Fisetin Clinical Trials: What the Human Evidence Actually Shows
As of September 2026, thirty-four clinical trials involving fisetin have been registered on ClinicalTrials.gov and the WHO International Clinical Trials Registry Platform. Six have been completed. Four of those six have results available, representing 11.8% of the total.[1] The rest are recruiting, suspended, terminated, withdrawn or have an unknown status.
That ratio, four out of thirty-four, is the single most useful number in this field. It means that fisetin's reputation in human health rests almost entirely on preclinical work and on extrapolation from a handful of small, early-stage studies. Some of those studies reported favourable changes in biomarkers. Others found no significant clinical benefit. None was large enough to establish efficacy.
For a product team, the evidence does not yet support claims of clinical benefit in people. What it does support is an ingredient with serious research interest, a distinctive dosing model, and a set of gaps that the next two years of trial results may begin to close.
This guide covers the trial landscape, what each completed study found, why a biomarker result is not the same as a health outcome, what "clearing senescent cells in humans" actually means in the published data, the dosing patterns used in research, the formulation gap, safety signals and drug interactions, the trials most likely to report next, and what all of this means for product design and label language.
01 Summary
The Short Version: What Has Been Shown in People
The positive signals from human studies of fisetin, as of September 2026, share a pattern. They come from studies that measured biomarkers rather than clinical outcomes, that lacked a placebo group, that were reported only as conference abstracts or preprints, or that combined fisetin with another intervention such as chemotherapy or thrombolysis. In the studies that had a placebo control and measured a clinical outcome, fisetin either showed no significant benefit or produced inconclusive results because the sample was too small.[1][2]
This does not mean fisetin is ineffective. It means the question has not been answered at the level of evidence that would support a product claim. The distinction matters for anyone building or marketing a fisetin product, and for suppliers like us who provide the ingredient.
02 Landscape
Thirty-Four Trials, Four With Results: The Current Landscape
The most complete account of fisetin's clinical pipeline was published on 14 September 2026 by Sandoval-Caballero and colleagues at the University of Minnesota. They searched ClinicalTrials.gov and the WHO ICTRP systematically and identified thirty-four registered trials. Aging and frailty was the most common focus, accounting for about 35% of registered trials. Other chronic age-related diseases, mainly osteoarthritis, accounted for about 24%. Cancer survivorship made up about 15%, followed by neuroimmune and neurodegenerative diseases at about 12%, cardiovascular diseases at about 9%, and metabolic diseases at about 6%.[1]
The phase distribution tells the same story. Phase 2 was the most common designation, at about 35% of trials. Only two trials were classified as Phase 2/Phase 3, and one as Phase 4. The clinical investigation of fisetin is still in its early stages.[1]
03 Scorecard
What Each Completed Study Actually Found
The table covers every human study of fisetin whose results are available through a registry, a peer-reviewed publication or a preprint as of September 2026. Where a trial is marked as completed in a registry but results have not been posted or published, it is noted as such.
| Study | Design and size | Fisetin dose | Control | Main finding |
|---|---|---|---|---|
| Krishnakumar 2022, pharmacokinetics[3] | Crossover, 15 healthy volunteers | 1,000 mg single dose | Plain fisetin as the reference arm | Plain fisetin barely detectable in plasma; a hydrogel formulation raised exposure about 27-fold. Free fisetin circulated for only about 2 hours |
| Tashman 2025, knee osteoarthritis[2] | Randomised, placebo-controlled, 74 participants | 20 mg/kg per day, 2 days on and 28 days off, 3 cycles | Placebo | No significant benefit for pain, function or cartilage. No significant safety concerns |
| NCT04313634, skeletal health[1][4] | Three arms (D+Q, fisetin, untreated control), 74 enrolled but only 11 analysed in the fisetin arm | About 20 mg/kg per day, 3 days every 4 weeks, 5 cycles over 20 weeks | Untreated | Inconclusive for fisetin due to sample size. D+Q arm showed bone formation marker increase only in women with high senescent-cell burden |
| NCT05416515, carpal tunnel syndrome[1] | Single-arm, 40 participants, no control | About 20 mg/kg per day, 2 days on and 28 days off | None | Changes in symptoms and senescence markers reported, but without a control group the changes cannot be attributed to fisetin |
