Fisetin

Fisetin: A Comprehensive Reference Article

1. Identity, Chemistry, and Natural Sources

Chemical Identity

Fisetin (7,3′,4′-flavon-3-ol) is a plant flavonol from the flavonoid group of polyphenols. It is also systematically named 3,7,3′,4′-tetrahydroxyflavone and is classified as a polyhydroxy flavonoid. Fisetin has a structure similar to quercetin, and is thus also named 5-deoxyquercetin; it is identified as a secondary metabolite of plants that occurs in fruits, green parts, barks, and hardwood. Its molecular formula is C₁₅H₁₀O₆. As a pure substance, fisetin presents as high-melting yellow needles, soluble in polar organic solvents and practically insoluble in water.

Historical Isolation and Chemical Elucidation

The first record of fisetin as an isolate from Venetian sumac (Rhus cotinus L.) dates back to 1833. Basic chemical characteristics of the compound were provided several decades later by Schmidt (1886). Its chemical structure was not fully elucidated and confirmed by synthesis until the 1890s by S. Kostanecki, who launched a broader study of plant pigments during this period and coined group names for flavonoid subcategories, including flavones, flavonol, chromones, and chalcones. Fisetin's chemical formula was first formally described by Austrian chemist Josef Herzig in 1891.

Botanical Sources

Fisetin is synthesized by many plants, including trees and shrubs of Fabaceae, acacias Acacia greggii and Acacia berlandieri, the parrot tree (Butea frondosa), the honey locust (Gleditsia triacanthos), members of the family Anacardiaceae such as Quebracho colorado, and species of the genus Rhus, which contains the sumacs. Along with myricetin, fisetin provides the color of the traditional yellow dye young fustic, an extract from the Eurasian smoketree (Rhus cotinus). It is also present in Pinophyta species such as the yellow cypress (Callitropsis nootkatensis).

Among dietary food sources, fisetin is a bioactive flavonol molecule found in fruits and vegetables such as strawberry, apple, persimmon, grape, onion, and cucumber at concentrations in the range of 2–160 μg/g. The highest concentration of fisetin was found in strawberries (160 μg/g), followed by apple (26.9 μg/g) and persimmon (10.5 μg/g). A pint of strawberries contains approximately 57 mg of fisetin, while a large apple could have up to 8 mg, a persimmon 2 mg, an onion or cup of grapes 1 mg, and kiwi fruit, cucumbers, and peaches less than 1 mg. Fisetin can also be extracted from fruit juices, wines, and teas.

The average intake of fisetin from foods in Japan is about 0.4 mg per day. This figure is far below the doses being tested for therapeutic purposes in current clinical research, meaning dietary intake alone cannot replicate supplemental or experimental dosing regimens.

Commercial and Supplement Forms

Because of its various bioactive properties, fisetin is considered a health-promoting agent, and some dietary supplements containing fisetin have been marketed. Food sources provide a relatively low daily intake of fisetin (0.4 mg on average), while fisetin supplements offer higher concentrations ranging from 100 mg to 500 mg per serving. Fisetin is commercially available in encapsulated powder, tablet, and liquid extract forms. In humans, a hybrid hydrogel formulation has successfully enhanced the bioavailability and absorption of fisetin by increasing the Cmax and AUC by 23-fold and 26-fold, respectively. Key challenges such as poor solubility and low bioavailability are well recognized, and emerging strategies may improve its clinical utility.

2. Traditional and Historical Use

Unlike many botanical compounds, fisetin was not traditionally recognized or used in its isolated form in herbal medicine systems. However, its source plants—particularly strawberries and onions—have a long history of medicinal and nutritional use in various cultures.

Fisetin-rich plants, fruits, and herbs were consumed for their therapeutic properties in various cultures throughout history. Ancient civilizations, including those in China, India, and the Middle East, may have utilized fisetin-containing plants for their purported health benefits. Traditional medicinal systems employed fisetin-containing herbs such as Rhus succedanea (Japanese wax tree) and Gleditsia sinensis (Chinese honey locust).

