Peptide for Wound Healing and Tissue Repair


Technology: The inventors have developed a wound-treating material for use in promoting wound healing, decreasing scarring, decreasing inflammation, or promoting formation of healthy tissue architecture post-injury. This JM2 peptide effectively works by blocking hemichannels and lessening ATP release from cells. The JM2 peptide is able to modulate the initial innate immune response to rebuild normal tissue instead of scar tissue. When utilizing the JM2 peptide, there is improved vasculature surrounding an implant capsule with a smaller connective tissue response. This technology has applications in not only surgical implants and dermatological applications, but also age-related macular degeneration and many other injuries or inflammation that are a result from trauma, surgery, or disease. JM2 can be administered as a pharmaceutical preparation, a wound dressing, or a medical implant. Researchers are currently working to demonstrate with FRAP techniques that JM2 blocks Cx43, while not affecting gap junction communication. This will demonstrate that the cell can have functional gap junctions while having critical hemichannels blocked to mute the inflammatory response.

Overview: There is a clinical unmet need for therapies that can reduce the inflammatory response and subsequent scarring that occurs with trauma, injury, surgery, implantation, etc. This novel peptide has applications for slow healing wounds, dermal ulcers cardiac injury, and other disease states in which scarring impacts tissue function.


Advantages: Increased normal tissue response versus scar tissue at site of surgical implant, increased vasculature at site of implant, reduction of capsular contracture, reduction of ATP release to reduce neutrophil invasion.

Key Words: Wound healing, tissue repair, regeneration, anti-scarring, anti-inflammatory, anti-fibrotic, peptide therapeutic, biologic, ATP, purinergic signalling, neutrophils

Publications: J. Matthew Rhett, Bennett W Calder, Stephen A Fann, Heather Bainbridge, Robert G. Gourdie, Michael J Yost. “Mechanism of Action of the Anti-Inflammatory Connexin43-Mimetic Peptide JM2 American Journal of Physiology - Cell Physiology (2017)

Rhett, J. Matthew, et al. "Connexin-Based Therapeutics and Tissue Engineering Approaches to the Amelioration of Chronic Pancreatitis and Type I Diabetes: Construction and Characterization of a Novel Prevascularized Bioartificial Pancreas." Journal of Diabetes Research 2015 (2015).

Calder, Bennett W., et al. "Inhibition of connexin 43 hemichannel-mediated ATP release attenuates early inflammation during the foreign body response."Tissue Engineering Part A (2015).

Rhett, J. Matthew, Stephen A. Fann, and Michael J. Yost. "Purinergic signaling in early inflammatory events of the foreign body response: modulating extracellular ATP as an enabling technology for engineered implants and tissues." Tissue Engineering Part B: Reviews 20.5 (2014): 392-402.

Inventors: M. Yost, R. Gourdie, E. Goldsmith, L.J. Jourdan, J.M. Rhett
Patent Status: US Patent 9,345,744, Continuation Filed US 15/135,780
MUSC-FRD Technology ID: P1204


Licensing Status: This technology is currently optioned to a company for the field of cancer. Please contact the FRD to be put in touch with the company if interested in this field.



Patent Information:
For Information, Contact:
Scott Davis
Associate Director, Licensing
MUSC Foundation for Research Development
Robert Gourdie
Edie Goldsmith
L. Jane Jourdan
J. Matthew Rhett
Michael Yost
wound care
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