Science
What Are Senolytics, and Do They Work?
Senolytics are experimental drugs meant to clear senescent cells. They help some mice; small human trials haven't shown slower aging or a longer life.
A few cells in your body have stopped dividing and, for reasons of their own, refused to leave. Scientists call them senescent cells, and the internet calls them zombie cells. A whole class of experimental drugs, senolytics, is designed to clear them out, on the theory that it might help people live longer and better. Humanic Blue traces that idea from the mouse work to the much smaller human trials.
So what are senolytics, and do they work? In mice, clearing these cells has improved health and, in some experiments, lifespan. In people, senolytics have reached only small, early trials. Those found that carefully screened volunteers could complete short treatment courses and that some laboratory markers changed. That does not establish long-term safety or better health. A randomized trial of the most studied combination missed its main goal. No human study has shown that a senolytic slows aging or helps anyone live longer.
In This Article
- Senescent cells stop dividing but keep signaling
- Clearing them helped mice, though not in every lab
- Human trials are tiny, and mostly uncontrolled
- A randomized bone trial missed its main target
- A company built on senescence drugs has closed
- Dasatinib is a leukemia drug; fisetin is a supplement
- The trials and numbers behind all of this
Key Takeaways
- Senescent cells can release inflammatory signals, but they also help with wound healing and tumor suppression.
- Clearing senescent cells improved health, and sometimes lifespan, in several mouse studies. A large federal mouse program found no lifespan gain from fisetin.
- Small human studies found that volunteers could complete short courses and that some senescence-related laboratory measures changed; they did not establish a health benefit.
- Three randomized trials aimed at a benefit, one from Mayo Clinic and two from a biotech company, all missed their main goals.
- Dasatinib is a prescription cancer drug with serious labeled risks. The FDA does not approve quercetin or fisetin dietary supplements for safety and effectiveness before sale.
What do senescent cells do?
Cellular senescence is a stress response. When a cell can no longer copy itself safely, it can switch off division and keep living. The National Institute on Aging (NIA) describes these cells as ones that “stop multiplying but don’t die off when they should,” releasing chemicals that can trigger inflammation. Researchers call that chemical output the senescence-associated secretory phenotype, or SASP.
Think of an employee who retired years ago but still sends emails to the whole office.
That’s not the whole story. The NIH’s Cellular Senescence Network says senescent cells can also protect health, by preventing tumor growth and helping wounds heal. The late Judith Campisi of the Buck Institute, whose lab built a mouse model for clearing senescent cells, put the problem plainly to the NIA in 2021: “But how are the good guys different from the bad guys?”
Senolytics remove; senomorphics quiet
Senescent cells resist the body’s normal self-destruct program. Senolytics are meant to switch off the survival defenses those cells rely on, so they die while healthy cells don’t. A related group, senomorphics, tries to quiet the harmful signals without killing the cell.
The most studied human combination is dasatinib plus quercetin, shortened to D+Q. Dasatinib is an FDA-approved leukemia drug. Quercetin is a plant pigment found in onions, grapes and tomatoes and sold as a supplement. Fisetin, a related plant compound, is also being tested.
Supplements don’t go through drug approval. The FDA explains that it “is not authorized to approve dietary supplements for safety and effectiveness before they are marketed.”
How does removing senescent cells differ from changing the signals they release?
The mouse evidence that started it
In 2015, a Mayo Clinic-led team, funded in part by the NIA, reported that D+Q cleared senescent cells in mice (NIA research summary). A single dose improved heart function in old mice within days, and repeated doses delayed age-related problems in mice bred to age quickly.
In 2018, the same group reported that very old mice given intermittent D+Q lived about 36% longer from the start of treatment than untreated mice. Another 2018 study, led by Laura Niedernhofer’s group at Scripps Research with Mayo co-authors, reported that fisetin extended median and maximum lifespan in mice. Several of the Mayo scientists hold a financial interest in Mayo Clinic’s senolytic patents, as their papers disclose.
Then the NIA’s Interventions Testing Program, which tests compounds in genetically varied mice at three separate labs, tried fisetin. It found no significant effect on lifespan in either sex. The program’s scientists noted their study used about 30 times as many mice as the earlier fisetin study, and said different mouse stocks or lab conditions might explain the gap. How the mouse studies compare
A mouse result is a reason to run a human trial. It isn’t a preview of the answer.
Have human trials shown that senolytics extend life?
