# Scientists develop drug extending lifespan by 25% in model organisms AMPK-targeting compound shows promise for delaying age-related diseases - **Source:** [Science & tech Articles | Mail Online](https://www.dailymail.com?ns_mchannel=rss&ns_campaign=1490&ito=1490) - **Published:** 2026-09-30 - **Original article:** - **On Brifing:** https://brifing.si/s/98c9b130-c41c-4904-96b3-fc7fcafed47c ## Breakthrough in longevity research UK researchers developed compound 991, demonstrating 25% lifespan extension in yeast, worms, and flies. The drug directly activates AMPK, a key cellular energy regulator. This protein normally responds to stress, exercise, or fasting. The study marks the first direct evidence that pharmacological AMPK targeting can extend longevity across species. Funded by the UK Medical Research Council, the work involved multiple academic institutions. ## AMPK's central metabolic role AMPK acts as the body's 'fuel gauge', monitoring cellular energy levels. During shortages, it shuts energy-intensive processes while boosting fuel production. The protein influences aging-related processes like metabolism and inflammation. Its dysfunction links to diabetes, obesity, and dementia. Existing diabetes drugs like metformin activate AMPK indirectly, complicating research interpretation compared to 991's direct mechanism. ## Strategic organism selection Researchers chose yeast, nematodes, and fruit flies for their short lifespans (3 weeks to 3 months). This enabled rapid longevity assessment compared to mammals. The cross-species effectiveness suggests conserved biological mechanisms. Dr. Cochemé notes such models accelerate discovery before mammalian testing. The team observed consistent lifespan extension despite evolutionary distance between test species. ## Clinical translation challenges Aging isn't classified as a disease, complicating clinical trial pathways. Professor Cabreiro emphasizes current focus on improving healthspan rather than lifespan. Direct AMPK activators show promise due to existing safety data from metabolic disorder trials. The team now plans mouse studies to assess mammalian effects. Successful translation could address multiple age-related conditions simultaneously. ## Potential healthcare impact Delaying aging could reduce risk for diseases like cancer, diabetes, and dementia. The researchers highlight societal benefits from extended healthspan. Current indirect AMPK activators show anti-aging potential but lack mechanistic clarity. Compound 991's specificity offers new research avenues. The study was published in Aging Cell, with contributions from London and Lyon institutions. ## Mechanistic advantages Unlike indirect activators, 991 allows precise AMPK pathway study. This clarity helps distinguish longevity effects from other metabolic changes. The direct approach simplifies dose-response relationships critical for clinical development. Researchers can now explore whether lifespan extension correlates with healthspan improvements in model organisms. ## Future research directions Mouse studies will test mammalian applicability. Researchers must determine if effects scale with organism complexity. Parallel work will examine health metrics beyond lifespan. The team notes AMPK's network position enables broad metabolic influence. Successful translation could revolutionize preventive medicine for aging populations. ## Balanced scientific optimism While excited about cross-species results, scientists caution about human applicability timelines. The study provides mechanistic proof-of-concept for targeted anti-aging interventions. Researchers emphasize that even partial success could significantly impact age-related disease burdens. This work establishes AMPK as a validated target for longevity research moving forward. ## Sources covering this story - https://www.dailymail.com/sciencetech/article-16168953/anti-aging-holy-grail-drug-lifespan.html?ns_mchannel=rss&ns_campaign=1490&ito=1490 — --- _Summary written by Brifing from the original reporting. Copyright in the original article belongs to its publisher; read the full piece at the link above._