LAUSR

Thymosin β4 is a naturally-occurring regenerative protein present in almost all cells and body fluids, including wound fluid. In multiple preclinical injury models, it promotes dermal repair and tissue regeneration. Thymosin β4 acts by increasing keratinocyte/epithelial cell migration, angiogenesis, and cell survival, and by decreasing inflammation, apoptosis, and scarring. It also modulates cytokines, including those that cause itching. Thymosin β4 promotes faster repair in various chronic human wounds, including pressure ulcers, stasis ulcers, and epidermolysis bullosa lesions. The faster healing time with increased keratinocyte migration and angiogenesis and reduction in both inflammation and scarring are especially important for epidermolysis bullosa patients who suffer from slow healing and inflammation that leads to itching, infections, pain, fluid loss, scarring, and tissue damage. These multiple mechanisms of action support thymosin β4’s role in accelerating dermal repair and suggest the potential to treat various types of severe wounds, including epidermolysis bullosa patients who suffer from frequent blistering wounds that can be life threatening. There is an urgent need at this time to develop a therapeutic, such as thymosin β4, for epidermolysis bullosa. Despite progress in gene/stem cell therapy, there is no cure for this disease and careful wound management is the standard of care.