No human trial has shown a longer life from senolytics. The studies so far have tested narrower questions.
The human evidence so far is a handful of small studies in people with specific diseases. Most had no comparison group, and every one listed a feasibility, safety or biomarker question as its main goal:
- Lung scarring, 2019. In a small group with idiopathic pulmonary fibrosis, a Wake Forest-led pilot found that three weeks of intermittent D+Q was feasible, and walking speed and distance improved. Lung function didn’t change. There was no placebo group.
- Lung scarring, 2023. A University of Texas Health San Antonio-led follow-up randomly assigned about a dozen people to D+Q or placebo (PubMed). The drug was generally well tolerated, but physical and lung measures didn’t appear to differ meaningfully between the groups.
- Kidney disease, 2019. In a small group of adults with diabetic kidney disease, a three-day course of D+Q reduced senescent cells in fat and skin samples 11 days later (EBioMedicine pilot study). That showed biological activity, not better kidneys.
- Memory and walking, 2025. Harvard-affiliated researchers at Hebrew SeniorLife gave D+Q to about a dozen older adults with slow walking and mild memory problems (STAMINA pilot). Average memory-test scores didn’t change significantly. The authors said the absence of an appropriate control group meant the data required cautious interpretation.
Scientists with a financial interest in Mayo Clinic’s senolytic patents are co-authors on all four. In a 2024 Nature Medicine column, London-based freelance writer Natalie Healey captured the gap in a single line: “Senolytics can prevent and treat age-related diseases in mice, but data in humans are lacking — for now” (Nature Medicine). See the pilot studies side by side
A phase 2 bone trial missed its main target
A bigger test of D+Q came from a Mayo Clinic randomized phase 2 trial published in Nature Medicine in 2024, led by researchers Joshua Farr and Sundeep Khosla (trial report). Postmenopausal women ages 62 to 88 took intermittent D+Q or nothing for 20 weeks.
The main goal was to lower a blood marker of bone breakdown. D+Q didn’t. A marker of bone building was about 16% higher relative to the untreated group during the first month, but that difference was no longer present at week 20. Women with the highest levels of a senescence marker in their blood seemed to respond better, including a small gain in wrist bone density.
The authors were careful about that last part. They wrote that exploratory analyses like this “do not definitively establish” a benefit, and that the idea needs its own trial. The trial didn’t measure fractures.
About half the women taking D+Q reported headaches, and stomach complaints were common. There were no serious drug-related side effects, but one woman was withdrawn after the QTc interval, a measure of how long the heart takes to reset electrically between beats, lengthened. Three authors disclosed a financial interest in senolytic patents held by Mayo Clinic. How the trial worked
What can a subgroup finding establish when the trial's primary outcome is not met?
A company built on senescence drugs has closed
Unity Biotechnology, a South San Francisco company, built its drug pipeline around senescent cells. In 2020, its knee-injection drug UBX0101 showed no significant difference from placebo on pain in people with knee osteoarthritis, according to the company’s filing with the Securities and Exchange Commission (SEC).
Unity then moved to an eye injection for diabetic macular edema, a swelling of the retina. In 2025 it reported that the drug met the trial’s criterion for being no worse than a standard eye treatment by more than an allowed margin at most time points. It failed that comparison at the main time point chosen before the trial. Meeting that criterion, called noninferiority, would not establish equal effects. By May 2025 it had cut all of its employees and ceased clinical development. On September 26, 2025, it filed a certificate of dissolution in Delaware, according to its SEC filings. What Unity’s trials found
What are the risks of senolytics?
Dasatinib’s FDA-approved uses are specific leukemias. Its prescribing information warns of severe drops in blood counts, “serious and fatal bleeding,” fluid buildup, heart problems, high blood pressure in the lungs and a lengthened QT interval on a heart tracing, among other risks. Trials screen people for these risks, check their other medicines and monitor them. A self-designed protocol at home skips all of that.
James Kirkland, the geriatrician who led much of Mayo Clinic’s senolytics research and who holds a financial interest in its patents, has urged people not to take senolytics outside a clinical trial. He told the NIA in 2021 that “anything that sounds too good to be true in mouse or cell culture models usually is.”
Quercetin has interaction questions of its own. Memorial Sloan Kettering Cancer Center notes that quercetin blocked two drug-processing liver enzymes in lab studies, though the clinical relevance isn’t known. It also describes a 79-year-old man on the blood thinner warfarin whose clotting test rose after he started quercetin, then normalized when he stopped.
