Plate Nº 55 · recorded October 10, 2026
Health & Medicine ResearchReported finding
Drug Extends Animal Lifespan by 25% by Switching On 'Energy Saver Mode'
A study published today in the journal Aging Cell reported that directly switching on the cellular enzyme AMPK with a drug called 991 extended the lifespan of yeast, worms and flies by more than 25% in some cases.
By Priya Raman3 min read628 words
In brief
- Study published today in Aging Cell; lifespan extended by more than 25% in yeast, worms and flies
- Drug 991 directly activates the AMPK enzyme, unlike metformin and semaglutide, which act indirectly
- Researchers tested 991 on fission yeast, nematode worms (C. elegans) and fruit flies (Drosophila)
- Model species live roughly three weeks (worms), three months (flies) and three years (mice, for comparison)
- Funded by the Medical Research Council (MRC) UK; collaborators included Imperial College London, University of Cologne, Queen Mary University of London, the Francis Crick Institute and the University of Lyon
A drug that directly switches on a cellular "energy saver mode" extended the lifespan of yeast, worms and flies by more than 25% in some cases, according to a study published today in the journal Aging Cell. The work, led by teams at the MRC Laboratory of Medical Sciences (LMS), Imperial College London and the University of Cologne, is the first to extend lifespan in living animals by targeting the enzyme AMPK with a drug.
What is AMPK and why does it matter?
AMPK stands for adenosine monophosphate-activated protein kinase. It works as a fuel gauge inside every cell, sensing how much energy is available at any moment.
When fuel runs low — during exercise, fasting or stress — AMPK halts energy-hungry activities such as building new proteins and storing fat. It then flips on energy-generating processes like burning stored sugar and fat.
Because AMPK sits at the center of metabolic control, glitches in its function contribute to type 2 diabetes and obesity. Turning it up, by contrast, brings measurable health benefits. Two widely used drugs — the diabetes medication metformin and the weight-loss drug semaglutide — activate AMPK, but only indirectly.
How did the new study differ?
Previous drugs activated AMPK as a side effect, which made it hard to confirm the enzyme's real role. To clean up that signal, the team used a small molecule called 991, designed to bind AMPK directly and switch it on.
The researchers tested 991 on three common lab species:
- Fission yeast (Schizosaccharomyces pombe)
- Nematode worms (Caenorhabditis elegans)
- Fruit flies (Drosophila)
These organisms live roughly three weeks, three months and three years, respectively. Their short lives let scientists screen ageing interventions far faster than in mice.
What did the experiments show?
Treating the animals with 991 stretched their lifespans by more than 25% in some cases. Dr Helena Cochemé, who leads the Redox Metabolism Group at MRC LMS, framed the finding as a first.
"The fact that we can extend lifespan in yeast, worms and flies is very exciting," Cochemé said. "Our study is the first demonstration that directly targeting AMPK using a drug can have longevity benefits in living organisms."
She compared AMPK to the "energy saving mode" on a mobile phone and pointed to the breadth of species tested as a sign of robustness.
"If a treatment works successfully in three such distantly related species, then these results give us confidence that in the longer-term, the effects could be translated to mammals and eventually humans," Cochemé said.
What comes next?
Professor David Carling, who heads the Cellular Stress Group at MRC LMS, said the direct activator lets researchers avoid off-target effects that muddy earlier results.
"By switching-on AMPK specifically using a direct activator, it is possible to achieve a much cleaner result, avoiding potential side-effects," Carling said.
The team's immediate goal is to repeat the experiment in mice. Direct AMPK activators have already passed early safety tests in human clinical trials for metabolic diseases, which could shorten the path to age-related studies.
How far are we from anti-ageing pills?
Professor Filipe Cabreiro, who leads the Host-Microbe Co-Metabolism Group at MRC LMS and runs a parallel lab at the University of Cologne, urged caution.
"The field is still a long way from anti-ageing clinical trials in humans," Cabreiro said.
Ageing is not classified as a disease, so regulators cannot approve drugs that aim to slow it. Still, Cabreiro said, sharpening health in later life would pay off because ageing drives much chronic illness, including heart disease, diabetes, cancer and dementia.
The study also involved scientists at Queen Mary University of London, the Francis Crick Institute and the University of Lyon. The Medical Research Council (MRC) UK funded the work.
via lms.mrc.ac.uk (Original)
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Senior reporter covering industry trends and analytics at SciBeat.
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