The research team found that an enzyme called cyclooxygenase-2 (COX-2), which is the molecular target of common drugs such as aspirin, ibuprofen and acetaminophen, mediates the transformation of omega-3 fatty acids into EFOX. Notably, cellular EFOX concentrations were significantly increased in the presence of aspirin, suggesting another mechanism for that drug's beneficial effects.

"There is a lot of evidence that supports minimizing inflammation as a fundamental therapy for many diseases," Dr. Freeman said. "Our new insights help explain in part the multitude of beneficial actions observed for both omega-3 fatty acids and aspirin, and the discovery of this new class of omega-3 fatty acid-derived anti-inflammatory mediators could point drug development activities in new and fruitful directions."

For example, drugs that, like aspirin, enhance the production of EFOX could be of value, or new agents might be synthesized that are able to induce anti-inflammatory signals that are similar to those induced by EFOX, he explained. Drs. Freeman and Schopfer and their drug discovery team now are working on some of these approaches.

Source: University of Pittsburgh Schools of the Health Sciences