Fisetin is sold online as a senolytic. As of September 26, 2026, ClinicalTrials.gov shows Mayo Clinic’s fisetin frailty trials still enrolling by invitation, with no posted results. No completed trial shows it slows aging or extends human life. Mayo’s bone trial originally planned a fisetin group but dropped it, citing the COVID pandemic and cost. There’s also no consumer test that shows whether a supplement cleared senescent cells in any tissue. Safety and fisetin details
What’s Interesting
The bone trial’s authors point toward a more selective future. If further trials confirm the exploratory finding in women with high senescence-marker levels, a blood marker might one day help identify who is likely to benefit. The NIH’s Cellular Senescence Network is building atlases of senescent cells across human tissues, partly to find those markers.
Researchers are also testing more precise tools. In 2024, NIA reported that engineered immune cells, called CAR T cells, cleared senescent cells in mice and improved metabolism and exercise capacity. It’s an old idea, getting rid of worn-out cells, now being tried with some very new equipment. It’s still mouse work.
What This Means in Practice
For living longer and better, no human trial has shown that dasatinib, quercetin or fisetin slows aging, and the one randomized D+Q trial in otherwise healthy older women missed its main goal. Kirkland, a co-author on every D+Q human study described here, has urged people not to use senolytics outside a clinical trial.
If you’re curious about a study, ClinicalTrials.gov lists senolytic trials by condition, phase and location. Questions to put to the study team before you join:
- What is the main outcome, and is it something you’d feel, like walking or memory, or only a lab marker?
- Is there a placebo or comparison group?
- What safety checks come with it, such as heart tracings and blood counts?
- Do the investigators hold patents or company interests in the drug?
Trial results are averages across small groups, and each person’s health history changes the risk. A geriatrician or your own doctor can help weigh a trial against your other medicines and conditions.
Senescent cells are one part of the framework in Hallmarks of Aging Explained, while What Is Geroscience? explains how interventions move from a mechanism to a human outcome test.
Bottom Line
Senolytics are experimental drugs designed to clear senescent cells. They improved health, and sometimes lifespan, in mice, though a large mouse program found no lifespan gain from fisetin. In people, small studies have found feasibility and biomarker changes, and three randomized trials aimed at a benefit missed their main goals. Nobody has shown that they help humans live longer. Until larger controlled trials report outcomes people can feel, Kirkland’s advice is to use senolytics only inside a clinical trial.
A NOTE FROM LONGEVITY365
We read research, consult expert perspectives and work to make complicated health information easier to understand. What you’re reading here reflects how we’ve interpreted and organized that information. It is educational content—not personal medical advice, diagnosis or treatment guidance.
We’re not perfect, and neither is the available research. Evidence changes, new studies emerge and what’s appropriate for one person may not be appropriate for another.
Use this article as a starting point for your own research and conversations with qualified professionals. Always talk with your doctor or another trusted healthcare professional before making decisions that could affect your health, particularly if you take medications, are receiving treatment, have existing health conditions, are pregnant or have other circumstances that could affect what’s appropriate for you.
Reader Questions
A few questions to carry into the comments or your next conversation. Please leave out identifying or personal medical details.
- 01What did this article make clearer about the gap between an aging mechanism and a proven human outcome?
- 02Which claim would you want to see tested in people before it affected a real health decision?
- 03What question should readers keep asking when "What Are Senolytics, and Do They Work" shows up in longevity marketing?
Extra Insights & Sources
For readers who want the details behind each claim above.
What We Know
- Senescence has beneficial and harmful roles, and senescent cells can contribute to inflammatory tissue dysfunction. Established biology.
- Targeted senescent-cell clearance can improve health and lifespan outcomes in some mouse models. Established preclinically.
- Fisetin did not extend lifespan in the NIA Interventions Testing Program’s genetically varied mice. Contested preclinically.
- D+Q can alter senescence-related biomarkers in small human studies. Preliminary human evidence.
- The randomized phase 2 D+Q bone trial did not meet its primary endpoint, and Unity Biotechnology’s UBX0101 phase 2 and UBX1325 ASPIRE trials missed theirs. Established trial results.
What We Don’t Know
- Whether any senolytic slows human aging or helps people live longer. Unknown.
- Which senescent-cell types should be removed, in which tissue, at what stage of disease. Unknown.
