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Fisetin
Fisetin
Fisetin
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Fisetin
Skeletal formula of fisetin
Fisetin structure
Ball-and-stick model of the fisetin molecule
Names
IUPAC name
3,3′,4′,7-Tetrahydroxyflavone
Systematic IUPAC name
2-(3,4-Dihydroxyphenyl)-3,7-dihydroxy-4H-1-benzopyran-4-one
Other names
2-(3,4-Dihydroxyphenyl)-3,7-dihydroxychromen-4-one
Cotinin (not to be confused with Cotinine)
5-Deoxyquercetin
Superfustel
Fisetholz
Fietin
Fustel
Fustet
Viset
Junger fustik
Identifiers
3D model (JSmol)
ChEBI
ChEMBL
ChemSpider
DrugBank
ECHA InfoCard 100.007.669 Edit this at Wikidata
KEGG
UNII
  • InChI=1S/C15H10O6/c16-8-2-3-9-12(6-8)21-15(14(20)13(9)19)7-1-4-10(17)11(18)5-7/h1-6,16-18,20H checkY
    Key: XHEFDIBZLJXQHF-UHFFFAOYSA-N checkY
  • InChI=1/C15H10O6/c16-8-2-3-9-12(6-8)21-15(14(20)13(9)19)7-1-4-10(17)11(18)5-7/h1-6,16-18,20H
    Key: XHEFDIBZLJXQHF-UHFFFAOYAQ
  • O=C1c3c(O/C(=C1/O)c2ccc(O)c(O)c2)cc(O)cc3
Properties
C15H10O6
Molar mass 286.2363 g/mol
Density 1.688 g/mL
Melting point 330 °C (626 °F; 603 K)
Except where otherwise noted, data are given for materials in their standard state (at 25 °C [77 °F], 100 kPa).
checkY verify (what is checkY☒N ?)

Fisetin (7,3′,4′-flavon-3-ol) is a plant flavonol from the flavonoid group of polyphenols.[1] It occurs in many plants where it serves as a yellow pigment. It is found in many fruits and vegetables, such as strawberries, apples, persimmons, onions, and cucumbers.[2][3][4]

Its chemical formula was first described by Austrian chemist Josef Herzig in 1891.[5]

Sources

[edit]

Fisetin is a flavonoid synthesized by many plants such as the trees and shrubs of Fabaceae, acacias Acacia greggii,[6] and Acacia berlandieri,[6] parrot tree (Butea frondosa), honey locust (Gleditsia triacanthos), members of the family Anacardiaceae such as the Quebracho colorado, and species of the genus Rhus, which contains the sumacs.[7] Along with myricetin, fisetin provides the color of the traditional yellow dye young fustic, an extract from the Eurasian smoketree (Rhus cotinus).

Many fruits and vegetables contain fisetin.[2] In one study, fisetin content was highest in strawberries, with content also observed in apples, grapes, onions, tomatoes, and cucumbers.[2] Fisetin can be extracted from fruit juices, wines,[8] and teas.[3] It is also present in Pinophyta species such as the yellow cypress (Callitropsis nootkatensis).

The average intake of fisetin from foods in Japan is about 0.4 mg per day.[1]

Plant source Amount of fisetin
(μg/g)
Toxicodendron vernicifluum[9] 15000
Strawberry[2] 160
Apple[2] 26
Persimmon[2] 10.6
Onion[2] 4.8
Lotus root[2] 5.8
Grape[2] 3.9
Kiwifruit[2] 2.0
Peach[2] 0.6
Cucumber[2] 0.1
Tomato[2] 0.1

Research

[edit]

Although fisetin has been under laboratory research over several decades for its potential role in senescence or anticancer properties, among other possible effects, there is no clinical evidence that it provides any benefit to human health, as of 2018.[1]