The traditional yellow/ochre dye known as young fustic used fisetin extracted from the wood of the smoke bush and was a popular way to color fabrics and clothes until synthetic dyes replaced it. This industrial use predates the scientific characterization of fisetin as a distinct bioactive molecule.

The specific identification of fisetin as a distinct chemical compound occurred in the late 19th century, but its biological activities were not extensively studied until the late 20th and early 21st centuries, with the rise of flavonoid research. There is no direct mention of fisetin as a named compound in classical herbal pharmacopeias such as the Caraka Samhita or Sushruta Samhita; its presence in those traditions is inferred retrospectively from the use of fisetin-containing plants.

3. Key Constituents and Mechanisms of Action

Chemical Structure and Antioxidant Activity

Fisetin is a flavonol with a diphenyl propane structure containing two aromatic rings linked via an oxygenated heterocyclic ring. As a flavonol, it belongs to a subgroup of flavonoid organic compounds; like other flavonols, fisetin contains a hydroxyl group (–OH) on the third carbon atom (C3) and a carbonyl group (C=O) on the fourth carbon atom of the central heterocyclic ring.

Fisetin not only has direct antioxidant activity but can also increase intracellular levels of glutathione, the major intracellular antioxidant. A key molecular mechanism underlying this antioxidant activity involves the Nrf2 pathway: fisetin upregulates the mRNA expression of heme oxygenase-1 (HO-1), glutamate-cysteine ligase catalytic subunit (GCLC), glutamate-cysteine ligase modifier subunit (GCLM), and NAD(P)H quinone oxidoreductase-1 (NQO1), and induces nuclear accumulation of Nrf2, with enhanced luciferase activity of antioxidant response element (ARE)-regulated transactivation observed. Fisetin translocates Nrf2 into the nucleus and upregulates the expression of downstream HO-1 gene by inhibiting the degradation of Nrf2 at the post-transcriptional level.

Anti-Inflammatory Mechanisms

Fisetin mediates its anti-proliferative and anti-inflammatory effects, in part, through modulation of the nuclear factor kappa-light-chain-enhancer of activated B cells (NF-κB) pathways. Of nine different flavones tested, fisetin was the most potent in suppressing tumor necrosis factor (TNF)-induced NF-κB activation; it also suppressed NF-κB activation induced by various inflammatory agents and carcinogens, and blocked the phosphorylation and degradation of IκBα, which in turn led to suppression of the phosphorylation and nuclear translocation of NF-κB/p65. Fisetin's anti-inflammatory properties are driven mainly by suppression of NF-κB signaling and inhibition of NLRP3 inflammasome activation.

Fisetin has anti-inflammatory activity against microglia and astrocytes and inhibits the activity of lipoxygenases, thereby reducing the production of pro-inflammatory eicosanoids and their by-products.

mTOR and Longevity Signaling

Fisetin modulates mTOR signaling, which intersects with NF-κB and MAPK pathways to fine-tune the transcription of inflammation-related genes. Fisetin activates the PI3K/Akt signaling cascade, which in turn stimulates Nrf2; activated Nrf2 boosts the production of enzymatic antioxidants including HO-1 and glutathione (GSH), helping to neutralize harmful reactive oxygen species (ROS). By reducing ROS levels, fisetin indirectly suppresses NF-κB signaling, causing a decline in pro-inflammatory cytokine release.

Senolytic Mechanism

Senolytics are drugs that selectively promote apoptosis of senescent cells by temporarily disabling the pro-survival pathways that enable senescent cells to resist the pro-apoptotic, pro-inflammatory factors that they themselves secrete. Fisetin exerts senolytic activity by selectively inducing apoptosis in senescent cells through coordinated inhibition of NF-κB and activation of p53, thereby reducing senescence-associated secretory phenotype (SASP) secretion. Fisetin, a naturally-occurring flavone with low toxicity, is senolytic and selectively induces apoptosis in senescent but not proliferating human umbilical vein endothelial cells (HUVECs).

