Derma Sciences is developing a way to help the body utilize its own stem cells more productively for wound healing.


Aclerastide is a patented analog of a naturally occurring peptide, Angiotensin. This analog has been designed to promote wound healing without the blood pressure effects of angiotensin. In laboratory studies, it has been shown to increase keratinocyte proliferation, increase extracellular matrix production, and increase vascularization. Additionally, histological examination in animal studies has shown that aclerastide accelerated collagen deposition six-fold. All of these activities help to accelerate dermal tissue repair.

One potential mechanism of action is the up-regulation of mesenchymal stem cells (MSCs) at the site of injury. MSCs originate in the embryo and are considered to be multipotent — a type of stem cell that has not yet adopted a specific cellular phenotype. Such cells have the ability to differentiate into various types of cells found within the body, including fibroblasts, adipose cells, muscle cells, bone cells, and skin cells.

Extensive pre-clinical studies have demonstrated the ability of aclerastide to accelerate healing and reduce scar formation. Pre-clinical studies thus far have shown:

  • Accelerated healing in full thickness skin excision wounds in rats and diabetic mice9
  • Accelerated healing in partial thickness thermal injuries in guinea pigs6,7
  • Accelerated healing in a random flap skin model in rats4
  • Scar reduction in rats8,10

A Phase I safety study in humans was completed in Q4 2007. A Phase II study of 77 subjects evaluating the percentage of diabetic ulcers completely healed over a 12-week period, among other outcomes, was completed in 20113. The subjects were randomized to receive 4 weeks once-daily topical application with 0.03% aclerastide, 0.01% aclerastide, or Placebo, followed by 20 weeks of standard care. Safety parameters among the intent-to-treat groups were comparable. Covariate analysis compared reduction in ulcer area, depth and volume from baseline, and reductions in the 0.03% aclerastide group were greater at Weeks 12 and 24. Placebo-treated ulcers healed in a median 22 weeks vs. 8.5 weeks for 0.03% aclerastide (p = 0.04).