In our last issue, I showed you how artificial intelligence went exploring through a massive database of DNA and came back with something that scientists didn’t even know existed.
Today, I want to show you how it’s starting to fundamentally change the way we develop medicine.
Because researchers tested an AI-designed drug in human patients that was originally created to treat a deadly lung disease.
But they recently discovered it could be doing something much more exciting.
It might be able to wind back our biological clock.
Turning Back the Clock
To understand what these results are — and why they’re so remarkable — we need to go back to how the drug was created.
It’s called rentosertib, and it comes from a biotech company called Insilico Medicine.
Insilico has spent more than a decade using AI to speed up one of the slowest and most expensive parts of medicine: discovering new drugs.
Normally, scientists begin by identifying something inside the body that appears to play a role in a disease. This is known as a drug target.
You can think of that target as a lock. The challenge is finding a molecular “key” that fits the lock and changes what it does.
Traditionally, researchers might spend years testing thousands of different molecules looking for the right one.
Insilico used AI for both parts of the process.
Its first AI system analyzed enormous amounts of biological data and identified a protein called TNIK as a promising target. TNIK was associated with idiopathic pulmonary fibrosis (IPF), a deadly disease that causes lung tissue to become thick and scarred.
But there was something else interesting about TNIK.
It was also connected to six different hallmarks of aging, the biological changes scientists believe contribute to our bodies getting older.
Insilico then turned to a second generative AI system to design an entirely new molecule capable of targeting TNIK.
That molecule became rentosertib.
In other words, AI helped scientists find the lock. Then it designed a key.
And it all happened incredibly fast. Insilico says it went from identifying the target to selecting a drug candidate for preclinical testing in about 18 months.
Of course, designing a drug on a computer is one thing. Proving it works in people is something else entirely.
But that’s where this story really takes a turn.
Last year, a Phase II clinical trial showed that rentosertib could improve lung function in patients with IPF. The results were promising enough that the drug has since advanced into a Phase III trial.
But researchers had also collected blood samples from patients during the earlier trial. And they recently went back to those samples to answer a very different question.
Could the drug also be affecting how quickly the patients were aging?
To find out, researchers measured thousands of proteins circulating in the patients’ blood and ran that information through six different “aging clocks.”
An aging clock is essentially a biological speedometer.
Instead of looking at the date on your birth certificate, it looks at patterns inside your body that tend to change as you get older. Researchers can use those patterns to estimate whether your body appears biologically older or younger than your actual age.
And when researchers compared the patients’ biological ages before and after treatment, all six clocks moved in the same direction.
The patients appeared to be getting younger.
Patients taking rentosertib showed reductions in their predicted biological age, while patients taking the placebo generally showed little change or slight increases. The strongest and most consistent results appeared in patients taking 30 milligrams twice a day.
Researchers then performed another test.
They compared the changes in the patients’ proteins with data from more than 55,000 older adults in the UK Biobank.
Think of normal aging as leaving thousands of tiny fingerprints in your blood. Some proteins tend to increase as you get older. Others decrease.
In the strongest treatment group, rentosertib appeared to push many of those proteins in the opposite direction.
In other words, at least according to these biological measurements, the patients weren’t simply aging more slowly.
Some of the signs associated with aging appeared to be moving backward.
Now, this is a completely different approach from the cellular reprogramming research I showed you a few months ago.
And I’m not saying that scientists have discovered a pill that makes people younger. The study included only 42 patients. All of them had IPF, and researchers only followed them for 12 weeks.
Even the scientists behind the study acknowledge that aging clocks aren’t perfect and that they can’t yet completely separate the effects of treating a serious disease from an effect on aging itself.
The real test will be whether they eventually see similar results in larger studies and, crucially, in healthy people.
So we’re still a long way from knowing whether rentosertib can actually slow the aging process.
But I believe we’ve crossed an important threshold.
Here’s My Take
AI helped scientists identify a promising target and design a new drug to go after it.
Now, six different aging clocks suggest that this drug might actually be able to turn back our biological clock.
To me, it’s another incredibly exciting example of how AI is helping us explore parts of biology we’re only beginning to understand.
And we’re just getting started.
In our next issue, I’ll show you how AI searched through 1.7 million possibilities to find a potential new weapon against one of medicine’s biggest problems.
Regards,
Ian King
Chief Strategist, Banyan Hill Publishing
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