| NCT02909686, Gulf War Illness[1] | Randomised, placebo-controlled, 36 participants | 200 to 800 mg per day | Placebo | No significant improvement in symptom severity compared with placebo |
| COVID-FIS, nursing home residents[1] | Randomised, placebo-controlled | About 20 mg/kg per day, 2 days on and 28 days off | Placebo | Terminated by the data safety monitoring board for futility |
| Farsad-Naeimi 2018, colorectal cancer[5] | Randomised, placebo-controlled, 37 patients undergoing chemotherapy | 100 mg per day for 7 weeks | Placebo | Within the fisetin group, IL-8 and hs-CRP fell. Between groups, only IL-8 reached significance. No effect on CRP, IL-10, MMP-7 or MMP-9 between groups |
| Wang 2019, ischaemic stroke[6] | Double-blind randomised placebo-controlled, single-centre, patients receiving rt-PA thrombolysis | 100 mg per day (as adjunct to rt-PA) | Placebo plus rt-PA | Lower NIHSS scores and reduced MMP-2, MMP-9 and CRP in the delayed-treatment subgroup. Fisetin was given alongside a powerful drug, not alone |
| Colorado vascular function trial, conference abstract[7] | Randomised, placebo-controlled, 41 older adults | 2 mg per kg per day, 3 days, repeated after 2 weeks | Placebo | Brachial artery flow-mediated dilation improved by about 41% from baseline; no change in placebo. Accompanied by reductions in senescence and oxidative stress markers. Conference abstract only, not yet peer-reviewed |
| Gao 2026, senescence gene expression, preprint[8] | Double-blind randomised, 81 adults over 55, no placebo arm | Daily 100 mg versus bolus 20 mg/kg for 2 days on and 28 days off | Two fisetin arms compared with each other; no placebo | Both regimens lowered GLB1 and P16 gene expression in blood cells at day 45. Bolus was more effective for MIF. No placebo means effect of time and expectation cannot be separated from the drug |
| Hambright 2024, C12FDG observational[9] | Observational, 10 participants self-reporting fisetin use (100 mg per day), within a larger cohort study | Self-reported, about 100 mg per day | Own baseline | Senescent-cell markers and sclerostin decreased compared with their own earlier values. No control group, no randomisation, self-selected participants |
| Alipour 2026, obesity[10] | Randomised, 4 arms (fisetin, exercise, fisetin plus exercise, placebo), 44 men with obesity | 200 mg per day for 12 weeks | Placebo | Fisetin plus exercise improved body weight and inflammatory markers more than either alone; fisetin alone also improved some outcomes versus placebo. Small sample per arm |
Read together, the table shows a field where interest is running well ahead of evidence. Of the studies with a placebo control and a clinical outcome, the results are either negative (knee osteoarthritis, Gulf War Illness) or driven by a subgroup or a co-intervention (bone trial, stroke trial).
04 Endpoints
Why a Biomarker Change Is Not a Health Outcome
Several of the studies above reported that fisetin reduced a senescence-associated marker in the blood. In the Hambright cohort, C12FDG-positive blood mononuclear cells and serum GDF15 both fell after participants started taking fisetin.[9] In the Gao preprint, gene expression of P16 and GLB1 in blood cells dropped in both dosing groups.[8] In the Colorado vascular trial, markers of cellular senescence and mitochondrial oxidative stress decreased alongside the improvement in flow-mediated dilation.[7]
A biomarker decline is a signal worth investigating. It is not the same as showing that a person feels better, moves better, lives longer or avoids a disease. The gap between the two was demonstrated directly in the Mayo skeletal health trial. Dasatinib plus quercetin increased the bone formation marker P1NP at 2 and 4 weeks, but the primary endpoint of bone resorption did not change. Only in an exploratory subgroup of women with the highest P16 levels did the combination show a meaningful skeletal response.[4] The drug moved a marker in everyone and moved a bone outcome in some. That distinction is exactly why regulators require clinical endpoints, not just biomarker changes, before allowing health claims.
The within-group trap
One pattern recurs in the supplement marketing built on these studies and is worth naming directly. In the colorectal cancer trial, hs-CRP fell significantly within the fisetin group from baseline to the end of treatment. Several consumer-facing sites cite this as evidence that fisetin lowers CRP. But the trial was randomised and placebo-controlled, and the between-group comparison, fisetin against placebo, showed no significant difference for CRP, IL-10, MMP-7 or MMP-9. Only IL-8 was significant between groups.[5] A within-group change in a placebo-controlled trial tells you very little, because the placebo group may have changed by the same amount. The between-group comparison is the one that counts, and it is the one most often left out of the marketing summary.
