19/10/2026
Duchenne muscular dystrophy (DMD) is characterized by progressive skeletal muscle degeneration, caused by cycles of muscle damage, chronic inflammation, and a declining capacity for muscle regeneration. With limited therapeutic options available, there’s a need for new strategies to support muscle repair and reduce inflammation.
In a study published in Biochemical Pharmacology, researchers examined the potential of niclosamide as a therapeutic strategy for DMD. Using primary macrophages from mdx mice, the researchers found that niclosamide reduced inflammation and reactive oxygen species and pushed macrophages toward an anti-inflammatory, pro-regenerative phenotype. In human DMD myoblasts, niclosamide enhanced myogenic differentiation and increased the levels of utrophin, which can functionally compensate for dystrophin. In vivo experiments using mdx mice showed that niclosamide treatment improved muscle strength during early treatment, lowered creatine kinase levels, and reduced muscle damage. Altogether, this proof-of-concept study supports the potential role of niclosamide as a therapeutic candidate for DMD.
To study myogenic differentiation in human DMD myoblasts, the researchers used our Skeletal Muscle Cell Growth Medium and Differentiation Medium. Optimized media specifically designed for skeletal muscle cell culture make it easier to capture consistent differentiation outcomes, a key consideration when testing how a compound affects cell phenotype.
Studies like this highlight the importance of reliable cell culture tools for evaluating emerging therapeutic candidates in disease-relevant models.
Milani M, Della Valle I, Torcinaro A, et al. Niclosamide reprograms macrophages and improves muscle integrity in Duchenne muscular dystrophy models. Biochem Pharmacol. Published online July 28, 2026.
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