New compound reduces joint inflammation in arthritis

Researchers have developed a compound that can significantly reduce joint inflammation in animal models of rheumatoid arthritis, paving way for an oral drug to treat the auto-immune disease.
Scientists from The Scripps Research Institute (TSRI) in Florida developed the compound, known as SR2211, that blocked development of virtually all symptoms of rheumatoid arthritis in mice within the first eight to ten days of treatment.
The mice also showed significantly reduced bone and cartilage erosion compared to animals that did not receive treatment.
The experimental compound targets the nuclear receptor RORy, a key regulator of TH17 cells, one of a family of white blood cells that play a role in the immune system.

Identified only a decade ago, TH17 cells have been implicated in numerous autoimmune diseases, including multiple sclerosis, rheumatoid arthritis, inflammatory bowel disease and lupus.
"This compound, and its precursors, showed the ability to block the release of specific inflammatory mediators from Th17 cells in culture, so we were confident that SR2211 would demonstrate good efficacy in rodent models of autoimmune disease," said biochemist Patrick R Griffin, chair of the TSRI Department of Molecular Therapeutics.

"Our newest study strongly supports the idea that by targeting the RORy receptor, we can therapeutically repress inflammation and joint destruction associated with rheumatoid arthritis," Griffin said.

While several treatments are currently available for rheumatoid arthritis, Griffin noted their use is associated with the increased risk of infections and pneumonia.
Since they have to be taken by injection, they are optimised for long, sustained immunosuppressive action, which is a disadvantage in managing opportunistic infections.
An oral medication could be taken daily and stopped immediately to allow the drug to leave the body in the case of a potentially life-threatening infection.
The study will appear in the journal Arthritis & Rheumatism.