- Whether a reliable biomarker can identify likely responders. Promising but unvalidated.
- The long-term benefit-to-harm balance of intermittent senolytic treatment in generally healthy adults. Unknown.
The mouse studies in detail
Mayo Clinic, 2015. Zhu and colleagues, with senior author James Kirkland, identified the pro-survival networks senescent cells rely on and tested drugs against them. In Aging Cell they reported that D+Q reduced senescent-cell burden in chronologically aged, radiation-exposed and progeroid (Ercc1-deficient) mice. In old mice, heart function and blood-vessel reactivity improved five days after a single dose; after one limb was irradiated, a single dose improved exercise capacity for at least seven months; and periodic dosing extended healthspan in the progeroid mice. The paper’s disclosures state that Mayo Clinic and six authors, including Kirkland and Tchkonia, have a financial interest, and that co-authors Laura Niedernhofer and Paul Robbins co-founded and hold equity in Aldabra Bioscience. The NIA summary notes the researchers cautioned “that it is far too early to suggest that they be considered as a clinical intervention for aging.”
Mayo Clinic, 2018. Xu and colleagues reported in Nature Medicine that transplanting small numbers of senescent cells into young mice caused persistent physical dysfunction, and that intermittent D+Q in naturally aged mice “increased post-treatment survival by 36% while reducing mortality hazard to 65%.” Treatment began at 24 to 27 months of age, which the authors equate to 75 to 90 years in humans. Six authors, including Kirkland and Tchkonia, disclosed a financial interest; the patents (PCT/US2016/041646) are held by Mayo Clinic. (Note 1)
Fisetin, 2018. Yousefzadeh and colleagues (senior author Laura Niedernhofer, then at The Scripps Research Institute in Jupiter, Florida; Kirkland and Tchkonia were co-authors) reported in EBioMedicine that fisetin given to wild-type mice late in life “extended median and maximum lifespan.” In the aged-mouse experiments, supplementation began after 20 months of age. (Note 1)
NIA Interventions Testing Program, 2024. The ITP runs each test simultaneously at the University of Texas Health Science Center at San Antonio, the University of Michigan and The Jackson Laboratory, in genetically heterogeneous UM-HET3 mice. Harrison, Strong and colleagues (senior author Richard A. Miller) fed fisetin at 600 parts per million (ppm) from 20 months of age, either continuously or 3 days on and 11 days off. Fisetin did not significantly affect lifespan in either sex “at the doses and schedules used.” The authors also could not reproducibly detect fisetin in the treated mice’s plasma. On the gap with the 2018 study they wrote: “Our study is more adequately powered, using 30 × larger numbers of mice compared to the earlier study. The discrepancy may reflect the use of different mouse stocks or inter-laboratory variations in husbandry conditions.” The paper’s disclosures state that Mayo Clinic holds patents on certain senolytic agents, “None is currently licensed,” that Tamara Tchkonia held shares from Unity Biotechnology, and that Paul Robbins co-founded Itasca Therapeutics, a startup developing senotherapeutics. (Note 2)
CAR T cells, 2024. Amor and colleagues at Cold Spring Harbor Laboratory, Memorial Sloan Kettering Cancer Center and other institutions reported in Nature Aging that CAR T cells targeting a protein on many senescent cells improved glucose tolerance and exercise capacity in old mice. In young mice, one treatment prevented metabolic decline for more than a year, according to the NIA’s summary.
