GLP-1 Pill Fails to Slow Alzheimer’s Progression in Clinical Trial

GLP-1 pill fails to slow progression of Alzheimer’s disease in clinical trial

By Lauren J. Young edited by Claire Cameron

The pill version of Novo Nordisk’s blockbuster weight loss drug semaglutide failed to slow the progression of Alzheimer’s disease in an early analysis of two Phase 3 clinical trials. The company behind the weekly injectable diabetes drug Ozempic and the weight loss drug Wegovy, also known as the GLP-1 drugs, announced its topline results today.

Endocrinologist Daniel Drucker says the trials were well done but the results are “a setback for the field.” Novo Nordisk confirmed in a statement to Scientific American that the company is ending its trials of semaglutide in Alzheimer’s disease, including tests involving the injectable version of the drug.

“GLP-1 [drugs] We’ve had so many wonderful results, but tackling these very difficult brain disorders has been disappointing,” says Drucker, who has consulted for Novo Nordisk in the past but does not currently. “No one expected it to stop the progression of Alzheimer’s disease, but the hope was that we would see a benefit, and we didn’t.”

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Animal models and analyzes of real-world data have already suggested that GLP-1 drugs could reduce the risk or slow the development of Alzheimer’s disease. The reason remains elusive, although researchers including Drucker suggest that these drugs may reduce inflammation associated with certain neurological diseases.

“GLP-1 reduces inflammation in many parts of the body, and inflammation drives some of the pathology of Alzheimer’s disease,” he says.

Novo Nordisk’s trials, called evoke and evoke+, included 3,808 people aged 55 to 85 with early-stage Alzheimer’s disease, classified as having mild cognitive impairment due to the disease. For most of the 156-week trial, researchers gave half of the participants 14 milligrams of oral semaglutide once a day, while the other half received a placebo.

Participants who took the drug showed some improvements in Alzheimer’s biomarkers, but the treatment did not delay disease progression, according to the company.

Drucker says there are many possible explanations for why oral semaglutide didn’t work as hoped. The fatty acid structure surrounding semaglutide could have prevented it from entering certain regions of the brain, such as the hippocampus, which controls memory and cognitive functions. Previous studies evaluating the link between GLP-1 treatment and the risk or development of Alzheimer’s disease have primarily relied on data on injectables, raising the question of whether changing how people take the drug or the dosage could lead to a different outcome, Drucker says, while adding that giving higher doses to some older adults may also carry additional risks.

“These are not miracle drugs that are going to fix everything that’s wrong with us, and that’s why we need to do clinical trials, and we need rigorous evidence,” Drucker says, adding that Novo Nordisk deserves credit for conducting these trials despite the low chance of success.

Novo Nordisk plans to present the results at the Clinical Trials in Alzheimer’s Disease (CTAD) Conference next week and the full datasets at the Alzheimer’s and Parkinson’s Diseases AD/PD Conference in March 2026.

“We will continue to analyze the data and may not have an answer to ‘why’ next week when we share the results at CTAD,” a Novo Nordisk spokesperson said. Scientific American.

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