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Methods To Treat Fatty Liver Disease

The National Cancer Institute's Laboratory of Metabolism is seeking statements of capability or interest from parties interested in collaborative research to further develop, evaluate, or commercialize therapeutics for fatty liver disease.

Currently, there are no adequate therapies for fatty liver disease, the most prevalent liver disease in the United States. Fat-Specific Protein 27 (FSP27) expression is regulated by PPAR??, a gene known to play a critical role in the development of fatty liver.  Over-expression of FSP27 results in an increase in triglyceride accumulation and an increase in cystolic vacuoles containing lipid droplets which are associated with development of fatty liver disease or hepatic steatosis.  This abnormal retention of lipids in liver cells occurs in diabetes and alcoholism and is correlated with decreased liver function which can often lead to cirrhosis and sometimes death. 

The inventors have discovered that an shRNA directed against FSP27 inhibits fatty liver. This invention could potentially lead to the development of a new shRNA based therapy for fatty liver disease. This invention also describes methods of inhibiting FSP27 using antisense compounds, small molecule inhibitors and antibodies that target FSP27. 
Further R&D Needed:

  • Develop new methods of delivery for the shRNA
  • Optimize shRNA inhibitors of FSP27 and test them in additional animal models
R&D Status: Preclinical

IP Status:  U. S. Provisional Application No. 61/043,330 filed 08 April 2008

Value Proposition:  Ability to inhibit Fat-Specific Protein 27 (FSP27)

Contact Information:
John D. Hewes, Ph.D.
NCI Technology Transfer Center
Tel: 301-435-3121
Email: hewesj@mail.nih.gov

Please reference advertisement #784

Revised 1/12/2008


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Page Last Updated: 12-17-2008