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Posted on 09/08/2026 7:47:27 AM PDT by SeekAndFind
Alex Zhavoronkov, founder and co-chief executive of techbio company Insilico, is among the scientists who have devoted countless hours to studying aging.
He has a reality-check for anyone who thinks that artificial intelligence means that the ability to double lifespans is tantalizingly close.
“Absolute nonsense,” said Zhavoronkov, whose company uses AI to discover and develop drugs.
In 150 years of discovery, no drug has been clinically proven to extend life, he said in an interview. “Regardless of how rich you are…you cannot buy one year of life with a drug.”
What could be within reach in the next decade or so—in the most optimistic scenario—is the ability to dial back a person’s biological clock, said Zhavoronkov.
In a study published in Nature Biotechnology, researchers evaluated Insilico’s investigational drug—known as rentosertib—for idiopathic pulmonary fibrosis, an age-related lung disease.
They used six independently developed proteomic aging clocks—machine-learning algorithms that analyze hundreds to thousands of proteins to establish a person’s biological age. Whereas chronological age measures years, biological age assesses the health of cells and organs to predict lifespan and risk of disease.
The clocks consistently indicated declines in the biological ages of rentosertib-treated patients. Zhavoronkov, who co-authored the paper, said the most significant reduction was six years.
“Six years is very promising, right? But I can tell you that it will take us a decade to prove that it’s anti-aging—if it gets approved,” he said.
A preliminary trial on a small group of patients—known as Phase 2a—of rentosertib for IPF concluded last year. It is now in Phase 3, the final stage before a drug gets approval to hit the market.
Zhavoronkov said the research by Insilico and scientists from institutions including Harvard, Peking University and Westlake University is the first clinical evaluation of an AI-driven innovative drug candidate in aging research.
(Excerpt) Read more at wsj.com ...
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Things AI should be used for and never use it to replace people
“The clocks consistently indicated declines in the biological ages of rentosertib-treated patients. Zhavoronkov, who co-authored the paper, said the most significant reduction was six years.” Doesn’t learning three languages do the same thing, or is that just appearance? My daughter , learning ancient Greek and Latin in the interim , on top of her French, looked younger in the second of two passport photos taken ten years apart.
Aubrey de Grey’s example: first-generation therapies that restore a 60–70-year-old to roughly age-40 biology might add 20–30 healthy years—enough time for second-generation therapies to be ready. Those then add still more time, and so on. Once this loop outruns aging, remaining life expectancy no longer shrinks with chronological age.
De Grey has given people now in their 40s roughly even odds of reaching that threshold if it arrives in the mid-to-late 2030s. Ray Kurzweil and others offer nearby dates. These are forecasts, not established facts; recent life-expectancy gains have slowed. LEV is the opposite of the “fourth-age event horizon”: instead of a point of no return into frailty, it is a technological threshold after which that horizon recedes faster than you approach it.
Some have posited that, if you can last another ten years, you would make it to the LEV point.
Two of the three research universities mentioned — Peking U and Westlake U — are in communist China.
‘ He has a reality-check for anyone who thinks that artificial intelligence means that the ability to double lifespans is tantalizingly close’
I have a reality check for those people too, which is there is a sucker born every minute.
Magic Beans CEO also hopeful the beans will cure cancer in addition to growing into the clouds.
Maybe this will improve peoples’ quality of life as they get older.
Maybe this will unleash the Zombie Apocalypse.
I guess we’ll find out.
What could be within reach in the next decade or so—in the most optimistic scenario—is the ability to dial back a person’s biological clock, said Zhavoronkov.
The first one has shown that promise in Phase 3 trials and he is talking about a decade ? We will dial back biological age by detecting chronic disease earlier, tailoring treatments more precisely, and shifting the focus from treating illness to preventing it in the first place.
Well that’s going to break social security and disability if people start living longer.
“I take exercise by walking behind the coffins of my friends who took exercise.” - Peter O’Toole.
Shorten the expensive end-of-life window requiring intensive medical intervention and you can use Medicare and Medicaid to pay off the deficit.
Or they are just making it up because AI loses so much $.
Canada is doing that by killing people.
This is the type of article that typically is the first in a series that ends with an article about investors losing hundreds of millions of dollars and the CEO living in a country where he can’t be extradited to the US.
Alas it comes along too late for Ruth Bader Ginsburg.
The whole-blood infusions from newborns could only keep her alive for so long.
IPF is a horrible disease with no current successful treatment. If the drug offers hope for those who suffer, that is more than enough.
They are using 3 of the 4 Yamanaka factors for partial epigenetic reprogramming.
First human dosed with cellular reprogramming drug in longevity trial
A Boston biotech company has administered what researchers are describing as the first human dose of a cellular rejuvenation drug, a milestone in the effort to treat age-related disease at the epigenetic level.
Life Biosciences Inc. announced June 9 that the first participant had been dosed in its Phase 1 clinical trial of ER-100 — the first cellular rejuvenation therapy using partial epigenetic reprogramming to receive FDA clearance to enter human clinical trials. The trial targets optic neuropathies, including open-angle glaucoma and non-arteritic anterior ischemic optic neuropathy, a common cause of sudden vision loss in adults.
ER-100 is administered by intravitreal injection — directly into the eye — and employs the controlled expression of three of the four Yamanaka factors, the transcription factors OCT-4, SOX-2 and KLF-4, to restore cells to more youthful patterns of gene expression without altering the underlying DNA sequence.
https://www.washingtontimes.com/news/2026/jun/16/first-human-dosed-cellular-reprogramming-drug-longevity-trial/
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