Furthermore, fisetin was shown to activate peroxisome proliferator-activated receptor gamma (PPARγ), which in turn activated PTEN and protected against senescence via PTEN-mediated inhibition of the mTOR Complex 2 (mTORC2)-Akt (Ser 473) signaling pathway and subsequent activation of the FoxO3a-autophagy signaling pathway.

Neuroprotective Signaling

Fisetin can activate key neurotrophic factor signaling pathways. Neuroprotective effects result from its capacity to reduce ROS accumulation, stabilize mitochondrial function, and modulate ERK1/2 and PI3K/Akt pathways. Fisetin can cross the blood-brain barrier (BBB) and enhances antioxidant defense while inhibiting MAPK-p38 mediated NF-κB activation, thereby reducing oxidative stress.

Modulation of Cell Cycle and Apoptotic Proteins

Several regulatory proteins such as anti-apoptotic and pro-apoptotic proteins, cyclin-dependent kinases (CDKs), cyclins, matrix metalloproteinases (MMPs), and growth factors have been shown to be modulated by fisetin. Fisetin has been co-crystallized with Cdk-6 and shown to inhibit its activity.

4. Scientific Evidence by Area of Use

4.1 Senolytic and Anti-Aging Activity

Preclinical Evidence (Strong; Animal Models): The landmark study in this area was published in EBioMedicine in 2018 by Yousefzadeh, Zhu, McGowan, and colleagues, associated with the Mayo Clinic and the University of Minnesota. Of 10 flavonoids tested, fisetin was identified as the most potent senolytic. Acute or intermittent treatment of progeroid and old mice with fisetin reduced senescence markers in multiple tissues, consistent with a hit-and-run senolytic mechanism. The research demonstrated that fisetin is a senolytic agent that alleviates multiple senescence-associated disorders in mice, decreases physical dysfunction if administered to old mice, attenuates age-related tissue damage and pathology, and extends remaining lifespan by 17%.

In preclinical arterial aging models, fisetin decreased cellular senescence in human endothelial cell culture. In old mice, vascular cell senescence and SASP-related inflammation were lower one week after the final dose of oral intermittent (1 week on—2 weeks off—1 week on) fisetin supplementation, and old fisetin-supplemented mice had higher endothelial function.

In skeletal muscle aging models, preclinical data indicate that genetic- and pharmacological-based clearance of excess senescent cells can improve skeletal muscle strength and reduce frailty in old mice, suggesting that decreasing excess senescent cell burden may be a promising therapeutic approach.

Human/Clinical Evidence (Preliminary; Trials Ongoing): As of 2024–2026, fisetin's senolytic activity in humans remains under active investigation in registered clinical trials, and no large, completed, randomized controlled human trials have yet published primary efficacy results for aging or senescence endpoints. Due to limited knowledge of fisetin's pharmacokinetics in humans, a combined phase I and II trial in healthy volunteers and older adults with multimorbidity (NCT06431932) is evaluating these properties.

One registered study (NCT07195318) is a 2-arm triple-blind randomized placebo-controlled trial in which middle-aged and older adults (n=120) will receive either one capsule (100 mg) fisetin daily for 7 weeks or placebo. However, the overwhelming majority of existing claims stem from preclinical studies in animal models (e.g., C. elegans, mice), and there is extremely limited evidence for beneficial effects, effective doses, or safety profiles of these supplements in humans.

A separate pilot randomized trial (NCT06399809) is gathering preliminary data to test the hypothesis that fisetin will reduce abundance of senescent cells in blood, skeletal muscle, and both subcutaneous and intermuscular adipose tissue, and improve 6-minute walk distance in people with peripheral artery disease.

Evidence Strength: Strong in animal and cell models; preliminary and insufficient to establish efficacy in humans. Ongoing human trials are expected to clarify this.

