Alzheimer’s drug succeeds in slowing cognitive decline, makers Eisai and Biogen

Sept 27 (Reuters) – Eisai Co Ltd (4523.T) and Biogen Inc (BIIB.O) on Tuesday said their experimental Alzheimer’s drug significantly slowed cognitive and functional decline in a large trial of patients in the early stages of the disease, marking a rare win in a field littered with failed drugs.

The drug, lecanemab, slowed progress of the brain-wasting disease by 27% compared with a placebo, meeting the study’s main goal, and potentially offering hope for patients and their families desperate for an effective treatment.

“It’s not a huge effect, but it’s a positive effect,” said Ronald Petersen, director of the Mayo Clinic Alzheimer’s Disease Research Center in Rochester, Minnesota.

The race to stem the progression of Alzheimer’s comes as the number of Americans living with the disease is expected to roughly double to 13 million by 2050, according to the Alzheimer’s Association.

Globally, the figure could reach 139 million by 2050 without an effective treatment, Alzheimer’s Disease International said.

Shares of Eisai jumped 17% to the daily limit in Tokyo, while Biogen shares were up 46% in premarket trading.

Eisai, leader of the 50-50 partnership’s lecanemab program, is seeking FDA approval under an accelerated pathway, with a decision expected in early January.

Eisai is aiming for full approval and commercialization of the drug in the United States, Europe, and Japan by the end of 2023, CEO Haruo Naito told reporters in Tokyo.

The company said results from the 1,800-patient trial prove the longstanding theory that removal of sticky deposits of a protein called amyloid beta from the brains of people with early Alzheimer’s can delay advance of the debilitating disease.

The lecanemab data suggest “a potentially new multi-billion dollar franchise,” Jefferies analyst Michael Yee said in a research note.

‘VERY EARLY DAYS’

Lecanemab, like the partners’ previous drug Aduhelm, is an intravenous antibody designed to remove amyloid deposits. Unlike Aduhelm, lecanemab targets forms of amyloid that have not yet clumped together.

“If you can slow a disease by almost 30% that’s fantastic,” said Dr Jeff Cummings, director of the Chambers-Grundy Center for Transformative Neuroscience at the University of Nevada Las Vegas.

The so-called amyloid hypothesis has been challenged by some scientists, particularly after the U.S. Food and Drug Administration’s controversial approval of Aduhelm in 2021 based on its plaque-clearing ability rather than proof that it helped slow cognitive decline. The decision came after the FDA’s own panel of outside experts had advised against approval.

While the top-line results for lecanemab are convincing, it’s still “very early days” in determining whether the effects are clinically meaningful, said Dr Kristian Steen Frederiksen, director of a clinical trial unit at the University of Copenhagen.

Alzheimer’s “is an extremely complex disease and amyloid-related pathology is unlikely to be the only player,” he said. “Therefore targeting a single target is not likely to produce large effect sizes.”

Aduhelm was the first new Alzheimer’s drug approved in 20 years after a long list of…