Small molecule therapeutic that can be delivered locally to enhance TGF-beta activity and promote cartilage growth.
- Increases production of protease inhibitors, simultaneously stimulating production and blocking degradation of extracellular matrix (ECM).
- Potentially reduces or eliminates need for joint replacements by regenerating articular cartilage
Each year, there are approximately one million knee and hip replacements performed in the United States, often due to osteoarthritis (OA), a joint disease that results from the breakdown of joint cartilage and underlying bone. Osteoarthritis is the most common form of arthritis, affecting an estimated 10 percent of men and 18 percent of women aged over 60 in developed countries. The number of people suffering from osteoarthritis is expected to continue to increase due to the aging population and growing prevalence of obesity. Current treatment may include patient education, physical therapy, weight control, use of medications, and eventually total joint replacement. There is currently no cure for osteoarthritis nor a small molecule capable of regenerating cartilage.
TGF-beta is believed to play key roles in the development, growth and maintenance of articular cartilage and several studies suggest that TGF-beta levels are down regulated in osteoarthritis cartilage. Researchers at Emory University have developed small molecule compounds that potentiate TGF-beta activity. TGF-beta inhibits terminal differentiation or “hypertrophy” of chondrocytes, blocking endochondral bone formation and allowing formation of articular cartilage at the end of the long bones. This small molecule therapeutic is capable of regenerating cartilage and can potentially reduce the total number of joint replacements worldwide.
Potential lead candidates have been identified.