The human pilot studies side by side
Idiopathic pulmonary fibrosis, open-label, 2019. Justice and colleagues (Wake Forest School of Medicine and UT Health San Antonio; senior author Kirkland) gave 14 people D 100 mg/day plus Q 1,250 mg/day, three days a week for three weeks. Retention was 100%. One serious adverse event was reported; the most frequent non-serious events were respiratory symptoms, skin irritation or bruising, and stomach discomfort. Six-minute walk distance, 4-meter gait speed and chair-stand time improved (p < .05); pulmonary function, clinical chemistries, a lab-based frailty index and reported health were unchanged. Effects on circulating SASP factors were inconclusive. Three authors disclosed a financial interest in Mayo Clinic’s senolytic patents. (Note 3)
Idiopathic pulmonary fibrosis, randomized, 2023. Nambiar and colleagues ran a single-blind, placebo-controlled pilot in 12 participants over 50, randomized 1:1 to three weeks of the same regimen or placebo. All 108 doses were taken. The D+Q arm reported more non-serious adverse events than placebo (65 vs 22), and sleep disturbances and anxiety occurred in 4 of 6 on D+Q versus 0 of 6 on placebo. There were no serious adverse events related to D+Q. The study was too small to evaluate change reliably, and frailty, lung and physical-function measures did not appear meaningfully different between the groups. Tchkonia and Kirkland disclosed a financial interest in Mayo Clinic’s patents. (Note 3)
Diabetic kidney disease, open-label, 2019. Hickson and colleagues at Mayo Clinic gave nine people (average age 68.7) D 100 mg plus Q 1,000 mg for three days. Eleven days later, adipose tissue had fewer p16- and p21-expressing cells and fewer senescence-associated β-galactosidase-positive cells, skin had fewer p16- and p21-positive cells, and circulating SASP factors including IL-1α, IL-6 and MMP-9 and -12 were lower. Four authors disclosed a financial interest in Mayo Clinic’s senolytic patents. (Note 3)
STAMINA, single-arm, 2025. Millar and colleagues (Hinda and Arthur Marcus Institute for Aging Research at Hebrew SeniorLife and Harvard Medical School; senior author Lewis Lipsitz) gave 12 adults aged 65 or older with slow gait and mild cognitive impairment D 100 mg plus Q 1,250 mg for two days every two weeks for 12 weeks. About 10% of telephone-screened people completed the intervention. There were no serious related adverse events. Montreal Cognitive Assessment scores rose a non-significant 1.0 point on average (95% confidence interval, or CI, −0.7 to 2.7), and 2.0 points (95% CI 0.1 to 4.0) in those with the lowest baseline scores; TNF-α fell a non-significant 3.0%. The overall confidence interval describes uncertainty around the average change: it includes zero, meaning no change, as well as lower and higher scores. The subgroup interval excludes zero, but this uncontrolled study cannot show that treatment caused the subgroup’s improvement. Kirkland and Tchkonia, by then at Cedars-Sinai Medical Center, disclosed a financial interest in Mayo Clinic’s patents; the first author disclosed study support from the US Highbush Blueberry Council. (Note 3)
Other early human studies. The bone-trial authors also list a phase 1 D+Q study in five people with mild Alzheimer’s disease (Gonzales and colleagues, Nature Medicine, 2023), focused on safety and biodistribution, and a phase 1 study of UBX1325 in eight people with diabetic macular edema.
| Human study | Population | What it could answer | What it could not answer |
|---|---|---|---|
| Diabetic kidney pilot | 9 adults | Whether D+Q reached senescence-related tissue signals | Whether it improved kidney disease or lifespan |
| Pulmonary-fibrosis pilots | 14 open-label; 12 randomized | Feasibility, tolerability and trial design | Durable disease benefit or longevity |
| STAMINA pilot | 12 older adults with slow gait and mild cognitive impairment | Feasibility and preliminary functional signals | Efficacy without a control group |
| Bone phase 2 trial | 60 postmenopausal women | Randomized comparison of bone biomarkers | Fracture prevention or longer life |
The bone trial in detail
The phase 2 trial (NCT04313634) enrolled its first participant on June 9, 2020, and its last on November 15, 2022. It was open-label, comparing D+Q with an untreated control group, 30 women each. D was 100 mg a day for two days and Q was 1,000 mg a day for three days, repeated every 28 days for five cycles over 20 weeks.
- Primary endpoint (main outcome): percentage change in CTx, a bone-breakdown marker, at 20 weeks did not differ (D+Q −4.1% vs control −7.7%; P = 0.611).
- Secondary endpoint: P1NP, a bone-building marker, rose relative to control at 2 weeks (+16%, P = 0.020) and 4 weeks (+16%, P = 0.024), but not at 20 weeks (−9%, P = 0.149).
- Exploratory analysis: in the top third for T-cell p16 mRNA, a senescence-related marker measured in immune cells (about 10 women per arm), D+Q raised P1NP 34% and lowered CTx 11% at 2 weeks, and increased radius bone mineral density 2.7% (P = 0.004) at 20 weeks.
The abstract concludes that D+Q “did not reduce bone resorption in the overall group of postmenopausal women.” In the discussion, the authors wrote: “We acknowledge, however, that exploratory analyses such as this, even if based on a plausible, prespecified hypothesis, do not definitively establish that women with high T cell p16 mRNA levels would achieve skeletal benefits following D + Q treatment, and further studies are needed to rigorously test this hypothesis.”