The same caution applies to the Hambright and Gao studies: without a placebo arm, every change is a within-group change, and the question of whether it would have happened anyway remains unanswered.
For product teams, the practical consequence is straightforward. A fisetin product can say the ingredient is under investigation. It can cite the number of registered trials and the research institutions involved. What it cannot do, on current evidence, is claim that it clears senescent cells in people or that it improves any specific health outcome.
05 Senolysis
Has Fisetin Been Shown to Clear Senescent Cells in People?
The short answer is: not in a controlled trial. The longer answer matters because "fisetin clears senescent cells" is the single most common claim on supplement labels and marketing pages, and every link in the evidence chain behind it has a qualifier.
The original demonstration was in mice. Fisetin reduced senescent-cell markers and extended median and maximum lifespan when given late in life to one strain,[11] but did not extend lifespan in the multi-site Interventions Testing Program using genetically diverse mice, and did not lower P16 in liver, kidney or brain at the doses used.[12]
In people, the published observations are these. Hambright and colleagues found that C12FDG-positive mononuclear cells decreased in 10 individuals who were already taking fisetin when they joined the cohort. These participants chose to take fisetin on their own; there was no randomisation, no blinding and no control group.[9] Gao and colleagues showed that gene expression of senescence-related genes fell in blood cells from 81 older adults after fisetin, but both groups received fisetin and there was no placebo arm, so the decline could reflect time, expectation or biological variability rather than the drug.[8]
The Colorado vascular trial did include a placebo group and did measure senescence markers alongside a functional endpoint, and both moved in the right direction.[7] But these findings exist only as a conference abstract, the full peer-reviewed paper has not been published, and the trial registry still lists the study as active and not recruiting.
Every statement that fisetin clears senescent cells in humans rests on uncontrolled observations, a preprint without a placebo arm, or a conference abstract. No peer-reviewed, placebo-controlled trial has yet demonstrated it.
This will likely change. The AFFIRM trials at Mayo are designed to test exactly this hypothesis in frail older adults, and results are expected. The senior investigator on the bone trial drew a practical conclusion in a 2025 conference address: the early human signals of biological effect for senolytic therapy came from dasatinib plus quercetin, not fisetin, and using either commercially without knowing the individual's senescent-cell burden is premature.[13] But until they arrive, a label that says "clinically proven to clear senescent cells" is ahead of the data.
06 Dosing
Three Dosing Patterns and What They Mean for Product Design
The registered trials use three distinct approaches to dosing, and each implies a different kind of product.
| Pattern | Dose for a 70 kg adult | Schedule | Capsules per dosing day at 500 mg each | Multiple of daily dietary intake | Examples |
|---|---|---|---|---|---|
| High-dose intermittent pulse | About 1,400 mg per day | 2 to 3 consecutive days, then 28 days off | About 3 | About 3,500 times | AFFIRM, knee OA trial, COVID-FIS, carpal tunnel[1] |
| Daily low to moderate dose | 100 to 500 mg per day | Every day for weeks to months | 1 | 250 to 1,250 times | Hvidovre healthy-ageing trial (100 mg), colorectal cancer (100 mg), Colorado vascular (140 mg)[1][5] |
| Daily dose versus pulse, head to head | 100 mg per day versus about 1,400 mg on dosing days | 60 days total | Varies | 250 to 3,500 times | Gao 2026 preprint[8] |
The dietary-intake column puts the doses in perspective. The average daily intake of fisetin from food was estimated at 0.4 mg in a Japanese survey, about twenty times less than quercetin in the same population.[14] Even the lowest clinical dose, 100 mg per day, is 250 times the dietary level. The highest, at 20 mg per kg, is 3,500 times. The further a dose sits from normal dietary exposure, the more weight falls on dedicated safety data, which is §08's subject.
