New Alzheimer’s drug slows mental decline by 27% in clinical trials

The Japanese pharmaceutical company owns Eisai and its partner, Cambridge-based Biogen announce Their drug slowed the cognitive decline of Alzheimer’s disease in a global trial.

The drug, an antibody called lecanemab, slowed the rate of cognitive decline in the volunteers by 27% compared to those receiving a placebo in the large, late trial.

The companies plan to present the full study results November 29 in clinical trials at the Alzheimer’s Conference (CTAD), with publication in a peer-reviewed journal. For now, the top-line data release is basically all we know.

Eisai and Biogen announced their Alzheimer’s drug that reduced cognitive decline by 27% in a clinical trial.

Scientific cemetery: Any sign of progress in treating Alzheimer’s disease puts scientists, doctors, patients and advocates on high alert. Previous medications either failed to work or gave cloudy results, at best – as was the case with previous Biogen, Controversial The Alzheimer’s drug, aducanumab.

The field is the cemetery of therapy.

Despite the setbacks, researchers have doggedly sought treatments for decades, and the need is dire — and will only increase as the population ages. The Alzheimer’s Association estimates that 6.5 million Americans will have the disease in 2022; By 2050, they expect the number of people over 65 with Alzheimer’s disease to double to 12.7 million.

Haru Naito, CEO of Eisai, said the results of the lecanemab study represent “an important milestone for Eisai in fulfilling our mission to meet the expectations of the Alzheimer’s disease community.”

Not only does Alzheimer’s disease present a major challenge to patients and their families, but it also negatively impacts society, including reduced productivity, increased social costs and anxiety associated with the disease. We believe that helping to ease these burdens will positively impact society as a whole.”

The drug is an antibody designed to bind to a protein in the brain linked to Alzheimer’s disease.

drugs: The drug is an antibody designed by Eisai and Swedish biotech BioArctic.

While we usually think of antibodies to bacteria or viruses, these Y-shaped proteins can be tuned to bind to numerous targets. In this case, lecanemab was designed to bind to a protein in the brain associated with Alzheimer’s disease.

The hallmark of Alzheimer’s disease is the buildup of two types of proteins in the brain, referred to as plaques and tangles. A protein called amyloid beta (Aβ) forms plaques, while another protein called tau produces tangles. Amyloid has long been a front-runner in the search for a cause of Alzheimer’s disease, with the amyloid hypothesis garnering the lion’s share of scientific attention and capital.

The new antibody binds to pools of amyloid beta (Aβ) in the brain that many researchers believe cause neurodegeneration. The idea is that the antibody could help slow or delay mental decline. Unlike the pre-approved aduhelm, lecanemad is aimed at proteins Before They have gathered together, Reuters reported.

the study: The study, called Clarity AD, was a phase 3 randomized, placebo-controlled, double-blind study designed to test whether the drug was working.

1,795 patients had early-onset Alzheimer’s disease, and were randomly assigned to the placebo and antibody groups, and neither the patients nor the researchers knew who was getting what. The treatment group received 10mg of lecanemab intravenously every two weeks.

According to the companies, the group included patients with a wide range of comorbidities, including diabetes, heart disease and obesity, as well as diverse racial and ethnic groups.

According to the companies, the group included patients with a wide range of comorbidities, including diabetes, heart disease and obesity, as well as diverse racial and ethnic groups.

“Given the comprehensive eligibility criteria and successful employment of a variety of racial and ethnic groups in the United States, the Clarity AD population is generally comparable to the Medicare population in the country,” the companies stated.

To assess the progression of neurodegeneration, the researchers used the Clinical Dementia Classification – Total Boxes (CDR-SB) model.

Results: Eisai and Biogen reached their conclusion — that the antibody was slower to decline compared to placebo — using scores from the CDR-SB.

as such STAT . explainedOn the 18-point CDR-SB scale, lecanemab patients had a 45-point difference from the placebo group after 18 months—a 27% reduction in the rate of cognitive decline.

Significant differences (meaning “distinguishable from random noise”, not necessarily Clinically Important) between groups as early as 6 months of treatment, according to the companies.

None of the patients experienced an improvement in their cognitive scores; The drug is not designed to make people better, but to slow their worsening.

Regarding the drug’s safety, 12.5% ​​of treated patients had signs of brain swelling – a common side effect of these types of treatments, Noted FierceBiotech – But symptoms appeared on only 2.8%.

The Alzheimer’s Association estimates that by 2050, 12.7 million Americans over the age of 65 will have the disease.

Evan Cheung, Chairman and CEO of Eisai, said at a press briefing that the results are “the first definitive positive clinical trial to show that you can actually slow down Alzheimer’s disease in this very early stage of symptoms.” The New York Times.

But exactly what these findings mean, both for the amyloid theory of Alzheimer’s disease and, more importantly, for patients, remains to be seen — and experts are divided.

Conversation: As pointed out by the experts, the results are currently taken at face value from a press release; More detailed data will be released later in the year.

Eisai and Biogen describe this 27% relative difference as very significant, but fair How The important thing is to discuss. Perhaps most important is the question of whether this slowing of deterioration would be noticeable to patients and their caregivers.

Lon Schneider, director of the California Alzheimer’s Center at UCLA, told the New York Times that the drug’s effect is “negligible and many would not consider it a clinically significant difference.”

However, Schneider recognizes that “others will strongly disagree and say that it is clinically beneficial,” he told the New York Times.

The drug may also be more effective in the early stages, which the study patients were. “I am cautiously optimistic that it could be beneficial for people who are in the mild stage,” said Mia Yang, MD, geriatrician at Wake Forest, STAT.

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