References

[edit]
Revisions and contributorsEdit on WikipediaRead on Wikipedia

Fisetin

View on Grokipedia
from Grokipedia
Fisetin is a naturally occurring , a subclass of within the family, characterized by its as 3,3',4',7-tetrahydroxyflavone with the molecular C₁₅H₁₀O₆ and a molecular weight of 286.24 g/mol. It is abundant in various fruits and vegetables, including strawberries, apples, persimmons, onions, and mulberry leaves, where it contributes to the plants' pigmentation and defense mechanisms. Fisetin, despite its low oral , has been shown in studies to exhibit potent activity by scavenging free radicals and upregulating levels, which helps mitigate in biological systems. Its effects involve the inhibition of pro-inflammatory mediators such as TNF-α, IL-6, and pathways, making it a candidate for managing conditions like and chronic inflammation. Fisetin has garnered significant attention for its neuroprotective properties, including the enhancement of formation and against neurodegenerative diseases through mechanisms like reducing oxidative damage and modulating function. In the realm of , it acts as a chemopreventive and chemotherapeutic agent by inducing in cancer cells, inhibiting DNA , and suppressing tumor growth in various models. Notably, fisetin functions as a senolytic agent, selectively eliminating senescent cells to extend healthspan and lifespan in preclinical studies, with high Trolox-equivalent capacity supporting its role in aging-related interventions. It also inhibits differentiation, potentially benefiting bone health by preventing excessive . Despite these promising effects, fisetin can cause , eye, and respiratory upon direct exposure, though it is generally considered low in dietary contexts. As of 2025, clinical trials are underway to assess its safety and efficacy in humans, including for age-related frailty and physical function in cancer survivors. Ongoing research continues to explore its therapeutic potential across diverse health domains, emphasizing its multifaceted pharmacological profile.

Chemical properties

Molecular structure

Fisetin is a naturally occurring flavonol with the molecular formula \ceC15H10O6\ce{C15H10O6} and a molecular weight of 286.24 g/mol. Its systematic IUPAC name is 2-(3,4-dihydroxyphenyl)-3,7-dihydroxychromen-4-one, though it is commonly referred to as 3,3',4',7-tetrahydroxyflavone in . This nomenclature reflects its classification within the family, specifically the flavonol subclass, which features a 3-hydroxyflavone core structure. The core structure of fisetin consists of two aromatic rings—an A-ring (a ring fused to a heterocyclic pyrone) and a B-ring (a phenyl )—linked by a central γ-pyrone ring (C-ring). This system is characterized by extensive π-conjugation, contributing to its stability and bioactive properties. Hydroxyl groups are positioned at the 3-position on the C-ring, the 7-position on the A-ring, and the 3' and 4' positions on the B-ring, with the 4-position of the C-ring bearing a . These functional groups, particularly the ortho-dihydroxy configuration on the B-ring, are key to its chemical reactivity and biological interactions. In comparison to the related flavonol (3,5,7,3',4'-pentahydroxyflavone), fisetin lacks a hydroxyl group at the 5-position of the A-ring, earning it the synonym ; this structural difference influences its solubility, , and interactions with biological targets. The absence of chiral centers in fisetin results in no stereoisomers, and its planar arises from the system across the conjugated rings, facilitating stacking interactions in molecular assemblies.

Physical characteristics

Fisetin is typically observed as a yellowish to orange crystalline powder. Its is approximately 330–333 °C, at which point it decomposes. Fisetin exhibits poor in (≈0.3 mg/mL at 25 °C) but is soluble in organic solvents such as (≈5 mg/mL), DMSO (≈30 mg/mL), and DMF (≈30 mg/mL), as well as in alkaline solutions; its logP value of ≈2.3 reflects moderate . The compound is sensitive to light and oxidation, remaining stable under acidic conditions but degrading in strong basic environments. Spectroscopically, fisetin displays UV-Vis absorption maxima at 254 nm and 368 nm, with characteristic IR absorption bands and NMR signals attributable to its backbone, including aromatic protons and hydroxyl groups.

History and occurrence

Discovery and isolation

Fisetin was first isolated in from the smoke tree (Rhus cotinus L.), also known as Venetian sumac, a plant historically valued for its properties. This extraction marked one of the earliest isolations of a compound, highlighting the compound's role in plant coloration and traditional applications. The of fisetin was determined in by Austrian Josef Herzig, who provided a foundational description of its structure as 3,3',4',7-tetrahydroxyflavone. Herzig's work built on initial characterizations and contributed to the emerging understanding of within plant chemistry. During the late 19th and early 20th centuries, fisetin was investigated as part of broader studies on pigments responsible for yellow hues in various plants, reflecting its natural occurrence in species like those in the Rhus genus. Fisetin was recognized early on for its use as a in traditional practices, derived from the wood and bark of the smoke tree to produce and tones in textiles and other materials. Key advancements in the early 1900s included the first of fisetin around 1904, which involved cyclization of protected chalcones, enabling improved purification and techniques for more precise . These methods facilitated its separation from complex plant extracts and supported ongoing research into its properties as a and chemical entity.

