A Cambridge-led clinical trial has raised hopes for a new class of multiple sclerosis (MS) treatments after finding that a combination of a diabetes drug and an antihistamine could partially repair nerve damage.
The CCMR Two trial tested metformin, widely used for type 2 diabetes, alongside clemastine, an antihistamine previously linked to myelin repair. Seventy patients with relapsing MS were recruited, with half receiving the drug combination and half a placebo for six months.
Researchers measured the speed of electrical signals between the eyes and brain, which are slowed in MS due to damaged myelin sheaths around nerves. Patients on the drug combination showed improved signal speed compared with the placebo group, but the effect – just 1.3 milliseconds faster – was too small to produce noticeable improvements in vision or disability over the trial period.
“It’s smaller than we were hoping for,” said lead researcher Dr Nick Cunniffe of the University of Cambridge. “My conclusion is that the drugs have a biological effect to promote remyelination, but people do not feel better on these drugs over six months.”
Despite the modest results, experts described the findings as an important proof of concept. Emma Gray of the MS Society, which funded the trial, said longer studies would be needed: “We would not expect them to have a clinical benefit after only six months. It will take longer for this to be seen.”
MS affects nearly 3 million people worldwide and more than 150,000 in the UK, most diagnosed in their 30s or 40s. Current therapies focus on reducing immune system attacks, but none can reverse the progressive damage caused once myelin is lost.
Fatigue and diarrhoea were reported side effects of the drug combination, and researchers stressed that patients should not attempt to obtain the drugs outside clinical trials.
Jonah Chan of the University of California, San Francisco, who previously led work on clemastine, said the results added weight to the long-term goal: “I’m more convinced than ever that remyelination is the critical path to preventing permanent disability in MS. It is also the only immediate hope for restoring function.”
Scientists say the next step will be larger and longer trials to determine whether the early signs of repair can translate into lasting improvements for patients.
