Pfizer Inc. and Merck & Co. have stopped research for new drug on
Eli Lilly's drug that targets amyloid plaques did not significantly
slow cognitive decline.
JANUARY 7, 2018 / 2:59 PM / A MONTH AGO
NEW YORK (Reuters) - Pfizer Inc (PFE.N) is abandoning research to find new drugs aimed at treating Alzheimer’s and Parkinson’s disease, the U.S. pharmaceutical company announced on Saturday.
The company said it expects to eliminate 300 positions from the neuroscience discovery and early development programs in Andover and Cambridge, Massachusetts, and Groton, Connecticut, as it redistributes the money spent on research, according to the emailed statement.
Pfizer is not making any changes to research and development funding for tanezumab, which is being tested as a treatment for joint pain from osteoarthritis, fibromyalgia treatment Lyrica, or its rare disease program.
“This was an exercise to re-allocate spend across our portfolio, to focus on those areas where our pipeline, and our scientific expertise, is strongest,” the company said.
Pfizer has invested heavily in research for Parkinson’s and Alzheimer‘s, and is one of several drugmakers, along with GlaxoSmithKline (GSK.L) and Eli Lilly (LLY.N), that is part of the Dementia Discovery Fund, a venture capital fund launched in 2015 by industry and government groups that seeks to develop treatments for Alzheimer‘s.
However, some of Pfizer’s investments have resulted in disappointment. In 2012, Pfizer and partner Johnson & Johnson (JNJ.N) called off additional work on the drug bapineuzumab after it failed to help patients with mild to moderate Alzheimer’s in its second round of clinical trials.
The company said on Saturday that it will launch a new venture fund to invest in neuroscience research projects.
Pfizer is expected to make a presentation on Monday at the JP Morgan healthcare conference in San Francisco, a key annual event for healthcare
By Michelle Cortez Feb 14, 2017 Updated Feb 15, 2017,
Merck & Co. will end a study of its once-promising Alzheimer’s disease drug in patients with mild-to-moderate forms of the condition, just three months after Eli Lilly & Co. announced its own setback in a field that’s been littered with failures.
There was “virtually no chance of finding a positive clinical effect,” according to an independent panel of experts that looked at the trial partway through. A separate trial of verubecestat in patients who are showing only symptomatic hints of the degenerative disease will continue, Merck said in a statement, since the panel didn’t find safety signals worrisome enough to also halt that test.
“It’s very disappointing, once again,” said David Knopman, a professor of neurology at the Mayo Clinic in Rochester, Minnesota.
Shares of Kenilworth, New Jersey-based Merck fell less than 1 percent to $65.24 at 9:32 a.m. in New York
Alzheimer’s affects about 44 million people worldwide, and robs people of their memories and ability to care for themselves. There hasn’t been a new drug for alleviating symptoms in more than a decade, and there are no medicines proven to slow the condition.
Merck’s drug and others target a plaque, called amyloid, thought to be a cause of the disease. While more such treatments are in development from companies including Biogen Inc. and Roche Holding AG, many researchers now believe that administering drugs after amyloid has built up in the brain may be too late.
“There is mounting evidence -- of which this is another piece -- that removing amyloid once people have established dementia is closing the barn door after the cows have left,” Knopman said.
It’s possible that patients in the study were getting the drug too far along in their disease to help. Verubecestat and similar drugs, called BACE inhibitors, operate before the amyloid has formed into plaques. In the Merck study, however, the patients with mild-to-moderate disease would already have buildup.
“You need to go in at the very earliest stage of disease to show the kind of improvement we are hoping for,” said James Hendrix, director of global science initiatives at the Alzheimer’s Association. “BACE isn’t going to do anything about the plaques that are already there. Maybe if you can go in before there is a lot of plaque buildup in the brain, that’s where you will have the most benefit.”
It’s also possible that the drug was too weak, or that not enough of Merck’s drug was making it into the brain, Knopman said. Previous studies have shown that the drug does have a powerful impact on amyloid levels, though doctors and others in the industry will have to wait for more details of the trial to draw any conclusions, he said.
While investors’ expectations for the study known as Epoch were low, analysts estimated the drug would hit peak sales of about $1.3 billion in 2024, said Mark Schoenebaum, an analyst at Evercore ISI in New York. Patients weren’t given imaging tests to ensure they had plaque buildup from Alzheimer’s disease before they started the trial, an issue that has caused problems in rival studies, he said.
“While it remains possible that BACE inhibition may still have a place in Alzheimer’s disease treatment, the failure of this study for futility will dampen investor enthusiasm for the mechanism,” Schoenebaum said.
Alzheimer's drug targeting soluble amyloid falls short in a large clinical trial
January 24, 2018 Columbia University Medical Center
Summary: Researchers report that solanezumab, a monoclonal antibody-based treatment for Alzheimer's disease developed by Eli Lilly that targets amyloid plaques, did not significantly slow cognitive decline.
FULL STORY: A paper published today in the New England Journal of Medicine reports that solanezumab, a monoclonal antibody-based treatment for Alzheimer's disease developed by Eli Lilly that targets amyloid plaques, did not significantly slow cognitive decline.
Columbia University Irving Medical Center (CUIMC) led the multicenter study.
Researchers have proposed that Alzheimer's disease is caused by the buildup of a sticky protein called beta-amyloid. According to this 'amyloid hypothesis,' the protein forms plaques in the brain that damage and eventually destroy brain cells. Solanezumab was designed to reduce the level of soluble amyloid molecules before they aggregate.
A total of 2,129 patients with mild dementia due to Alzheimer's disease participated in the double-blind, placebo-controlled, phase 3 multicenter trial. This study was the first major Alzheimer's clinical trial to require molecular evidence of amyloid deposition in the brain for enrollment. While the treatment did have some favorable effects, in the main measure of outcome -- measured with a cognitive test called the Alzheimer's Disease Assessment Scale-cognitive subscale -- the researchers did not observe any statistically significant benefit compared with placebo.
The authors suggest that while it is not certain that this particular strategy or drug could be effective, it is possible that either not enough drug was administered or that the drug needs to be administered earlier in the disease course.
In other studies ongoing at CUIMC, solanezumab is being evaluated in presymptomatic patients at risk of Alzheimer's disease. Other Alzheimer's drugs are also in development and being tested at higher doses.
"Although we are disappointed that this particular drug did not prove successful, the field is benefiting from each study," says lead author Lawrence Honig, MD, PhD, professor of neurology at CUIMC. "There is hope that one of the newer ongoing studies may result in an effective treatment for slowing the course of Alzheimer's disease."
The results of this study were first released in late 2016 at the international Clinical Trials on Alzheimer's Disease meeting in San Diego.
The study is titled, 'Trial of Solanezumab for Mild Dementia Due to Alzheimer's Disease.'
The study was designed and funded by Eli Lilly and Company.