The regenerative peptide thymosin β4 accelerates the rate of dermal healing in preclinical animal models and in patients.

Chronic nonhealing cutaneous wounds are a worldwide problem with no agent able to promote healing. A naturally occurring, endogenous repair molecule, thymosin beta 4 (Tβ4), has many biological activities that promote dermal repair. It is released by platelets at the site of injury and initiates the repair cascade. Tβ4 accelerated dermal healing of full-thickness punch wounds in various animal models, including normal rats and mice, steroid-treated rats, diabetic mice, and aged mice. Furthermore, in two phase 2 clinical trials of stasis and pressure ulcers, it was found to accelerate healing by almost a month in those patients that did heal. Tβ4 likely acts to repair and regenerate wounds by promoting cell migration and stem cell mobilization and differentiation, and by inhibiting inflammation, apoptosis, and infection. We conclude that Tβ4 is a multifunctional regenerative peptide important in dermal repair.