4.2 Neuroprotection, Cognitive Function, and Neurodegenerative Disease

Preclinical Evidence (Substantial): Researchers used a phenotypic screening platform based on old age-associated brain toxicities to identify the flavonol fisetin as a potential therapeutic for Alzheimer's disease (AD) and other age-related neurodegenerative diseases. Based on earlier results with fisetin in transgenic AD mice, researchers hypothesized that fisetin would be effective against brain aging and cognitive dysfunction in rapidly aging senescence-accelerated prone 8 (SAMP8) mice, a model for sporadic AD and dementia. Fisetin reduced cognitive deficits in old SAMP8 mice while restoring multiple markers associated with impaired synaptic function, stress, and inflammation.

In animal studies, fisetin has shown efficacy against many of the risk factors associated with an increased risk of developing dementia and also exhibits direct neuroprotective effects. Thus, further human research on fisetin in the context of dementia risk factors is clearly warranted.

Fisetin also targets the Nrf2-regulated heme oxygenase-1 (HO-1) antioxidant system and attenuates hydrogen peroxide-induced DNA damage and apoptosis, supporting its role in ROS protection. Fisetin upregulated the expression of autophagy genes (Atg-3 and Beclin-1), sirtuin-1 (Sirt-1), and neuronal markers (neuron-specific enolase [NSE] and neuroglobin [Ngb]), and downregulated the inflammatory genes (IL-1β and TNF-α) and Sirt-2 genes in aged rat brains.

Human/Clinical Evidence: No published human randomized controlled trials have directly evaluated fisetin for Alzheimer's disease, Parkinson's disease, or cognitive impairment. Fisetin's ability to selectively target senescent cells, reduce neuroinflammation, and enhance synaptic function positions it as a potential therapeutic for brain aging; however, future research focusing on clinical trials and dosing optimization is crucial to establishing fisetin as a viable treatment for neurodegenerative conditions and cognitive decline associated with aging.

Evidence Strength: Promising preclinical evidence; no published human efficacy data for neurodegenerative indications as of mid-2026.

4.3 Cancer Biology

Preclinical Evidence: The anticancer activity of fisetin has been widely documented in numerous in vitro and in vivo studies. Its wide biological activities involve significant anticancer activity against lung cancer, colon cancer, prostate cancer, pancreatic cancer, and skin cancer. These activities are mediated through various pathways involving mTOR, Wnt/β-catenin, NF-κB, and TRAIL-induced apoptosis, making fisetin a multi-targeted pharmacological agent. Several studies have demonstrated its ability to target various cancer cells while sparing healthy ones. Additionally, fisetin has exhibited potential as an adjuvant to regular cancer treatments, augmenting their efficacy, lowering their side effects, and surmounting acquired chemoresistance.

Flavonols present in the diet may prevent cancer initiation, promotion, and progression by modulating important enzymes and receptors in signal transduction pathways related to proliferation, differentiation, apoptosis, inflammation, angiogenesis, metastasis, and reversal of multidrug resistance.

Human/Clinical Evidence: In a clinical study of colon cancer patients, 100 mg/day fisetin was reported as effective for reducing inflammation. Beyond this limited finding, robust human clinical trial data specifically evaluating fisetin's anticancer efficacy are absent from the published literature.

Evidence Strength: Strong mechanistic and preclinical data; human clinical evidence for cancer endpoints is extremely limited.

4.4 Cardiovascular and Vascular Health

Endothelial cells were found to be highly susceptible to becoming senescent with aging, and were effectively eliminated by senolytic treatment with fisetin in vascular models. Fisetin has been assessed as a senolytic to reduce vascular cell senescence and SASP factors and improve arterial function in old mice. Cellular senescence and the SASP contribute to age-related arterial dysfunction, in part, by promoting oxidative stress and inflammation, which reduce the bioavailability of the vasodilatory molecule nitric oxide (NO).

The natural flavonoid fisetin was recently identified as a lead compound that stabilizes endothelial cell microtubules. These cardiovascular effects have been primarily demonstrated in cell-based and animal models. No dedicated human clinical trials examining cardiovascular endpoints with fisetin have reported primary outcomes in the published literature as of mid-2026.

