging-wire test. Compared with vehicle-treated mdx mice, treatment with ibudilast (10mg/kg/day, i.p.) for 4 weeks attenuated compensative increase in soleus weight and muscle wasting, as well as the increases in creatine kinase, MuRF, Col1a1 and aSMA levels. Proxymity ligation assay revealed that the number of TRPC3-Nox2 protein complex-positive signals were significantly increased in soleus, which was canceled in ibudilast-treated mdx mice. These results suggest that ibudilast prevent the progression of muscle atrophy and wasting in mdx mice, mainly through inhibiting TRPC3-Nox2 complex formation.