The high-dose pulse follows from the senolytic hypothesis: senescent cells need a brief, concentrated hit, after which the drug should be cleared before the next cycle, in what the researchers call a "hit-and-run" approach.[11] Most Mayo-led trials use this pattern. But it is not the only one being tested. The Hvidovre trial in Copenhagen is using 100 mg per day for 7 weeks, a dose and schedule that fits a standard daily supplement capsule.[15] The Colorado vascular trial used 2 mg per kg, roughly 140 mg for a 70 kg person, which is also within the range of commercial products.[7]
The Gao preprint compared the two approaches directly and found that the pulse regimen produced a more consistent reduction in senescence-related gene expression across multiple blood cell genes, particularly MIF, than the daily dose.[8] That is a single study, it is a preprint, it has no placebo arm, and gene expression in blood cells is not a clinical outcome. But it is the first human data directly comparing the two schedules, and the result is consistent with the hit-and-run model.
For a product team, the dosing pattern drives the format. A daily 100 mg capsule is the simplest retail product. A monthly pulse pack of three to six high-dose capsules is a different product entirely, with different label directions, a different price per serving, and a different conversation with the consumer about how and when to take it. Neither format has been validated by a positive outcome trial in people.
07 Formulation
What the Trials Are Not Telling You About Formulation
The Sandoval-Caballero review flagged a problem that most commentary on fisetin trials ignores: the majority of registered trials do not report which formulation of fisetin they used.[1] This matters because the only human pharmacokinetic study showed that formulation can change systemic exposure by a factor of twenty-seven. After a 1,000 mg dose of plain fisetin, the compound was barely detectable in plasma. A hydrogel-based formulation of the same dose produced 27-fold higher exposure and a slightly longer half-life, from about 1.1 to about 1.5 hours.[3]
The review catalogued what was missing from the trial records: for several multi-component and proprietary interventions, the amount of fisetin itself was not even reported. Among trials that did report a dose, most gave only milligrams per day or milligrams per kilogram without stating the source plant, the purity grade, the dosage form (capsule, tablet, powder), whether a carrier or excipient was present, or whether any bioavailability-enhancing technology was used.[1]
If two trials use the same nominal dose but different formulations, the amount of fisetin that actually reaches the bloodstream can differ by an order of magnitude. A negative result in one trial and a positive result in another may reflect formulation rather than the molecule itself. Yet most trial registrations say only "fisetin" without specifying the source, purity or delivery form.
For the ingredient supply side, this is both a problem and an opportunity. The problem is that a trial result obtained with an unspecified formulation cannot be assumed to apply to any particular grade or preparation on the market. The opportunity is that brands and clinical researchers need raw materials whose identity, purity and physical form are documented well enough to support a reproducible protocol. That is what a specification with HPLC assay, a certificate of analysis and an identity test are for. Our fisetin powder grades and specifications are set out on the product page.
08 Safety
Safety, Drug Interactions and Who the Trials Actually Tested
What the completed trials reported
None of the completed fisetin trials reported serious adverse events attributable to the compound. The knee osteoarthritis trial reported no significant safety concerns.[2] The pharmacokinetic study reported one case each of bloating and reduced appetite after a 1,000 mg dose.[3] The Sandoval-Caballero review concluded that the available human evidence is insufficient to establish a long-term safety profile, and that drug interactions remain insufficiently characterised.[1]
What the exclusion criteria reveal
Trial exclusion criteria are designed to protect participants from foreseeable risks, and they also reveal what the researchers themselves consider potentially unsafe. The AFFIRM-LITE protocol excluded participants who could not stop taking any of the following during the dosing period: all statins, lithium, digoxin, cyclosporin, tacrolimus, sirolimus, methotrexate, corticosteroids, proton pump inhibitors, quinolone antibiotics, strong CYP3A4 inhibitors (including azole antifungals and several antivirals), repaglinide, bosentan, and a list of about twenty other drugs.[16] The Gao trial similarly excluded people on warfarin, metformin, senolytic agents and drugs that induce cellular stress.[8]
These lists are long, and they describe the medicine cabinet of a typical supplement buyer in the target age range. A 65-year-old taking a statin for cholesterol, omeprazole for reflux and perhaps metformin for early diabetes would have been excluded from these trials. The safety and efficacy data that exist for fisetin were therefore collected in people who are healthier and less medicated than the population most likely to buy a fisetin supplement.
The trials excluded the very people most likely to use the product. That gap between trial populations and real-world consumers is a safety question that the current data do not answer.
