SCIENTISTS in Bradford have found a new way of treating inflammatory diseases using medicines already treating diabetics and an ingredient found in an everyday headache tablet.

Researchers at the University of Bradford have discovered that a molecule thought to play a key role in flaring up some inflammatory diseases such as rheumatoid arthritis and some cancers, can be switched off by using metformin – a medicine used by diabetics to control blood sugar levels – and then salicylate, the main ingredient in aspirin.

The researchers, which included scientists from the University of Glasgow, now hope to carry out more studies and eventually clinical trials with the drugs, which are already prescribed to millions of patients around the world.

Professor Tim Palmer, a pharmacologist at the University of Bradford who led the research, said: “While our studies are at a very early stage, we’ve identified a new biochemical process that suggests certain anti-diabetic drugs could potentially be repurposed to treat diseases caused by activated Janus kinase proteins.”

He explained that Janus kinase (JAK) proteins, named after the ancient Roman two-faced god, are involved in controlling inflammation in certain tissues.

“They act like gatekeepers at the surface of cells, reacting to signals released by the immune system and transmitting these messages inside the cell.

“These Janus kinase proteins, however, can also carry mutations that make them faulty so they are permanently turned on and become overactive. A fault like this in Janus kinase 1 (JAK1) has been found to occur in several diseases.”

Professor Palmer and his colleagues have discovered that another protein, known as AMP-activated protein kinase (AMPK) which can be activated by metaformin and salicylate, can turn JAK1 off even when it is faulty.

Their findings have now been published in the journal Science Signalling.

Professor Palmer said: “We found this AMPK pathway is able to profoundly inhibit JAK signalling and it seems to work in a way that other drugs that target the JAK proteins do not.”

The researchers believe this approach could also be used to turn off other inflammation controlling proteins, which are known to be overactive in other diseases.

Co-author Dr Ian Salt, a senior lecturer at the Institute of Cardiovascular and Medical Sciences at the University of Glasgow, added: “Although it is still early in our work, our findings suggest we can design future therapies for those disorders that target this pathway.”

The British Heart Foundation and Diabetes UK funded the study.