Across laboratories in London, Cologne, and beyond, scientists have demonstrated that directly activating a single cellular protein — AMPK, the body's ancient energy regulator — can extend the lives of yeast, worms, and flies by more than 25 percent. The drug used, called 991, cuts through the ambiguity of indirect approaches to reveal something that may be fundamental to life itself: that how cells manage energy is inseparable from how long they endure. The consistency of this effect across three distantly related species suggests humanity may be looking at a mechanism deep enough to matter,
Drug Targeting AMPK Enzyme Extends Lifespan by 25% Across Multiple Species
AMPK is the body's equivalent to energy-saving mode
Mark
So they've actually extended lifespan in living animals, not just in cells?
Mimi
Yes—in yeast, worms, and fruit flies. All three showed lifespan extensions of more than 25 percent when treated with this drug called 991.
Luke
But we should be clear: these are model organisms with very short natural lifespans. The jump from flies to humans is enormous.
Mimi
Absolutely. That's why the researchers chose them—you can run a complete lifespan study in weeks or months instead of years. It's a proof-of-concept.
Mark
What exactly does AMPK do that makes it so important?
Mimi
It's a cellular energy sensor. When energy runs low, it tells cells to stop expensive processes like building proteins and storing fat, and instead focus on generating fuel.
Luke
And we know this works in humans already? Metformin and Semaglutide both activate AMPK.
Mimi
Right, but they do it indirectly. This drug, 991, targets AMPK directly, which gives cleaner results and makes it easier to see what AMPK activation alone actually does.
Mark
What's the next step?
Mimi
Mouse trials. If it works in mice, that's a much bigger step toward humans.
Luke
And even then, aging isn't classified as a disease, so getting approval for human trials would be complicated.
Mimi
True. But the researchers point out that aging is a major risk factor for almost every serious disease. Keeping people healthier longer would be transformative, even if it's not technically treating a disease.
The Pulse
- A drug called 991 has extended lifespans by over 25% across three different species — yeast, worms, and flies — by directly switching on AMPK, the cellular engine that decides when to conserve and when to burn.
- The urgency lies in what AMPK's failure already costs us: when this metabolic gatekeeper falters, type 2 diabetes, obesity, and metabolic disease follow — making its activation not just a longevity question but a present-day health crisis.
- Previous drugs like Metformin and Semaglutide nudge AMPK indirectly, muddying the science; 991's direct targeting finally isolates the mechanism, giving researchers a cleaner signal and potentially fewer side effects.
- Mouse trials are the immediate next step, and the path to humans is not purely theoretical — direct AMPK activators have already cleared safety testing in human clinical trials for metabolic conditions.
- The road to anti-aging treatment in humans remains long: aging is not classified as a disease, regulatory frameworks are unprepared, and the leap from flies to people is vast — but the biological logic is growing harder to dismiss.
Across laboratories in London, Cologne, and beyond, scientists have demonstrated that directly activating a single cellular protein — AMPK, the body's ancient energy regulator — can extend the lives of yeast, worms, and flies by more than 25 percent. The drug used, called 991, cuts through the ambiguity of indirect approaches to reveal something that may be fundamental to life itself: that how cells manage energy is inseparable from how long they endure. The consistency of this effect across three distantly related species suggests humanity may be looking at a mechanism deep enough to matter, one day, for us as well.
A research team spanning London, Cologne, and several partner institutions has shown that a drug called 991 can extend the lifespan of multiple animal species by more than 25 percent. Their findings, published in the journal Aging Cell, center on AMPK — a metabolic enzyme that acts as the body's energy monitor, determining in real time whether cells should conserve resources or burn through them.
AMPK works much like a smartphone's battery-saving mode. When the body faces stress, fasting, or exertion, AMPK shuts down costly processes like protein synthesis and fat storage, redirecting energy toward fuel generation. When AMPK functions poorly, metabolic diseases such as type 2 diabetes and obesity can take hold. Some existing drugs, including Metformin and Semaglutide, activate AMPK — but indirectly, making it difficult to isolate what AMPK alone is doing. Drug 991 targets it directly, producing cleaner results and a clearer scientific picture.
