Novo Nordisk and Eli Lilly presented early data at the Aging Research & Drug Discovery (ARDD) conference at Harvard suggesting that their GLP-1 receptor agonists may slow molecular measures of biological aging. Novo's Global Project Leader for Research and Development, Nikolaj Roed, presented evidence that semaglutide and other GLP-1 receptor agonists "may" support healthier aging, citing survival and physical function data and class-level evidence pointing to broader longevity potential. Roed said the company has been seeing "improved biological age in our patients across trials and across different tissues," with an overall difference of around two to three years.
Alejandro Aguayo-Orozco, a senior scientific director at Novo, told the meeting that the question is no longer whether semaglutide reaches diseases relevant to health span and aging. "If the question is, 'Can semaglutide reach several diseases relevant to health span and aging?' we know we can say the answer is yes," he said. The next question, he added, is whether those effects are accompanied by 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." Novo's study drew blood from 10,052 people, half on the drug and half on placebo, at baseline and again months later. The samples were measured with proteomic clocks, which use levels of key proteins to predict a person's age and risk of dying.
The company found the drugs caused a broad slowdown in aging clocks, as much as four years on a clock that looks at heart proteins. "I think it's pretty clear that the organ age is shifting," Aguayo-Orozco said. Semaglutide showed lower proteomic biological age estimates across cardiovascular outcome trials, with a rapid effect within 13 to 20 weeks that was either sustained or enhanced over 150 weeks. Proteomic signatures suggested improvements in vitality and locomotion.
Modeled from SELECT trial effect estimates in a UK real-world semaglutide cohort of 19,117 people, remaining life-year gains of 1.9 years overall were projected across every age group, with the largest gain at younger treatment ages. Lilly's Epigenetic Sub-Study: Within SURMOUNT-5, Kevin Duffin, vice president for aging research at Eli Lilly, presented early epigenetic data suggesting tirzepatide "may" slow biological aging, framing it as a small pilot to test methods and check consistency rather than a definitive result. "All the clocks are telling a consistent story that we're seeing a reduction in age," Duffin said. "It's not like we're going to reverse age by 30 years or something, but it's a significant reduction." The data came from an epigenetic sub-study within SURMOUNT-5, Lilly's head-to-head trial of tirzepatide against semaglutide. The sub-study took paired whole-blood samples from tirzepatide-treated participants at baseline and at week 72, equivalent to 1.38 elapsed years, with 91.5% of participants on the 15 mg dose by week 72.
Zymo Research and Tru Diagnostic independently generated the methylation data so the two sets could be checked against each other. After quality control, the analysis covered 82 unique subjects, 71 of whom had paired baseline and week 72 data. All 15 age-unit epigenetic clocks showed less aging than the 1.38 years of chronological time that had passed.
Two clocks reached statistical significance, with median gains of 1.1 and 0.7 years over the study period. On pace-of-aging measures, the Zymo data showed Dunedin PACE falling from a median of 1.13 to 1.08. Tru Diagnostic's data reproduced the direction of travel across six second-generation clocks, including Grim Age V1 and V2, and showed larger effects on the Dunedin PACE and Framingham PACE pace clocks.
Organ clocks suggested lower predicted age in the immune system.
Source: Hacker News · Summarized by HeadlinesBriefing