INmune Bio, Inc. in collaboration with Professor Armando Villalta, Ph.D. of University California, Irvine School of Medicine, has shown targeting soluble TNF (sTNF) using a Dominant-Negative TNF (DN-TNF) biologic significantly decreased muscle damage in a murine mdx model of Duchenne Muscular Dystrophy (DMD) and showed a statistically significant increase in muscle regeneration. Current clinical approaches to limiting muscle damage and inflammation in DMD patients, such as corticosteroids, can be immunosuppressive and promote metabolic problems, leading to significant long-term side effects including muscle atrophy with chronic use. There are currently no approved drugs that promote muscle regeneration in DMD patients.

DMD and other muscle disorders are the focus of a diverse array of drug development efforts to slow disease progression, such as decreasing inflammation and fibrosis, or by restoring/replacing missing dystrophin. Prior pre-clinical attempts using non-selective TNF inhibitors to target TNF as a therapeutic approach for treatment of DMD were limited by some of the same side effects identified in clinical and commercial use of these non-selective TNF inhibitors. Duchenne muscular dystrophy is a rare, genetic condition characterized by progressive muscle damage and weakness caused by the inability of skeletal muscle cells to produce dystrophin.

Without dystrophin, muscles become damaged and weakened as they are used. The muscle cells lose the ability to repair themselves and are replaced by scar tissue. Individuals with DMD will develop problems walking and breathing, and eventually, the heart and the muscles that help them breathe will stop working.

DMD primarily affects males, with 1 in 3500 to 5000 boys born worldwide having Duchenne. In rare cases, it can also affect females. Duchenne is an irreversible, progressive disease - there is no cure at present.