Lonvi Biosciences says its procyanidin C1 capsule could, one day, stretch human life towards 150. The data behind the claim come from old mice, not long-lived humans — and they tell a more modest, but still interesting, story about how we might age better rather than forever.
A 150-year promise in a 73-year world
Global life expectancy today hovers around 73 years; in the richest countries it pushes into the mid-80s, while the verified record for any individual remains Jeanne Calment’s 122 years. Against that backdrop, a Shenzhen startup suggesting that 150-year lifespans are “definitely realistic” was always going to grab attention.
Lonvi Biosciences, a self-described “longevity laboratory”, has unveiled a capsule built around procyanidin C1 (PCC1), a molecule found in grape seeds. In its own mouse experiments, the company says the treatment increased overall lifespan by about 9.4% and extended remaining life expectancy after treatment by more than 60%.
From those numbers, Lonvi executives have leapt to the suggestion that humans might one day live to 150, especially if the pill is combined with healthy lifestyle choices.
The underlying science is more grounded — and more limited — than the headlines suggest.
What PCC1 actually did in the lab
PCC1 is not a brand-new discovery from Lonvi’s lab. It was first flagged in 2021 by researchers in Shanghai, the Buck Institute and others, who screened natural compounds for their ability to affect senescent cells — aged cells that have stopped dividing but refuse to die, and instead secrete inflammatory molecules known as the SASP.
In a Nature Metabolism paper, the group showed that PCC1, a polyphenolic component of grape seed extract, has a dual personality:
- at low doses, it damped down SASP signalling (“senomorphic” behaviour)
- at higher doses, it selectively killed senescent cells (“senolytic” behaviour) while sparing many healthy cells.
When given intermittently to very old mice — roughly 24 months of age, near the end of a normal laboratory lifespan — PCC1 reduced senescent-cell burden, improved physical performance and modestly increased survival. The study reported that overall lifespan rose by around 9–10%, while remaining lifespan from the start of treatment extended by roughly 60% in these late-life animals.
Subsequent work has pushed PCC1 into specific organs and systems:
- A 2024 PNAS study found that PCC1 reduced senescent cells in the aged retina of mice, improved retinal structure and function, and altered inflammatory signalling, again acting with both senolytic and senomorphic effects.
- A 2025 study in npj Aging profiled the mouse hematopoietic and immune systems at single-cell resolution and reported that PCC1 reduced senescent signatures, restored stem-cell function, and improved grip strength in aged mice fed PCC1-supplemented chow for four months.
- Other preclinical papers suggest benefits in models of kidney fibrosis and diabetic wound healing, again via targeted clearance of senescent cells.
Taken together, the mouse data support a cautious but real claim: PCC1 appears to improve late-life health and survival in rodents by pruning back senescent cells in multiple tissues.
That is a long way from proving that a daily PCC1 capsule lets humans live 50–70 years beyond today’s longest-lived outliers.
From “zombie cells” to senolytics: what we actually know
Lonvi’s marketing language leans hard on “zombie cells” — senescent cells that accumulate with age and pump out inflammatory factors. That framing is not entirely hype. A large body of work now links senescent cells to age-related tissue damage, cardiovascular disease, osteoarthritis, lung fibrosis and neurodegeneration.
Senolytics, the drug class that aims to selectively kill these cells, began with cancer agents such as navitoclax and combinations like dasatinib + quercetin, which were shown to clear senescent cells and rejuvenate tissues in aged mice.
In humans, the data are still early and disease-specific:
- Small open-label trials in idiopathic pulmonary fibrosis and diabetic kidney disease have shown that intermittent dasatinib/quercetin regimens can reduce senescence markers in fat tissue and modestly improve physical function or biomarkers over weeks to months.
- Pilot studies in Alzheimer’s disease and other conditions are ongoing, but so far no senolytic has demonstrated that it can extend human lifespan, only that it may tweak disease endpoints or frailty scores in small cohorts.
Crucially, senescent cells are not purely harmful. They play roles in wound healing, development and possibly cancer suppression. Clearing the wrong populations, or clearing too aggressively, could have unintended consequences — one reason mainstream researchers are wary of over-the-counter “senolytic supplements” that are ahead of the evidence.
PCC1 slots into this picture as one more promising senotherapeutic: a compound with preclinical evidence for organ-specific benefits and survival gains in mice, but no published human trial data yet.
Stretching mouse months into human decades
Even if we take Lonvi’s mouse results at face value, the leap to 150-year humans is more marketing than math.
A 9–10% increase in overall lifespan in mice is meaningful but not unprecedented. Calorie restriction, certain genetic manipulations and other compounds (such as the flavonoid fisetin) have extended mouse median lifespan by similar or larger margins in well-controlled experiments.