Safety: headache affected 53% of the D+Q group, and gastrointestinal complaints were common. No serious or severe adverse events related to D+Q occurred. One D+Q participant was withdrawn because of QTc prolongation after dasatinib and was lost to follow-up after week 4; another stopped at week 9 because of fatigue and other nonspecific side effects; a third withdrew after week 2 over COVID concerns. The trial excluded people with a QTc above 450 ms and people taking antiarrhythmic, antiplatelet or anticoagulant drugs.
Disclosures: Nathan LeBrasseur, Tamara Tchkonia and James Kirkland “have a financial interest related to this research, including patents and pending patents covering senolytic drugs and their uses that are held by Mayo Clinic.” (Note 4)
Unity Biotechnology’s trials in detail
UBX0101, knee osteoarthritis. Unity’s August 17, 2020 release, filed with the SEC, reported that the phase 2 double-blind, placebo-controlled study randomized 183 patients to placebo or a single knee injection of 0.5, 2.0 or 4.0 mg. “UBX0101 failed to meet 12-week primary endpoint,” with no statistically significant difference from placebo on WOMAC-A pain.
UBX1325 (foselutoclax), diabetic macular edema. In a randomized, sham-controlled trial (NCT04857996) published in NEJM Evidence in 2025, 65 people received one eye injection or a sham. The primary objective was safety; the difference in vision at week 48 was 5.6 letters on an eye chart (95% confidence interval −1.5 to 12.7, a range that includes no difference), which the authors described as “trends suggestive of potential efficacy.” The trial was funded by Unity. In the phase 2b ASPIRE trial against aflibercept, Unity’s May 5, 2025 release said UBX1325 was non-inferior at most time points through 36 weeks “except for the average of weeks 20 and 24, the primary endpoint.” Noninferiority means meeting the trial’s statistical criterion for being no worse than the comparator by more than a margin set in advance; it does not mean equal effects. The main comparison averaged weeks 20 and 24, and that comparison failed the criterion.
Corporate status. Unity’s filings state that in May 2025 it implemented a reduction in force affecting all of its employees and ceased clinical development. Its board approved dissolution on June 27, 2025, stockholders approved it on September 18, 2025, and the certificate of dissolution became effective at 5:00 p.m. Eastern on September 26, 2025.
Safety and fisetin in detail
Dasatinib label. The current DailyMed label for dasatinib tablets (Teva; version published August 17, 2026) lists indications in Philadelphia chromosome-positive chronic myeloid leukemia and acute lymphoblastic leukemia. Its warnings and precautions cover myelosuppression, bleeding-related events (“Dasatinib can cause serious and fatal bleeding”), fluid retention including pleural effusions, cardiovascular toxicity, pulmonary arterial hypertension, QT prolongation, severe dermatologic reactions, tumor lysis syndrome, embryo-fetal toxicity, effects on growth in children and hepatotoxicity. Strong CYP3A4 inhibitors and inducers change dasatinib dosing.
Kirkland in full. From the NIA’s 2021 feature, when Kirkland was at Mayo Clinic: “We haven’t so far seen serious or severe adverse events in clinical trials with some of these agents, but it doesn’t mean they won’t happen,” he said. “They could take a long time to develop, and anything that sounds too good to be true in mouse or cell culture models usually is. We need many more long-term studies and human trials.” In the same feature, Viviana Perez Montes, an NIA program officer for senescence research, said, “We have to remember that senolytics are going to kill senescent cells and we believe that some of those senescence functions could be beneficial,” and added that the consequences of eliminating cells that won’t be replaced aren’t yet known.
Quercetin interactions. Memorial Sloan Kettering’s quercetin monograph (last updated October 10, 2023) says quercetin “was shown to significantly inhibit the constitutive CYP3A4 and CYP2C19 activity, in vitro,” and that “Clinical relevance is not known.” It also lists preclinical interactions with losartan and tamoxifen, and a case report of a 79-year-old man on stable warfarin for atrial fibrillation whose INR rose after quercetin supplementation and normalized after he stopped.