The absence of long-term data
The longest completed fisetin trial ran for 20 weeks.[1] Several ongoing trials plan follow-ups of one to three years, but none has reported long-term safety data. Unlike quercetin, which has a two-year carcinogenicity study in rats and a detailed safety review from Germany's Federal Institute for Risk Assessment,[17] fisetin does not have an equivalent body of chronic toxicology work. A comparison of their safety profiles is covered in our fisetin vs quercetin guide.
09 Pipeline
Trials Most Likely to Report Next
Three trials are worth tracking because they address the biggest gaps in the current evidence.
| Trial | Why it matters | Expected timing |
|---|---|---|
| NCT07195318, Hvidovre University Hospital, Copenhagen: low-dose fisetin for healthy ageing[15] | 120 participants, triple-blind, placebo-controlled, 100 mg per day for 7 weeks. This is the first adequately powered, placebo-controlled trial at a dose that matches a standard supplement capsule. If positive, it would be the first controlled evidence that a daily consumer dose produces a measurable biological effect | Primary completion estimated October 2026 |
| NCT06431932, Hvidovre: Phase 1 pharmacokinetics plus Phase 2a in older adults with multimorbidity[18] | 60 participants, 20 mg/kg for 2 days. Provides the first formal pharmacokinetic data in older adults and the first efficacy signal in people with multiple diseases, the population most fisetin supplements are marketed to | Recruiting since March 2026, estimated completion December 2028 |
| NCT06133634, University of Colorado: fisetin for vascular function in older adults[7] | 70 participants, placebo-controlled, 2 mg per kg per day. Preliminary conference abstract reported improved flow-mediated dilation. If the full peer-reviewed results confirm it, this would be the first positive outcome from a controlled fisetin trial at a commercially relevant dose | Active, not recruiting; primary completion estimated March 2026, final completion March 2027 |
| NCT03675724 and NCT03430037, Mayo Clinic: AFFIRM and AFFIRM-LITE[16] | The two original Mayo fisetin trials in frail older adults. AFFIRM tests a single 2-day pulse; AFFIRM-LITE tests two monthly pulses. Primary outcomes are inflammatory markers and physical function. Currently listed as enrolling by invitation | Timing uncertain; registered since 2018 and 2019 |
The Hvidovre and Colorado trials are the ones most likely to report soon. The AFFIRM trials have been running longest and would carry the most weight because they test the core hypothesis, fisetin versus placebo in frail elderly people, at the dose most trials have adopted. Two by the same group in Copenhagen, and together they cover both sides of the dosing debate: the daily low dose and the intermittent pulse. The Colorado trial sits between the two in dose. Between them, these three studies could shift the evidence picture substantially within the next one to two years.
10 Implications
What This Means for Product Teams
What the evidence supports saying
The ingredient is under active clinical investigation at multiple research institutions, including Mayo Clinic and the University of Colorado. Thirty-four trials have been registered. The preclinical rationale centres on the clearance of senescent cells. Human studies are in their early stages, with results expected from several placebo-controlled trials in the near term.
What it does not support saying
That fisetin has been clinically proven to clear senescent cells in humans, slow ageing, improve joint health, or produce any specific health benefit. Each of these claims requires a positive, adequately powered, placebo-controlled trial with a clinical endpoint, and none exists as of September 2026.
Choosing a dose and format
If modelling the product on the senolytic pulse trials, the reference is 20 mg per kg for 2 to 3 consecutive days per month, which translates to roughly 1,400 mg per day for a 70 kg adult. If modelling on the daily trials, the reference is 100 to 500 mg per day. Neither has been validated by a positive outcome trial. The trial regimens were administered under medical supervision and should be presented as research context, not as serving recommendations.
What to ask a fisetin supplier
Given that most trials do not report formulation details, the burden falls on the brand to document its own ingredient. The questions that matter are the botanical source and plant part, the HPLC assay and what it separates fisetin from (quercetin is a co-occurring flavonoid in smoke tree wood), the physical form, and whether stability data exist for the intended finished product format. PhytoVale supplies fisetin extracted from the trunk and thick-branch wood of Cotinus coggygria at 10%, 50%, 85% and 98% by HPLC. Grades, specifications and what the assay measures are set out on the fisetin powder product page. Samples are free, MOQ is 1 kg, and quotations are returned within 24 hours.
