In 2025, longevity has made headlines, sometimes in surprising ways. There’s been big news in epigenetic reprogramming and promising studies from mice to monkeys—and both AI leaders and world leaders talking about doubling human lifespan.

But breakthroughs and media attention also came with setbacks: a drought in both public and private funding, and a resurgent risk of longevity hype swamping serious science.

At The Longevity Initiative, we’re welcoming the new year with five articles reviewing the old one. Our round-up of 2025 in longevity starts today with science and, through the rest of the week, business, funding, medicine, and comms, policy and politics on Friday.

Let’s start with some of the top results in ageing research in 2025:

2025’s top longevity cocktail

The year’s most significant animal result came from combining two drugs: a cocktail of the cancer drug trametinib and longevity science favourite rapamycin. Together, they extended mouse lifespan by 30%—the biggest effect seen in 2025.

Why is this exciting? The fact that these drugs’ effects add up suggests that they work in independent ways. It’s also another example showing that combining treatments targeting different pathways could be more effective than single drugs. We also know that rapamycin plus acarbose or metformin (both diabetes drugs) work better than rapamycin on its own—could a combination of rapa, acarbose and trametinib be even more effective? (Conversely, substances sometimes subtract from each other’s effect—for example, some supplements may work less well in combination.)

What’s the catch? The dose of trametinib used in mice was much higher than that normally given to cancer patients, and that could mean unacceptable side-effects if we tried to copy and paste this idea into people. It’s also hard to do rigorous studies on combinations just because there are so many combinations—trying three drugs at three different doses in every permutation would require 27 different experiments.

Let’s talk about sex differences

Other notable results in 2025 included a combination of oxytocin (sometimes known as the ‘love hormone’) with a drug called an Alk5 inhibitor, which resulted in a 14% increase in median lifespan even though treatment was started late in life.

The Interventions Testing Program (ITP) also found three new molecules that make mice live longer:

• Epicatechin (a flavanol found in cocoa) increased average lifespan by 5%
• Halofuginone (which simulates eating less protein) increased average lifespan by  9%
• Mitoglitazone (an experimental diabetes drug) also added 9% to average mouse lifespan

Why is this exciting? It’s always good to find new ways to make mice live longer, and the oxytocin plus Alk5 inhibitor is particularly interesting because the idea arose out of work on exchanging blood between young and old mice. Recapitulating the effect with drugs would be a far more practical and likely safer approach than transfusions of young blood for older people.

What’s the catch? All of these only worked in male mice—continuing a strange trend for longevity drugs to only work in males. In fact, of 14 previous ITP successes, eight made only male mice live longer, while none only worked in female mice. We don’t yet know if this means that human men are more likely to benefit from these treatments than women—or perhaps it hints at some as-yet-undiscovered interesting biology that, if we understood it, could help us all live longer, healthier lives.

Your organs are ageing at different rates

Scientists have been measuring people’s and animals’ ‘biological age’ for more than a decade now, but 2025 saw the development of clocks that could measure not just overall age, but the ageing of specific organs like the brain and heart.

One used blood samples from nearly 45,000 people, while another used images from MRI scans to estimate organ age.

Why is this exciting? These clocks can predict disease risk, which is often organ-specific: when someone’s heart was biologically old, their risk of heart failure significantly increased, while people whose brains aged more quickly were at higher risk of dementia. This might make it easier for doctors to identify people at risk, and intervene earlier.

The catch? Like with all biological age measures so far, we don’t know what exactly these clocks are measuring. Whether they will be more useful in the clinic than conventional measurements like cholesterol and blood pressure will need further studies to confirm.

Ageing like a fine naked mole-rat

Naked mole-rats are rodents, closely related to rats and mice. And they’re not just a pretty face—where a mouse might survive two or three years in the lab, naked mole-rats can live over 30 years, and are surprisingly resistant to cancer, cognitive decline and frailty.

How do they do it, and are their abilities transferable to other animals? Scientists tried splicing the naked mole-rat version of a gene involved in repairing DNA called cGAS into mice reduces frailty, inflammation and hair greying.

Why is this exciting? DNA damage accumulates as we age, contributing to many age-related diseases—not least, cancer—so better repair mechanisms could have broad benefits. It also highlights an underappreciated approach in longevity science: while short-lived species are convenient for rapid experiments, we mustn’t neglect the importance of learning from creatures that nature already optimised for longevity.

What’s the catch? We’re not quite ready to start transferring naked mole-rat genes into humans! However, clinical trials are already testing drugs that target cGAS, which might help us emulate the effect without gene editing.

Year of the monkey

Despite the lunar zodiac, 2025 has also been the year of the monkey and of ‘extracellular vesicles’, aka EVs, which are tiny bubble-like packages that cells use to send messages to each-other. These have been mooted as a potential anti-ageing intervention for a while after various promising results in mice showing that EVs can improve health in old age.

Two separate studies treated middle-aged rhesus macaques with EVs and saw improvements in health. One used EVs derived from deer antlers (which regrow every year, so have incredible regenerative capacity) to demonstrate a number of improvements, while another group used EVs from stem cells to improve memory test scores and brain imaging. A third gave monkeys stem cells directly, and attributed some of the improvements in markers of ageing to the EVs these cells produced.

Why is this exciting? EVs might be a very different way to deliver anti-ageing medicines, and monkeys are much closer to humans than mice are, improving the odds that EVs could translate to people. 

The catch? The studies were small (as monkey studies usually are for practical and ethical reasons), and none measured whether the monkeys actually lived longer—just whether certain health markers improved.

Reality check

However, one paper provided a sobering counterpoint: researchers examined 667 studies of longevity drugs in the DrugAge database and found that many studies were too small to be useful, alongside evidence of ‘publication bias’, where scientists only publish experiments that work, depriving the field of knowledge of what didn’t.

What does this mean? Be sceptical when reading about the latest ‘lifespan-extending’ miracle molecule in 2026: many compounds found in small studies probably won’t hold up when tested more rigorously. Longevity science needs more methodological rigour and, crucially, more funding for larger studies early on to avoid wasting time on interventions that won’t work when tested properly.

This is part of our New Year 2026 series on 2025 in longevity. Read the next piece, on private funding for longevity companies here.