SBIR/STTR Award attributes
PROJECT SUMMARY/ABSTRACT Diabetes Mellitus (DM), a metabolic disorder characterized by defective insulin signaling and elevated blood glucose, has become a public health epidemic with half of the US population diagnosed with either DM or pre- diabetes. One of the most common and devastating sequelae of uncontrolled DM is the development of chronic non-healing wounds. An estimated 25% of diabetic patients develop chronic non-healing ulcers in their lifetime that, given the poor vascularity and immunodeficiency associated with diabetes, are highly susceptible to infection and frequently result in limb amputation. DM is currently the seventh leading cause of death in the U.S. Current management primarily focuses on controlling wound bioburden to promote wound healing, which includes pressure off-loading, antimicrobial medications and dressings, judicious wound care, and optimization of lifestyle factors. However, complete wound closure is complicated by impairment of cellular migration and function in DM wounds. Therefore, there is a pressing need to develop novel therapeutic methods for diabetic wounds that directly restore the molecular and cellular processes required to promote proper cutaneous repair.Injuries in diabetic patients often persist and progress. Chronic DM causes significant alterations to several physiologic wound healing mechanisms that impair timely cell infiltration/migration, granulation tissue formation, and wound contraction. Based on more than 20 years of research on wound healing management, we have developed a technologically innovative fibromodulin (FMOD)-based amino acid peptide sequence, SLI-F06, that markedly stimulates fibroblast and endothelial cell migration and myofibroblast differentiation/contraction to promote timely wound closure. Previously, we demonstrated that SLI-F06 significantly promotes acute wound healing without eliciting any adverse effects in preclinical animal studies at maximal feasible dosing as well as in ongoing Phase 1/2a clinical trial targeting acute wound healing. Excitingly, we have shown that repeated SLI- F06 administration significantly accelerates diabetic wound closure in a mouse model (NONcNZO10/LtJ) that closely simulates human type 2 DM. The goal of the current Fast-track SBIR application is to obtain the key preclinical efficacy and mechanism of action data for SLI-F06 as a repeatedly administered, locally applied therapeutic for diabetic wounds for expanding the clinical indication of SLI-F06. Overall, this proposal will accomplish key efficacy and mechanism of action (MOA) objectives to expedite commercialization of SLI-F06-based therapy for diabetic wounds. This product can significantly improve the quality of life of diabetic patients suffering from chronic wounds that can lead to amputations and death.PUBLIC HEALTH RELEVANCE Up to 25% of diabetic patients develop chronic non-healing ulcers in their lifetime, which present significant infection risks given the poor vascularity and immunodeficiency related to diabetes. More generally, chronic non-healing wounds affect an estimated 6.5 Million Americans with annual cost of $50 billion dollars. This project seeks to develop an effective, novel peptide-based treatment to promote wound healing and to improve the quality of life for patients suffering from chronic wounds, especially in the diabetic populations.
