Duchenne Muscular Dystrophy (DMD) is a fatal muscle disease with an incidence of 1 in 5000 males. DMD results from mutations in the gene encoding dystrophin, a 427 kDa scaffolding protein responsible for providing a mechanical link between the muscle fiber actin cytoskeleton and laminin in the extracellular matrix. The 7β1 integrin is a transmembrane linkage protein in skeletal and cardiac muscle that also links laminin to the actin cytoskeleton. Studies have demonstrated that transgenic and virally mediated overexpression of the 7 integrin alleviates disease progression and improves survival of mouse models of DMD. Loss of the 7 integrin in dystrophin-deficient mdx mice results in a severe muscle disease and a maximum lifespan of around 4 weeks. Together these studies demonstrate that the 71 integrin protein serves in an overlapping capacity to that of dystrophin in muscle and is a target for drug-based therapies. The Burkin lab has previously shown treatments with compounds that increase the 7 integrin in dystrophic muscle lead to enhanced muscle regeneration, improved skeletal muscle strength and decreased myofiber damage. In collaborative efforts between Sarcomatrix, Strykagen, and the Burkin lab at UNR, here we will display our ongoing efforts to advance our lead alpha7 Integrin enhancing small molecule called S969 towards the clinic. These studies include in vitro assessments, mdx mouse and GRMD canine efficacy studies, and primate safety and PK evaluation. Our results show S969 treatments are effective as a therapeutic intervention for DMD animal models and will be an effective and affordable option to treat DMD patients in the future.