Lilly and Novo Say GLP-1 Drugs Show Signs of Slowing Biological Aging

Aging clocks estimate a person’s biological age by tracking DNA changes that accumulate over time or, in newer versions, by measuring levels of key proteins. Both companies reported that overweight or diabetic patients on the drugs scored younger than those on placebo, though the gap varied widely depending on which clock was used and which organ was tested.

Novo Nordisk drew blood from 10,052 people, half taking semaglutide and half taking a placebo, at the start of the study and again months later, and measured the samples with proteomic clocks. The company found the drugs produced a broad slowdown across the clocks, reaching as much as four years on a clock that looks at heart proteins. Nikolaj Roed, a global project leader at Novo, said the company has been seeing “improved biological age in our patients across trials and across different tissues,” describing the overall difference as around two to three years.

“If the question is, ‘Can semaglutide reach several diseases relevant to health span and aging?’ we know we can say the answer is yes,” Alejandro Aguayo-Orozco, a senior scientific director at Novo, told the meeting. The next question, he said, was whether those effects come with changes to molecular measures of biological aging. “When you intervene with semaglutide, does it actually move the clocks in any direction? And the answer is yes.” He added that organ age appears to be shifting.

Eli Lilly ran a smaller study of its GLP-1 drug tirzepatide using epigenetic clocks, which count accumulated DNA changes. It also found that molecular time generally moved more slowly for people taking the drug. “All the clocks are telling a consistent story that we’re seeing a reduction in age,” Kevin Duffin, vice president for aging research at Lilly, said at the conference. “It’s not like we’re going to reverse age by 30 years or something, but it’s a significant reduction.”

The results feed long-running speculation that GLP-1 drugs act on basic causes of aging. “Two years is a pretty strong effect, in my book,” said Steve Horvath, a University of California, Los Angeles, professor credited with inventing aging clocks. He said the data could support the idea that the drugs are geroprotectors, medicines that slow or possibly reverse biological aging. Vadim Gladyshev, a Harvard biologist who assisted Novo with its molecular measurements, was more cautious: “In an unhealthy population, I do think it’s an anti-aging drug. But in a healthy population, no one knows.”

The drugs work by stimulating the GLP-1 receptor, which signals the brain that a person is not hungry, but real-world studies have shown wider benefits including improved kidney function, lower blood pressure and a sharply reduced overall chance of death. The compounds have become the world’s best-selling medicines: Lilly’s tirzepatide, sold as Mounjaro for diabetes and Zepbound for obesity, brought the company more than $36 billion last year, with Novo’s semaglutide a close second.

The findings also give a boost to aging-clock science, whose readouts have been of uncertain value as biomarkers. “The clock people have been pushing for a decade to get this kind of study done,” said Yuge Ji, a biologist who formerly worked in the field and now runs a startup, Reflector Bio. “It’s huge for them.” Alex Zhavoronkov, founder of Insilico Medicine and organizer of the Boston meeting, said extending lives by even one year across the world’s population would equal tens of millions of lifetimes. He said last month that one of his company’s drugs, for a lung disease, also reversed aging-clock signals.