This article was first published in The Australian. 1 June 2017.
A “game changing” analgesic could bring relief to millions of Australians, after Melbourne researchers discovered why so many previous attempts to develop new pain drugs have floundered.
In a proof-of-concept study, Monash University scientists unravelled the molecular workings of a “receptor” protein long implicated in chronic pain. When they used the insights to tweak a failed drug, it doused pain in laboratory mice and rats.
Co-researchers at New York’s Columbia University are now laying plans to trial the technique in humans. The team hopes the breakthrough, outlined this morning in the journal Science Translational Medicine, will help suppress a global pain epidemic afflicting tens of millions of people worldwide.
Chronic pain is considered the most common cause of disability, affecting more people than diabetes, heart disease and cancer combined. Current drugs often do not work and carry serious side effects, with anti-inflammatories like ibuprofen thought to increase the risk of heart attacks, while morphine and other opioids cause around 600 accidental deaths a year in Australia alone.
Co-author Meritxell Canals, from the ARC Centre of Excellence in Bio-Nano Science, said the “NK1” receptor had long been known to play a role in pain transmission. She said researchers had spent a decade developing drugs to control pain by blocking the receptor, but none of them had worked.
The new study found that the protein transmitted pain signals not when it was lurking on the surface of nerve cells, as researchers had assumed, but after it had migrated inside the cells. “They were targeting the right receptor, but in the wrong location,” Dr Canals said.
The team devised a way of forcing drugs through cell walls by attaching them to fat molecules. Tests using an existing drug, spantide, found that the technique provided “prolonged” pain relief in rodents.
Dr Canals said analgesics re-engineered in this way could prove effective against aching joints and backs and the pain caused by cancer, among other things. “The challenge now is to translate the technology into human clinical trials.”
Lead researcher Nigel Bunnett, who joined Columbia last year from Monash’s Institute of Pharmaceutical Sciences, said more than one-third of current drugs targeted receptor proteins on cell surfaces. He said modifying them in similar ways could boost the effectiveness of “many different classes of medications”.