Three underrated molecules the longevity field is still catching up with
Some molecules don't get the attention they deserve. Not because the science is thin, but because they haven't been packaged, marketed or hyped into the mainstream yet. That's exactly the category we pay attention to at Dr Yan Labs: bioactives with a serious biological rationale, not just marketing potential.
Three of them are worth a proper look. All three sit in peer-reviewed literature. All three act on mechanisms central to how we age. And all three come with the same honest caveat, which we'll get to.
Fisetin: the senolytic flavonoid
Fisetin is a flavonoid you already eat, in strawberries, apples and onions. Its biological relevance goes well beyond the fruit bowl.
Fisetin is a senolytic. It acts on senescent cells: the dysfunctional, non-dividing cells that accumulate with age and drive chronic inflammation through what researchers call the senescence-associated secretory phenotype, or SASP.
The recent data is striking, and it's from the same research group at the University of Colorado Boulder. A 2024 study in Aging Cell found that intermittent fisetin supplementation reduced vascular cell senescence and SASP-related inflammation in old mice, and improved endothelial function, through genuine senolysis. A 2025 study in the same journal showed fisetin improved physical function and reduced skeletal muscle senescence in aging mice, with effects comparable to synthetic senolytics and to the genetic clearance of senescent cells. Tellingly, it did nothing in young, healthy animals, which is what you'd expect if it truly works through senescence.
Bioactives with a serious biological rationale, not just marketing potential.
Apigenin: an ally to NAD+
NAD+ declines with age. It's one of the most replicated findings in longevity biology. Less discussed is how certain plant compounds interact with that decline.
Apigenin is a flavonoid found in chamomile, parsley and celery. Its relevance here comes from a specific mechanism: it inhibits CD38, a glycoprotein that consumes NAD+ and becomes more active as we age. A 2024 review in Frontiers in Nutrition summarised the evidence: in animal models, apigenin elevated NAD+ levels by inhibiting CD38, improved learning and memory in older mice, and extended survival in fly models of neurodegenerative disease.
A separate 2024 study in Mechanisms of Ageing and Development, from Colorado State University, found that apigenin shifted brain gene expression related to innate immune activation and inflammation in aging mice, and reduced markers of inflammation and cellular senescence in aged astrocytes in vitro. In other words, it shows a senomorphic profile: calming the behaviour of senescent cells and the excess SASP that fuels chronic inflammation.
Betulinic acid: the triterpene from birch bark
Birch bark has been used in traditional medicine for centuries. The compound behind much of it has a name most formulators don't recognise yet: betulinic acid.
It's a pentacyclic triterpene, structurally different from the flavonoids above, but with a well-documented antioxidant and anti-inflammatory profile. A 2024 study in Nutrients, from Inha University in South Korea, tested it on lifespan in Drosophila melanogaster. The finding: betulinic acid extended mean lifespan by 13% in males and 6% in females, an effect that disappeared in flies lacking functional Sir2 or FoxO, two of the most studied longevity-associated signalling pathways in biology.
A 2022 review in Frontiers in Pharmacology confirmed its anti-inflammatory activity across multiple pre-clinical models, including inhibition of NF-κB, the same pathway central to inflammaging.
Why this science matters
What makes these compounds worth watching is not a single headline result. It is the biology underneath it. Across different research models, the same themes keep appearing: cellular defence, oxidative stress, inflammatory signalling, metabolism and the pathways that help organisms maintain function under stress. Different molecules reach those systems in different ways, but together they are helping researchers map the biology of healthy ageing with increasing precision.
That is what makes this field so compelling. Longevity research is moving deeper than broad ideas like “antioxidants” or “healthy ageing” and into specific molecular pathways, cellular responses and measurable biological mechanisms. The more clearly we understand those mechanisms, the more intelligently we can choose which compounds deserve to be developed further.
For us, that is where the real opportunity begins: not with a trend, but with a molecule whose biology gives us a reason to pay attention.
Where we fit
This is exactly how we approach our own work. We start with the molecule: its chemistry, its biological activity and the research around it. Then we ask the next question: how do we turn that potential into an ingredient that can actually be used well?
Xanthohumol is our flagship example. Its research spans oxidative stress, inflammatory signalling, cellular defence and other areas central to modern longevity science. Its chemistry also creates a genuine delivery challenge, which is why we developed both highly standardised xanthohumol extract and liposomal delivery systems around it. That combination defines the way we think: strong molecules, serious science and delivery technology built around the chemistry of the active. And xanthohumol is only the beginning. As our work expands into new bioactive compounds, the principle stays the same: follow the biology, understand the molecule, and build the technology that allows more of its potential to be used.
That is where Dr Yan Labs fits into longevity. At the ingredient level where the science becomes something you can actually build with.
Sources
- Murray et al. Intermittent Supplementation With Fisetin Improves Physical Function and Decreases Cellular Senescence in Skeletal Muscle With Aging. Aging Cell. 2025;24(8):e70114. https://doi.org/10.1111/acel.70114
- Mahoney et al. Intermittent supplementation with fisetin improves arterial function in old mice by decreasing cellular
