Intellectual Property Office

Non-Confidential Disclosures

“Protein Kinase C Zeta Inhibition to Treat Vascular Permeability”

PSU Invention Disclosure Number 2006-3228

Field of the Invention:

Vascular Biology (retinopathy of prematurity; diabetic retinopathy, age-related macular degeneration)

Inventors:

David A. Antonetti, Jeffrey M. Sundstrom

Patent status:

Patent Pending

Background:

The vasculature of the central nervous system normally provides tight control over the flow of fluids, nutrients, and toxins to and from the nervous tissue. Unfortunately, in a variety of diseases, the overproduction of vasculature-targeting cytokines leads to the accumulation of fluid in the nervous tissue causing neuronal dysfunction and neuronal death. This alteration in blood vessel permeability is related to the three leading causes of vision loss in the United States: diabetic retinopathy, retinopathy of prematurity, and age-related macular degeneration. Although protein kinase C beta (PKC beta) inhibitors are currently under investigation as potential therapies to prevent vascular permeability in diabetic retinopathy, these compounds are only partially effective at reducing cytokine induced permeability. Novel therapies are clearly needed for the treatment of vascular permeability in retinal eye disease

Invention description:

Our group has identified a novel signaling pathway and a specific enzyme, Protein Kinase C Zeta, that regulates cytokine-induced vascular permeability. We have also identified a small molecule inhibitor of this enzyme which completely prevents cytokine-induced vascular permeability in both in vitro and in vivo disease models. Furthermore, the current body of literature suggests that the targeted enzyme is not essential for growth and development making it an ideal target to prevent excess vascular permeability in diseases such as diabetic retinopathy, retinopathy of prematurity, and age-related macular degeneration.

Advantages:

• Vascular permeability is important to a wide number of diseases including: diabetic retinopathy, retinopathy of prematurity and age-related macular degeneration
  
• The small molecule′s target enzyme is not necessary for normal growth and development thus reducing the likelihood of unwanted complications
  
• We have developed a specific small molecule inhibitor that is effective at preventing cytokine-induced vascular permeability in both in vitro and in vivo disease models.
  

Contact:

Dr. James F. Kolonay, Ph.D.
Technology Licensing Officer
Intellectual Property Office
The Pennsylvania State University
113 Technology Center
University Park, PA 16802-7000
Phone: (814) 863-7070
Fax: (814) 865-3591
E-mail: jfk11@psu.edu