Evidence Strength: Preclinical; human clinical evidence is absent.

4.5 Metabolic Health (Diabetes, Obesity, Metabolic Syndrome)

Fisetin's wide biological activities include antidiabetic and antiobesity effects, as observed in preclinical settings. Rodent studies have shown improvements in glucose tolerance and insulin sensitivity, and fisetin has also been investigated in models of non-alcoholic fatty liver disease (NAFLD). Fisetin has shown promise in a variety of liver pathologies, including non-alcoholic fatty liver disease (NAFLD), alcoholic liver disease (ALD), drug-induced liver injury (DILI), and hepatic fibrosis, further supporting its broad hepatoprotective profile.

Evidence Strength: Preliminary; rodent and cell-based data only; no published human clinical trials for metabolic disease endpoints.

4.6 Inflammation and Immune Modulation

Fisetin's anti-inflammatory properties have been extensively characterized at the molecular level. Fisetin mediates its anti-inflammatory effects through modulation of NF-κB pathways, and of nine different flavones tested, fisetin was the most potent in suppressing TNF-induced NF-κB activation. Fisetin prevented D-galactose-mediated ROS accumulation by regulating endogenous antioxidant mechanisms, such as Sirt1/Nrf2 signaling, and suppressed the activated p-JNK/NF-κB pathway and its downstream targets, including inflammatory cytokines.

Evidence Strength: Strong mechanistic evidence in cell and animal models; human data are limited.

5. Dosage Forms and Doses Reported in Studies

Fisetin is found in the range of 2–160 μg/g in different food plants, and the average daily intake of this flavonol in humans is estimated at about 0.4 mg. This dietary exposure is orders of magnitude lower than doses used in experimental or clinical settings.

In registered human clinical trials, the following doses have been used or proposed:

• A pilot trial (NCT06431932) is assessing the safety and tolerability of oral treatment with fisetin at a dose of 20 mg/kg/day for two consecutive days in healthy volunteers and in older medical patients.
• A randomized placebo-controlled trial (NCT07195318) is testing one capsule (100 mg) of fisetin daily for 7 weeks.
• Participants treated with up to 800 mg fisetin daily reported dizziness, upset stomach, nausea, fatigue, migraines, and headaches in the trial in men with Gulf War Illness (Hodgin et al., 2021).
• In a clinical study of colon cancer patients, 100 mg/day was used for reducing inflammation.
• In an ongoing clinical trial examining effects on inflammation, bone health, and frailty in the elderly, fisetin was used at a high dosage of 20 mg/kg for two consecutive days, which would be around 1,400 mg/day for a 155-lb person.

Commercially available supplements typically provide 100–500 mg per serving, though these doses have not been validated in large clinical trials. Further safety and pharmacokinetic studies will be required to establish safety and determine appropriate dosing regimens.

6. Pharmacokinetics and Bioavailability

The pharmacokinetic study by Shia and colleagues suggests that fisetin, after administration, is bio-transformed quickly by conjugating to glucuronides or sulfates. This rapid conjugation contributes to fisetin's characteristically low oral bioavailability. Key challenges such as poor solubility and low bioavailability have been recognized, and emerging strategies such as novel formulation approaches may improve clinical utility.

In humans, a hybrid hydrogel formulation successfully enhanced the bioavailability and absorption of fisetin by increasing the C_max and AUC by 23-fold and 26-fold, respectively. These formulation advances are still under investigation, and standard commercial fisetin preparations based on simple powder may have substantially lower systemic exposure than what is reported in modified-release studies.