Natural sources

Fisetin is a found in various plant families, including (such as acacias like Acacia greggii and Acacia berlandieri), (such as mulberry, Morus species), and (such as smoke tree, , and wax tree, Rhus succedanea). Among dietary sources, fisetin occurs at varying concentrations in fruits and , with strawberries containing the highest levels at approximately 160 μg/g, followed by apples at 26.9 μg/g and persimmons at 10.5 μg/g. Onions provide about 4.8 μg/g, grapes around 3.9 μg/g, and cucumbers roughly 0.1 μg/g, while tomatoes and other like also contribute smaller amounts. The following table summarizes representative fisetin concentrations in select high-content foods:
FoodFisetin Concentration (μg/g)
Strawberries160
Apples26.9
Persimmons10.5
Onions4.8
Grapes3.9
Cucumbers0.1
Fisetin is also present in nuts, though typically at lower levels than in fruits like strawberries, which remain the richest source overall, as well as in additional and such as smoke tree bark. Concentrations can vary significantly depending on factors like the specific plant part used, degree of , growing conditions, , and light exposure. In Western diets, the average daily dietary intake of fisetin is estimated at approximately 0.4 mg, reflecting its presence in common foods but at modest levels overall. For commercial purposes, fisetin is often extracted from plant byproducts such as waste or peels, as well as from sources like smoke tree bark, to produce supplements.

Biosynthesis and metabolism

Biosynthetic pathway

The exact biosynthetic pathway of fisetin in remains elusive. A proposed pathway, assembled heterologously, starts from , with the initial step involving conversion to catalyzed by tyrosine ammonia-lyase (TAL). Subsequent activation by 4-coumarate:CoA ligase (4CL) forms p-coumaroyl-CoA. synthase (CHS) and chalcone reductase (CHR) produce isoliquiritigenin from p-coumaroyl-CoA and three molecules of . isomerase (CHI) then cyclizes isoliquiritigenin to liquiritigenin. Flavanone 3-hydroxylase (F3H) introduces a hydroxyl group at the 3-position, yielding garbanzol. Flavonol synthase (FLS) oxidizes garbanzol to resokaempferol, and 3'-hydroxylase (F3'H) hydroxylates at the 3' and 4' positions of the B-ring to form fisetin. The expression of genes encoding flavonoid biosynthetic enzymes is regulated by environmental cues, with upregulation observed under UV light exposure, attack, and various abiotic stresses such as and wounding, enhancing flavonoid accumulation as a protective response. Tissue-specific expression predominates in fruits and leaves, where fisetin contributes to defense and pigmentation. Heterologous biosynthesis of fisetin has been engineered in by assembling this proposed pathway with nine enzymes starting from L-tyrosine, achieving titers of approximately 0.3 mg/L. Further optimizations in have reported titers up to 2.3 mg/L as of 2017.

Pharmacokinetics and metabolism

Fisetin exhibits low oral , approximately 8-32% in depending on dose, primarily due to its poor water and extensive first-pass . It is rapidly absorbed in the through passive , with peak plasma concentrations achieved within 1-2 hours post-administration in animal models. can be enhanced significantly—up to 24-fold—using formulations such as nanoemulsions or co-administration with dietary fats, which improve and reduce enzymatic degradation. As a lipophilic compound, fisetin readily crosses the blood-brain barrier and distributes to various tissues, with notable accumulation in the liver, kidneys, intestines, and . In mice, following intraperitoneal or intravenous administration, the highest concentrations are observed in these organs, supporting its potential for effects. Fisetin undergoes extensive phase II metabolism in the liver, primarily through and sulfation, yielding metabolites such as fisetin-3-O-glucuronide, fisetin-4'-O-glucuronide, and various sulfated forms, including the 3,4'-diglucuronide. Methylated derivatives, like geraldol (3,4',7-trihydroxy-3'-methoxyflavone), are also formed via O-methylation. Phase II conjugation predominates. The plasma is short, ranging from 3-7 hours in and approximately 1.5 hours in humans. Excretion occurs mainly via the biliary-fecal route (60-70%), with sulfate conjugates showing high biliary clearance mediated by , and the remainder (20-30%) through as glucuronides and other metabolites detectable up to 48 hours post-dose. In humans, oral doses of approximately 20 mg/kg (around 1000-1400 mg for a 70 kg ) yield peak plasma concentrations (Cmax) of 100-500 ng/mL with enhanced formulations, compared to under 10 ng/mL with unformulated fisetin. Animal intravenous studies confirm a rapid elimination of about 1.5 hours.