Converting those gains into “human years” is not as simple as multiplying by a factor. A common rule-of-thumb equates an extra 9% in mouse lifespan to perhaps 5–8 human years in average life expectancy, not a doubling of maximum lifespan.
The more eye-catching figure — 64% longer remaining life expectancy from the start of treatment — says that very old mice given PCC1 lived much longer than other very old mice, not that young animals were transformed into Methuselahs.
And while debate continues about whether there is a hard ceiling to human lifespan, no verified individual has yet passed 122, and recent analyses suggest that maximum human lifespan has changed little even as average lifespans rose dramatically over the 20th century.
In other words: if PCC1 translated perfectly from mice to humans — a very big “if” — it might shave some risk off age-related disease and add a handful of healthy years for some people. It would not, on current evidence, vault large numbers of us to 150.
China’s longevity push – and why Lonvi is a useful symbol
If Lonvi’s numbers are modest, its context is not. China is turning ageing into a national economic strategy.
- Government documents and industry reports frame the “longevity market” — spanning eldercare, biotech, wellness and financial products — as a strategic growth area alongside AI and advanced manufacturing.
- China’s anti-ageing products market is estimated at around US$4–5 billion in 2024 and forecast to more than double over the next decade; globally, the wider anti-ageing market is projected to rise from roughly US$76 billion in 2024 to ~US$130 billion by 2034.
Within that surge, Lonvi positions itself at the “deep science” end: a company with a PCC1-based capsule, a slick English-language website and white-paper-style blog posts describing PCC1’s dual senomorphic and senolytic actions.
Yet the small print matters. Like many supplement brands selling biologically plausible compounds ahead of regulatory approval, Lonvi’s site carries the familiar disclaimer that its products are not evaluated by the U.S. Food and Drug Administration and are “not intended to diagnose, treat, cure or prevent any disease.”
That places the capsule in a grey zone: marketed with language that edges toward medical benefit, grounded in preclinical science, but not yet backed by human trials robust enough for drug approval in the U.S., Europe or most other jurisdictions.
It also reflects a broader trend. China is trying to become a global hub for longevity biotech, combining central-government support, domestic capital and a huge ageing population. Western investors and policymakers are watching closely, both for scientific opportunities and for the regulatory tensions that emerge when pills with drug-like mechanisms are sold as lifestyle products.
How regulators might view a “150-year pill”
So far, no major regulator has approved any therapy — senolytic or otherwise — explicitly for extending healthy human lifespan. Trials instead target specific diseases or frailty syndromes, where endpoints such as walking distance, lung function or kidney markers can be measured over months, not decades.
If a company were to bring a PCC1-based product to the U.S. or EU as a drug, promising to slow or reverse ageing, regulators would almost certainly:
- demand phase 1–3 trials to show safety and efficacy in defined patient groups
- insist on clear disease indications (for example, macular degeneration, fibrosis, or an immune-aging syndrome), not vague anti-ageing claims
- scrutinise off-target effects, given the dual senolytic and senomorphic actions of PCC1 and the fact that some senescent cells are beneficial.
If the same capsule is marketed as a supplement, regulators have less leverage, especially outside the U.S. or EU. Most oversight then comes after the fact — if safety issues emerge, or if advertising crosses the line into making explicit therapeutic claims.
That makes Lonvi’s “150 years” rhetoric more than a scientific question. It is also a test of how far companies can go in promising radical life extension before consumer-protection and drug regulators step in.
Healthspan, not immortality
For ageing researchers, the Lonvi story has an odd double effect. On one hand, it stokes unrealistic expectations: there is no credible evidence that any pill can push large numbers of humans to 150 in the foreseeable future, and many experts still suspect the practical upper bound of human life is closer to 120–130.
On the other hand, it shines useful light on senolytics and PCC1, where the near-term opportunity is more modest but potentially real:
- Targeted clearance of senescent cells may help treat specific age-related diseases — from fibrosis to eye disorders — and improve late-life function in defined patient groups.
- Multi-organ mouse data suggest PCC1 can be part of that toolkit, especially as a natural compound with a senolytic profile distinct from existing drugs.
- The right question, then, is not “Will this make me live to 150?” but “Can careful senolytic therapy help me live healthier into my 80s and 90s — and with what risks?”
Answering that requires slow, conventional work: dose-finding, safety profiling, and disease-specific trials, not just glossy diagrams of “zombie cells” and viral headlines.
For now, PCC1 is a promising senotherapeutic in mice and a speculative supplement in humans. The distance between those two roles is the distance between a well-designed figure in a journal and a pill that regulators, clinicians and patients can trust.
This article is for information and analysis only. It does not constitute medical advice or an endorsement of any supplement or therapy. Anyone considering new treatments or supplements should discuss them with a qualified healthcare professional.