11 Questions
Fisetin Clinical Trials: Frequently Asked Questions
Has fisetin been proven to work in humans?
Not yet. As of September 2026, the completed placebo-controlled trials have been either negative (knee osteoarthritis, Gulf War Illness) or inconclusive (skeletal health, with only 11 participants in the fisetin arm). Several ongoing trials, particularly the Hvidovre and Colorado studies, may provide stronger evidence within one to two years.
What is the right dose of fisetin?
There is no established dose. Trials have used two main patterns: an intermittent pulse of about 20 mg per kg of body weight (roughly 1,400 mg per day for a 70 kg person) for 2 to 3 days per month, and a daily dose of 100 to 500 mg. A direct comparison of the two in a preprint found the pulse more effective at reducing senescence-related gene expression, but neither has been validated by a positive clinical outcome trial. These are research protocols given under medical supervision, not consumer dosing recommendations.
Is fisetin safe to take with statins or other medications?
The trial data do not answer this. Most fisetin trials excluded participants taking statins, proton pump inhibitors, anticoagulants, immunosuppressants and strong CYP3A4 inhibitors. Until interaction studies are conducted, the safety of combining fisetin with these medications is unknown.
Does fisetin clear senescent cells in humans?
There are observational and preliminary signals in that direction, but no peer-reviewed, placebo-controlled trial has demonstrated it. The published observations come from an uncontrolled cohort, a preprint without a placebo arm, and a conference abstract. Properly controlled results from the AFFIRM trials and others are expected.
Why do so many fisetin trials fail or get withdrawn?
Four of the 34 registered trials were withdrawn before enrolling any participants, and one was terminated. Reasons include loss of supplement supply (the glaucoma trial), lack of funding (the diabetic kidney disease trial), and futility (the COVID trial). Early-phase research in a new compound carries a high attrition rate, and fisetin is no exception.
How does fisetin compare with dasatinib plus quercetin?
D+Q is further along in human testing and has produced the first controlled evidence of senescent-cell reduction and bone-marker changes in people, although its primary bone endpoint was also negative overall.[4] Fisetin's advantage is that it is a single compound sold as a supplement, not a combination that includes a prescription oncology drug. The two are being compared head to head in the childhood cancer survivors trial. A broader comparison between fisetin and quercetin is covered in our fisetin vs quercetin guide.
12 Evidence base
References
[1] Sandoval-Caballero, C., Roemer, Z., Kotz, C. M., Puskarich, M. A., Mavanji, V., Schmidt, E. L., Sibley, S. D. (2026). Clinical translation of fisetin for age-related diseases: current evidence and future opportunities. Nutrients, 18(18), 2999. DOI: 10.3390/nu18182999
[2] Tashman, S., et al. (2025). Results from a randomized clinical trial evaluating the senolytic fisetin for treating knee osteoarthritis. Osteoarthritis and Cartilage, 33(Suppl S), abstracts from the 2025 OARSI World Congress. View source
[3] Krishnakumar, I. M., Jaja-Chimedza, A., Joseph, A., Balakrishnan, A., Maliakel, B., Swick, A. (2022). Enhanced bioavailability and pharmacokinetics of a novel hybrid-hydrogel formulation of fisetin orally administered in healthy individuals: a randomised double-blinded comparative crossover study. Journal of Nutritional Science, 11, e74. DOI: 10.1017/jns.2022.72
[4] Farr, J. N., Atkinson, E. J., Achenbach, S. J., et al. (2024). Effects of intermittent senolytic therapy on bone metabolism in postmenopausal women: a phase 2 randomized controlled trial. Nature Medicine, 30(9), 2605–2612. DOI: 10.1038/s41591-024-03096-2
[5] Farsad-Naeimi, A., Alizadeh, M., Esfahani, A., Darvish Aminabad, E. (2018). Effect of fisetin supplementation on inflammatory factors and matrix metalloproteinase enzymes in colorectal cancer patients. Food and Function, 9(4), 2025–2031. DOI: 10.1039/c7fo01898c