Pharmacology

Mechanisms of action

Fisetin exhibits properties primarily through direct scavenging of (ROS) facilitated by its phenolic hydroxyl groups, which donate hydrogen atoms to neutralize free radicals. Additionally, fisetin upregulates the Nrf2 signaling pathway, leading to increased expression of enzymes such as (SOD), , and (GPx). In terms of effects, fisetin inhibits the activation of , a key in inflammatory responses, thereby reducing the production of pro-inflammatory cytokines including TNF-α and IL-6. It also suppresses the expression of inducible enzymes such as COX-2 and iNOS, which contribute to inflammation by generating prostaglandins and , respectively. Fisetin modulates several critical signaling pathways, including inhibition of the PI3K/Akt/ pathway, which regulates and survival; this inhibition occurs through direct suppression of complexes and upstream Akt activation. Furthermore, fisetin activates AMPK, an energy sensor that promotes catabolic processes, and upregulates SIRT1, a NAD+-dependent deacetylase associated with anti-aging effects via enhanced cellular stress resistance. As a agent, fisetin selectively induces in senescent cells by modulating the of proteins, including downregulation of anti-apoptotic members like and , while promoting pro-apoptotic pathways through activation. Studies indicate that fisetin is more effective than quercetin in eliminating senescent cells in both in vitro and in vivo models, thereby promoting cell health by clearing dysfunctional cells and reducing the inflammatory burden associated with the (SASP) without broadly affecting healthy cells. Fisetin interacts with receptors such as acting as an agonist for estrogen receptor β (ERβ), which influences gene expression related to cell proliferation and differentiation. It also modulates ABC transporters, including inhibition of ABCG2, thereby reducing drug efflux and overcoming multidrug resistance in cancer cells.

Biological activities

Fisetin exhibits potent antioxidant activity by scavenging free radicals and protecting cellular components from oxidative damage. In vitro assays demonstrate its ability to inhibit DPPH radical scavenging with an IC50 value of approximately 9.7 μM, indicating strong radical-quenching capacity comparable to other flavonoids. Additionally, fisetin preserves mitochondrial function by enhancing biogenesis through pathways such as AMPK/SIRT1/PGC-1α and reducing oxidative stress-induced impairments in electron transport chain activity. These effects contribute to overall cellular protection against reactive oxygen species in various models. The compound also displays significant anti-inflammatory effects, particularly in suppressing inflammatory responses in immune cells. Fisetin inhibits (LPS)-induced production of pro-inflammatory cytokines such as TNF-α, IL-1β, and IL-6 in macrophages, while reducing and levels through downregulation of iNOS and COX-2 expression. In animal models, it attenuates formation and inflammatory infiltration, demonstrating efficacy in modulating acute inflammatory processes. Fisetin promotes neurotrophic effects by enhancing neuronal survival and plasticity. It upregulates (BDNF) expression, which supports differentiation and maintenance, as observed in models of where fisetin restores BDNF levels and prevents cell death. Furthermore, fisetin improves by modulating function and hippocampal [long-term potentiation](/page/Long-term_p potentiation), fostering adaptive neural responses. In terms of antifibrotic activity, fisetin inhibits transforming growth factor-β (TGF-β) signaling, thereby reducing phosphorylation of SMAD3 and subsequent extracellular matrix deposition in fibrotic tissues. This leads to decreased collagen accumulation and fibrosis progression in experimental settings. Other notable activities include vasodilatory effects via upregulation of endothelial nitric oxide synthase (eNOS) expression, which enhances nitric oxide production and improves endothelial function. At higher concentrations, fisetin shows antimicrobial properties against select bacteria like Staphylococcus species and fungi such as Cryptococcus neoformans, by disrupting cell membranes and inhibiting growth.