Fisetin trials, as of September 26, 2026. A ClinicalTrials.gov search lists 36 registered studies with fisetin as an intervention. Mayo Clinic’s fisetin frailty trials in older adults (NCT03675724) and older women (NCT03430037), each with a planned 40 participants, are enrolling by invitation with no results posted. A 75-person osteoarthritis trial at the Steadman Philippon Research Institute (NCT04210986) is listed as completed with results posted. The University of Minnesota’s STOP-Sepsis trial (NCT05758246), with 220 planned participants, is recruiting. The Mayo bone trial’s report says “because of the COVID pandemic and cost issues, the study was modified to a two-arm study (control versus D + Q).”
Aging as an FDA indication. No drug is approved to treat aging itself. The American Federation for Aging Research, which is raising money for the TAME trial of metformin, writes that it hopes “the FDA will approve aging as an indication.”
Sources
- National Institute on Aging: Feature on cellular senescence and healthier aging (July 13, 2021)
- National Institute on Aging: NIH-funded researchers identify drugs to eliminate senescent cells in mice, improving health and function (March 9, 2015)
- National Institute on Aging: Cellular therapy targeting senescent cells may improve health in mice (August 22, 2024)
- NIH Common Fund: Cellular Senescence Network (SenNet) (last reviewed February 2, 2026)
- US Food and Drug Administration: Information for Consumers on Using Dietary Supplements (content current as of October 21, 2022)
- Zhu Y, et al. The Achilles’ heel of senescent cells, Aging Cell, 2015: PubMed 25754370
- Xu M, et al. Senolytics improve physical function and increase lifespan in old age, Nature Medicine, 2018: PubMed 29988130
- Yousefzadeh MJ, et al. Fisetin is a senotherapeutic that extends health and lifespan, EBioMedicine, 2018: PubMed 30279143
- Harrison DE, et al. Astaxanthin and meclizine extend lifespan in UM-HET3 male mice; fisetin … do not, GeroScience, 2024: PubMed 38041783
- Justice JN, et al. Senolytics in idiopathic pulmonary fibrosis: first-in-human, open-label pilot, EBioMedicine, 2019: PubMed 30616998
- Nambiar A, et al. Dasatinib and quercetin in idiopathic pulmonary fibrosis: randomized, placebo-controlled pilot, EBioMedicine, 2023: PubMed 36857968
- Hickson LJ, et al. Senolytics decrease senescent cells in humans (diabetic kidney disease), EBioMedicine, 2019: PubMed 31542391
- Millar CL, et al. A pilot study of senolytics to improve cognition and mobility in older adults at risk for Alzheimer’s disease (STAMINA), eBioMedicine, 2025: PMC11907475
- Farr JN, et al. Effects of intermittent senolytic therapy on bone metabolism in postmenopausal women: a phase 2 randomized controlled trial, Nature Medicine, 2024: PubMed 38956196
- Healey N. Senolytics target cellular senescence — but can they slow aging? Nature Medicine (The Clinical Pipeline), September 2, 2024: Nature Medicine
- Klier S, et al. Safety and Efficacy of Senolytic UBX1325 in Diabetic Macular Edema, NEJM Evidence, 2025: PubMed 40261111
- Unity Biotechnology, SEC filings: UBX0101 phase 2 results, August 17, 2020; ASPIRE 36-week results, May 5, 2025; certificate of dissolution 8-K, September 26, 2025
- DailyMed, US National Library of Medicine: Dasatinib tablets prescribing information
- Memorial Sloan Kettering Cancer Center: Quercetin (last updated October 10, 2023)
- ClinicalTrials.gov: studies listing fisetin as an intervention (searched September 26, 2026)
- American Federation for Aging Research: TAME Trial
Notes
Note 1: The 2015 and 2018 Mayo Clinic mouse studies and the 2018 fisetin study were funded by NIH grants plus private donors and foundations, including the Glenn, Ted Nash Long Life and Noaber Foundations, the Glenn Foundation/American Federation for Aging Research, the Connor Group and Robert J. and Theresa W. Ryan.
Note 2: Funded in part by NIA grants to the three Interventions Testing Program sites, with some University of Michigan work supported by the Glenn Foundation for Medical Research.
Note 3: The human pilot studies were funded by National Institutes of Health grants, with additional support from private donors and foundations for the Mayo-linked lung and kidney studies. The kidney study also lists Satellite Healthcare, and the 2019 lung study states it “was not supported in any way by pharmaceutical companies, private industry, or other for-profit agencies.” STAMINA was funded by NIA grants R21AG073886 and R33AG061456.
Note 4: Funded by National Institutes of Health grants; the paper states “The funders played no role in the conduct or analyses in this study.”
Leave a Reply