You can't change the age written on your ID. But what about the age of your body?
A drug designed with the help of artificial intelligence made the blood profiles of people with lung disease look biologically younger, new research reveals.
The result came from six computer models that estimate biological age by examining proteins in the blood. Scientists call them biological aging clocks.
Each clock produced different estimates depending on the dose and stage of treatment. Remarkably, however, all six detected a shift in the same direction.
The drug examined in the study published in Nature Biotechnology is called rentosertib.
It was designed to treat a condition that scars the lungs and makes breathing increasingly difficult, while also targeting biological processes associated with aging.
The condition, known as idiopathic pulmonary fibrosis, or IPF, usually affects older adults. It involves inflammation, cell damage, and problems with tissue repair – changes that overlap with some of those seen during aging.
That connection raised a question: Could a drug developed for lung disease also affect biological processes linked to aging?
Researchers from Insilico Medicine, Harvard Medical School, and other institutions decided to investigate. They returned to blood samples collected during an earlier clinical trial of rentosertib.
The original trial involved 71 people with IPF. Participants received one of three doses of rentosertib or a placebo. For the new analysis, the researchers examined samples from 42 participants with an average age of 67.
They measured nearly 3,000 proteins in the blood. Inflammation, disease, energy use, tissue damage, and aging can all leave recognizable traces in these molecules.
The researchers then analyzed those patterns using six biological aging clocks. Some had been developed to estimate a person's age, while others were designed to predict health and mortality risks.
Why does using six clocks matter?
There is no perfect way to measure biological aging. A result from one clock could be influenced by the proteins it examines or the way its calculations work.
But when several independently developed models detect a similar change, it becomes less likely that the result is simply a quirk of one model.
In the new analysis, all six clocks detected a shift toward a lower predicted biological age among people treated with rentosertib. The placebo group showed little change, with some clocks suggesting an increase in biological age.
The clearest results emerged after four weeks. In the 60-milligram once-daily group, clocks designed to estimate chronological age showed reductions ranging from 2.71 to 3.46 years.
Other clocks and dosing groups produced different figures, including much larger estimates from some exploratory models designed to examine individual organs. The researchers therefore did not identify one number as the overall amount by which rentosertib reduced biological age.
The important finding was the direction of the change: despite being built in different ways, all six clocks detected younger-looking protein patterns in people who received the drug.
Rentosertib also altered the levels of 326 proteins, compared with only two in the placebo group. Some were linked to lung scarring and tissue repair. Others were involved in inflammation, energy use, cellular stress, and the behavior of old or damaged cells.
Many protein changes continued through the 12-week study. However, the apparent movement toward a younger biological age stopped increasing after week four and reached a plateau.
The researchers do not yet know why. The body may have adapted to the drug. A different dosing schedule may be needed, or the aging clocks may have reached the limit of what they could detect during such a short study.
The results are intriguing, but they come with important limitations.
Every participant had a serious lung disease. If rentosertib reduced fibrosis or otherwise improved their lung disease, that improvement alone could have made their blood look biologically younger.
The clocks may therefore have detected an improvement in the disease rather than a change in aging itself. The study could not fully separate those two possibilities.
The analysis also included only 42 people and lasted 12 weeks. It did not demonstrate that the participants had become younger, would remain healthier for longer, or would live longer.
It's also worth noting that several authors work for Insilico Medicine, the company developing rentosertib. Lead author Alex Zhavoronkov is the company's founder and co-CEO.
Related: Scientists Are Trying to Define What 'Reversing Aging' Really Means
For now, at least, rentosertib cannot yet be described as an anti-aging drug. The findings will need to be tested in larger and longer studies, including trials involving people who do not have IPF.
But six different clocks pointing in the same direction is difficult to ignore, and the research points to a future where drugs developed to treat diseases of old age might do more than target a single condition, helping scientists discover whether wider biological processes linked to aging can be changed as well.
The study was published in Nature Biotechnology.
This article was fact-checked by Peter Dockrill and edited by Peter Dockrill. While we pride ourselves on our process, we are only human. If you spot a mistake, please let us know.