The team tested 991 in fission yeast, nematode worms, and fruit flies — organisms chosen for their short lifespans, which compress years of biological data into months. Dr. Helena Cochemé of the MRC Laboratory of Medical Sciences called it the first demonstration that directly targeting AMPK with a drug can produce longevity benefits in living organisms. The fact that the effect held across three evolutionarily distant species suggests something more fundamental than a single biological quirk.
Professor David Carling outlined the next phase: mouse trials. Direct AMPK activators have already been safely used in human clinical trials for metabolic diseases, which opens a potential pathway forward. Professor Filipe Cabreiro acknowledged the distance still to travel — aging is not classified as a disease, complicating the route to human anti-aging trials. Yet the stakes are significant. Aging underlies heart disease, diabetes, cancer, and dementia. A drug that keeps cells energetically balanced for longer could represent a meaningful shift in how medicine approaches the human lifespan.
A team of researchers working across London, Cologne, and other institutions has demonstrated that a drug called 991 can extend the lifespan of multiple animal species by more than 25 percent. The findings, published today in the journal Aging Cell, center on a cellular protein called AMPK—a metabolic enzyme that acts as the body's energy monitor, deciding in real time whether cells should conserve resources or burn through them.
AMPK operates like an energy-saving mode on a smartphone. When the body faces depletion—during exercise, fasting, or stress—AMPK shuts down expensive cellular processes such as protein synthesis and fat storage, redirecting energy instead toward fuel generation by burning existing fat and sugar. This mechanism sits at the core of how organisms manage their metabolism. When AMPK functions poorly, metabolic diseases like type 2 diabetes and obesity can develop. When AMPK activity increases, health benefits follow. Some existing drugs, including the diabetes medication Metformin and weight-loss treatments like Semaglutide, activate AMPK, but they do so indirectly, which makes it harder for researchers to isolate and confirm exactly what AMPK activation alone accomplishes.
To cut through this ambiguity, the research team used drug 991 to target AMPK directly. They tested it across three model organisms chosen specifically because their short lifespans allow rapid experimentation: fission yeast, nematode worms, and fruit flies. Worms live roughly three weeks in the laboratory, flies about three months, compared to three years for mice. This compressed timeline lets researchers gather years of biological data in months rather than decades.
Dr. Helena Cochemé, who leads the Redox Metabolism Group at the Medical Research Council Laboratory of Medical Sciences, emphasized the significance of seeing the same effect across such distantly related species. "The fact that we can extend lifespan in yeast, worms and flies is very exciting," she said. "Our study is the first demonstration that directly targeting AMPK using a drug can have longevity benefits in living organisms." The consistency of results across three evolutionary branches suggests the effect is not a quirk of a single organism but something more fundamental—a finding that increases confidence the mechanism might eventually translate to mammals and, further down the line, to humans.
Professor David Carling, who leads the Cellular Stress Group at the same institution, noted that using a direct activator like 991 produces cleaner results than indirect approaches, potentially avoiding unwanted side effects. He outlined the next phase: testing whether the drug can improve health and extend lifespan in mice. Direct AMPK activators have already been used safely in human clinical trials for specific metabolic diseases, which opens a pathway for future exploration in humans, though significant hurdles remain.
Professor Filipe Cabreiro, whose laboratory spans the Medical Research Council and the University of Cologne, acknowledged the distance still to travel. Aging itself is not classified as a disease in medical terms, which complicates the path to human anti-aging trials. Yet the potential impact is enormous. Aging is a major risk factor for heart disease, diabetes, cancer, and dementia. If a drug could keep people healthier for longer by pharmacologically balancing energy metabolism through AMPK activation, it would represent a major shift in how medicine approaches the aging process. The research was primarily funded by the Medical Research Council, part of the UK Research and Innovation agency, with contributions from scientists at Queen Mary University of London, the Francis Crick Institute, and the University of Lyon.
Notable Quotes
The fact that we can extend lifespan in yeast, worms and flies is very exciting. Our study is the first demonstration that directly targeting AMPK using a drug can have longevity benefits in living organisms.— Dr. Helena Cochemé, Redox Metabolism Group, MRC Laboratory of Medical Sciences
The field is still a long way from anti-ageing clinical trials in humans. But improving health in older age would be hugely beneficial from a societal and healthcare perspective, since ageing is a major risk factor for so many diseases.— Professor Filipe Cabreiro, Host-Microbe Co-Metabolism Group, MRC LMS
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