Research and applications

Preclinical studies

Preclinical studies have demonstrated fisetin's potential therapeutic effects across various disease models, primarily through cell culture experiments and animal studies. In , fisetin has shown antiproliferative and pro-apoptotic activity in multiple cell lines. For instance, it induces in cells such as and MDA-MB-231 by activating caspases-7, -8, and -9, leading to mitochondrial depolarization and PARP cleavage, with reported IC50 values in the range of 10-50 μM across , prostate (e.g., ), and (e.g., NCI-H460) cancer lines. In prostate cancer models, fisetin triggers G1-phase arrest and modulates networks to promote cell death. Similarly, in cells, it increases the Bax/ ratio and activates executioner caspases-3 and -9 via mitochondrial pathways. In vivo, fisetin inhibits tumor progression in xenograft models. Administration of fisetin at 223 mg/kg alongside suppressed Lewis lung carcinoma tumor growth by 92% in mice, partly through anti-angiogenic effects including downregulation of (VEGF). In xenografts, fisetin reduced primary tumor growth and lung metastasis by targeting pathways that limit . Regarding neuroprotection, fisetin mitigates amyloid-β (Aβ1-42)-induced toxicity in (AD) mouse models. Intraperitoneal administration of 20 mg/kg/day for two weeks post-Aβ injection decreased Aβ accumulation, BACE-1 expression, and tau hyperphosphorylation at serine 413, while restoring synaptic proteins like PSD-95 and SNAP-25 to improve memory performance in the Morris water maze test. Fisetin also upregulates brain-derived neurotrophic factor (BDNF) expression, contributing to its neuroprotective effects against neurodegeneration. In models of memory impairment, fisetin at 40 mg/kg orally prevented scopolamine-induced in mice by enhancing cognitive function and reducing . Fisetin exhibits properties by selectively clearing in animal models. Intermittent high-dose fisetin is preferred over daily low-dose for senolytic effects because daily low doses (100–500 mg) are unlikely to achieve the threshold needed for senolytic clearance, while high pulses support targeted senescent cell reduction, as demonstrated in preclinical studies. In progeroid Ercc1−/∆ mice, intermittent dietary supplementation at 500 ppm reduced senescence markers such as ^Ink4a and p21 across multiple tissues, leading to a 10-20% extension in median and maximum lifespan with late-life intervention. These lifespan extensions were associated with improved healthspan, including benefits to brain function through reduced age-related pathology, kidney health via decreased senescence markers like p16^Ink4a and p21 in renal tissues, and muscle performance through lowered senescent cell burden in skeletal muscle. It also diminished (SASP) factors, including IL-6, IL-1β, and TNF-α, thereby alleviating chronic inflammation. In anti-aging contexts, fisetin improves healthspan metrics in aged rodents. Intermittent dosing at approximately 100 mg/kg enhanced grip strength and reduced frailty scores in old mice, correlating with decreased senescent cell burden in skeletal muscle and improved physical function without effects in young controls. In the SAMP8 accelerated aging mouse model, chronic administration at ~25 mg/kg/day over seven months mitigated cognitive decline and restored locomotor activity. Additional preclinical evidence supports fisetin's protective role in other conditions. In streptozotocin-induced models in mice, fisetin at 5-20 mg/kg attenuated injury, reduced , and inhibited activation to preserve renal function. It also reduced the accumulation of senescent tubular epithelial cells in kidney tissues, further supporting its renoprotective effects. For skin protection, topical or oral fisetin in UVB-irradiated hairless mice decreased , degradation via MMP-1/2 suppression, and inflammatory markers like COX-2 and IL-6, while upregulating Nrf2 for defense.

