An experimental drug developed by Japanese firm Eisai and US biotech firm Biogen is found to have brought about significant decline in the progression of early-stage Alzheimer’s disease (AD).
Nearly 1,800 global participants – some diagnosed only six months earlier with AD – were given the drug lecanemab in its phase-III trials.
It was found that the disease progressed 27 per cent slower with the use of this drug compared to a placebo.
“It’s not a huge effect, but it’s a positive effect,” Ronald Petersen, director of the Mayo Clinic Alzheimer’s Disease Research Center in Rochester, Minnesota, was quoted as saying by news agency Reuters. “This means that treating amyloid is a step in the right direction,” he said.
After decades of research the new drug shows promise for Alzheimer’s.
Lecanemab is a synthesised antibody that targets the amyloid beta protofibrils — the initial form of the sticky amyloid beta plaques in the brain that is known to cause Alzheimer’s.
The clinical trials, called Clarity AD, included participants from diverse ethnic and racial groups with various comorbidities. The study was placebo-controlled, double-blind, parallel-group and randomised.
The participants were given a bi-weekly dose of lecanemab and assessed at the end of 18 months. Their cognitive and functional performance was evaluated based on interviews with people living with AD and their caregivers and other standardised assessment methods.
Although the trial reports indicate associated side effects such as brain swelling and micro-haemorrhaging (21.3 per cent in people with AD and 9.3 per cent in placebo), the company statements say that the figures are within tolerable limits.
The companies are seeking the US Food & Drug Administration’s approval of the drug as well as market authorisations in Japan and Europe.
With the increase in longevity and population of older people, Alzheimer’s poses a high disease burden on nations globally.
“The lecanemab Clarity AD study results prove the amyloid hypothesis, in which the abnormal accumulation of Amyloid beta in the brain is one of the main causes of Alzheimer’s disease, when targeted with a protofibril-binding therapy,” said Haruo Naito, Chief Executive Officer at Eisai in a statement.