7. Body Systems Associated with Fisetin

• Central nervous system: Neuroprotective, anti-neuroinflammatory, memory-enhancing effects demonstrated in preclinical models; blood-brain barrier penetration reported.
• Cardiovascular system: Endothelial senescence reduction, improvement in arterial function, nitric oxide bioavailability — preclinical data.
• Immune system: Inhibition of NF-κB-mediated inflammation, NLRP3 inflammasome suppression, cytokine downregulation.
• Metabolic system: Antidiabetic and antiobesity effects in rodent models; hepatoprotective activity in NAFLD and ALD models.
• Oncology: Anti-proliferative, pro-apoptotic, and anti-angiogenic properties in multiple cancer cell lines.
• Musculoskeletal system: Reduction of skeletal muscle senescent cell burden and improvement in physical function in animal aging models.
• Vascular system: Senolytic clearance of senescent endothelial cells; improvement of arterial function in aged animal models.

8. Safety Considerations and Drug Interactions

General Safety Profile

Human clinical data about fisetin's toxicity and safety are limited, with reported side effects generally being mild. To date, no reports of significant toxicity for fisetin in vivo have been made. No adverse effects were found in mice at up to 25 times the dose used in mouse effectiveness studies, in old Rhesus monkeys at up to 5 times the dose proposed for humans, or in humans so far.

Adverse Effects Reported in Human Studies

No significant adverse events or clinical signs related to fisetin administration were observed in the bioavailability and pharmacokinetic study by Krishnakumar et al., though two cases of gastrointestinal issues (bloating and decrease in appetite) were reported. Participants treated with up to 800 mg fisetin daily reported dizziness, upset stomach, nausea, fatigue, migraines, and headaches in the trial in men with Gulf War Illness.

Potential Off-Target and Cytotoxic Effects at High Doses

While many studies show that fisetin selectively targets senescent cells without affecting non-senescent cells, treatment at higher doses (above 20–100 µM, depending on the study) may also affect non-senescent proliferating cells. Although such high doses and exposure times are unlikely to be achieved in humans due to fisetin's low bioavailability and rapid metabolism, off-target effects are possible and remain a concern for human trials and therapeutic applications, potentially causing unintended side effects or toxicity.

Drug Interactions

Fisetin, along with other flavones and flavonoids, has been shown to inhibit cytochrome P450 2C9; therefore, precaution is warranted to avoid significant drug-drug interactions, such as with warfarin. Fisetin along with other flavones and flavonoids has been shown to inhibit cytochrome P450 2C9, CYP3A4, and others. These cytochrome P450 inhibitory effects could theoretically elevate plasma concentrations of co-administered medications that are substrates of these enzymes.

Preclinical work shows fisetin can prolong clotting times and inhibit platelet aggregation in animal and in vitro models; human bleeding risk at supplement doses is not well defined.

Genotoxicity

Fisetin's toxicological profile includes safety concerns such as genotoxicity at higher concentrations. These concerns are based primarily on in vitro data and have not been confirmed at doses achievable through typical oral supplementation given fisetin's low bioavailability.

Long-Term Safety

In small human pharmacokinetic and pilot studies, fisetin has been generally well tolerated over short periods, with occasional reports of mild gastrointestinal symptoms. Long-term safety at higher exposures is unknown. The overwhelming majority of efficacy and safety claims stem from preclinical studies in animal models, and there is extremely limited evidence for beneficial effects, effective doses, or safety profiles of these supplements in humans.

9. Regulatory and Research Status

Fisetin is commercially available as an over-the-counter dietary supplement in many countries and is not approved by any major regulatory body (such as the U.S. FDA) as a drug or for treatment of any specific disease. Fisetin supplements have not been approved by the FDA for medical use, and regulatory bodies are not assuring the quality, safety, and efficacy of supplements. Multiple human clinical trials are underway, primarily evaluating senolytic properties, pharmacokinetics, and safety in older adults with various chronic conditions. Further randomized, controlled clinical trials using different senolytics are underway or planned; the Translational Geroscience Network, headed by the Kirkland team at the Mayo Clinic, is conducting senolytic clinical trials targeting fundamental aging mechanisms to extend healthspan and delay, prevent, or treat age- and cellular senescence-related conditions.

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