[6] Wang, L., Cao, D., Wu, H., Jia, H., Yang, C., Zhang, L. (2019). Fisetin prolongs therapy window of brain ischemic stroke using tissue plasminogen activator: a double-blind randomized placebo-controlled clinical trial. Clinical and Applied Thrombosis/Hemostasis, 25, 1076029619871359. DOI: 10.1177/1076029619871359
[7] Mahoney, S. A., et al. (2024). Fisetin to improve vascular function in older adults. Preliminary results reported as conference abstract. ClinicalTrials.gov NCT06133634
[8] Gao, X., Roder, J., Minas, L. T., Singer, J., Barton, C., et al. (2026). Effects of two fisetin dosing regimens on reducing senescence-related genes in peripheral blood mononuclear cells in aged humans. Preprints.org, 202607.1685.v1. DOI: 10.20944/preprints202607.1685.v1 (preprint, not yet peer-reviewed)
[9] Hambright, W. S., Duke, V. R., Goff, A. D., et al. (2024). Clinical validation of C12FDG as a marker associated with senescence and osteoarthritic phenotypes. Aging Cell, 23(5), e14113. DOI: 10.1111/acel.14113
[10] Alipour, M., Saeidi, A., Hejazi, K., Supriya, R., Zouhal, H. (2026). The effects of interval resistance-aerobic training and fisetin supplementation on asprosin and selected adipokines in obese men: a double-blind randomized control trial. Nutrients, 18(3), 433. DOI: 10.3390/nu18030433
[11] Yousefzadeh, M. J., Zhu, Y., McGowan, S. J., Angelini, L., Fuhrmann-Stroissnigg, H., Xu, M., et al. (2018). Fisetin is a senotherapeutic that extends health and lifespan. EBioMedicine, 36, 18–28. DOI: 10.1016/j.ebiom.2018.09.015
[12] Harrison, D. E., Strong, R., Reifsnyder, P., et al. (2024). Astaxanthin and meclizine extend lifespan; fisetin, SG1002, dimethyl fumarate, mycophenolic acid and 4-phenylbutyrate do not significantly affect lifespan at the doses and schedules used. GeroScience, 46(1), 795–816. DOI: 10.1007/s11357-023-01011-0
[13] Khosla, S. (2025). Translating senolytics from mice to humans. Innovation in Aging, Gerontological Society of America Annual Scientific Meeting abstract. DOI: 10.1093/geroni/igaf122.679
[14] Kimira, M., Arai, Y., Shimoi, K., Watanabe, S. (1998). Japanese intake of flavonoids and isoflavonoids from foods. Journal of Epidemiology, 8(3), 168–175. DOI: 10.2188/jea.8.168
[15] Fisetin Supplementation for Healthy Aging (Fisetin LOW). Triple-blind, randomized, placebo-controlled trial, 120 participants, 100 mg per day for 7 weeks. Hvidovre University Hospital, Copenhagen. ClinicalTrials.gov NCT07195318
[16] AFFIRM-LITE: A Phase 2 Randomized, Placebo-Controlled Study of Alleviation by Fisetin of Frailty, Inflammation, and Related Measures in Older Adults. Protocol and exclusion criteria. ClinicalTrials.gov NCT03675724
[17] Andres, S., Pevny, S., Ziegenhagen, R., Bakhiya, N., Schäfer, B., Hirsch-Ernst, K. I., Lampen, A. (2018). Safety aspects of the use of quercetin as a dietary supplement. Molecular Nutrition and Food Research, 62(1), 1700447. DOI: 10.1002/mnfr.201700447
[18] Pilot Trial of Fisetin in Healthy Volunteers and Older Patients With Multimorbidity (Fisetin HIGH). Phase 1 and pilot Phase 2a study. Hvidovre University Hospital, Copenhagen. ClinicalTrials.gov NCT06431932
Reviewed by
Prof. Bingji MaScientific Advisor at PhytoVale. Professor and medicinal plant science expert. Research focus covers Chinese medicinal materials, phytochemistry, natural products and medicinal plant quality.
Written by
FloraContent Editor at PhytoVale. Product content and editorial specialist, focused on botanical ingredient specifications, sourcing information and B2B technical content.
This article is intended for ingredient sourcing, formulation and technical information only. It summarises registered clinical trials and published research on fisetin and is not medical advice or a claim for any PhytoVale product. Trial descriptions are based on registry records and publications available as of September 2026; status, results and interpretations may have changed since that date. Nothing here should be treated as a recommended dose, a safety assessment for any individual, or a basis for health claims. Finished-product manufacturers remain responsible for regulatory status, permitted claims and labelling in their target markets.
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