Clinical trials and safety

Fisetin has demonstrated a favorable profile in early clinical , with no serious adverse events reported at doses up to 20 mg/kg per day for two consecutive days. In a completed phase 2 pilot (NCT03675724) involving older adults, oral fisetin at this dose was well-tolerated, reducing inflammatory markers such as IL-6 and CRP, and showing preliminary improvements in frailty and physical function. Mild gastrointestinal upset, such as or decreased , has been occasionally noted but is not common. Additionally, fisetin exhibits no genotoxic potential, as confirmed in assessments of novel formulations. A 2022 bioavailability study in healthy individuals evaluated a hybrid-hydrogel liposomal of fisetin (FF-20), reporting a maximum plasma concentration (Cmax) of 238.2 ng/mL following a single 1000 mg dose, representing a 26.9-fold increase in area under the curve compared to unformulated fisetin. This study, the first comparative pharmacokinetic investigation, confirmed no significant adverse events, supporting fisetin's for . Several clinical trials are exploring fisetin's therapeutic potential as a agent. A phase II trial (NCT05595499) is investigating fisetin combined with exercise versus to prevent frailty and improve physical function in stage I-III survivors post-chemotherapy; as of November 2025, the study remains ongoing with estimated completion in December 2025 and is recruiting participants. Another trial (NCT07195318) examines daily 100 mg fisetin supplementation for healthy aging in volunteers, with an estimated completion in 2026; as of November 2025, it is not yet recruiting. A planned phase I/IIa trial (NCT06431932) will assess , safety, and efficacy of fisetin in healthy volunteers and older patients with , with recruitment expected to begin in 2026. Additionally, a phase 1/2 trial (NCT06133634) is evaluating intermittent fisetin treatment at 2 mg/kg/day for three days, repeated after two weeks, in older adults to improve vascular function and reduce markers of cellular senescence; as of November 2025, it is active but not recruiting, with estimated completion in March 2027. The preference for intermittent high-dose fisetin over daily low-dose for senolytic effects stems from evidence that daily low doses (100–500 mg) are unlikely to achieve the threshold needed for senolytic clearance, while high pulses support targeted senescent cell reduction as shown in preclinical and human studies. This preference extends to human studies, where such dosing aims to replicate the targeted clearance seen in preclinical models, with trials evaluating safety and efficacy of intermittent regimens. Preliminary efficacy signals from completed pilot studies include reductions in markers and improvements in physical function in older adults. For instance, fisetin supplementation has shown potential to preserve strength and alleviate frailty symptoms in preliminary human data. As of 2025, fisetin holds self-affirmed (SA-GRAS) status for use as a ingredient, particularly in formulations like BeFisetin®, but it lacks FDA approval for any therapeutic indications.

References

  1. https://pubchem.ncbi.nlm.nih.gov/compound/Fisetin
  2. https://www.sciencedirect.com/topics/neuroscience/fisetin
  3. https://pmc.ncbi.nlm.nih.gov/articles/PMC9298084/
  4. https://pmc.ncbi.nlm.nih.gov/articles/PMC3689181/
  5. https://www.sciencedirect.com/topics/pharmacology-toxicology-and-pharmaceutical-science/fisetin
  6. https://pmc.ncbi.nlm.nih.gov/articles/PMC9589363/
  7. https://pmc.ncbi.nlm.nih.gov/articles/PMC6197652/
  8. https://www.sciencedirect.com/topics/chemistry/fisetin
  9. https://clinicaltrials.gov/study/NCT05595499
  10. https://clinicaltrials.gov/study/NCT07195318
  11. https://pmc.ncbi.nlm.nih.gov/articles/PMC6842927/
  12. https://pmc.ncbi.nlm.nih.gov/articles/PMC6572624/
  13. https://www.mdpi.com/2218-273X/9/5/174
  14. https://pmc.ncbi.nlm.nih.gov/articles/PMC5067175/
  15. https://pubs.acs.org/doi/10.1021/acsomega.3c03105
  16. https://www.chemicalbook.com/ChemicalProductProperty_EN_CB8451569.htm
  17. https://www.mdpi.com/1424-8247/16/2/196
  18. https://www.sciencedirect.com/science/article/pii/S0047637424000952
  19. https://liposomes.bocsci.com/resources/exploring-the-benefits-of-liposomal-fisetin-a-breakthrough-in-bioavailability.html
  20. https://pmc.ncbi.nlm.nih.gov/articles/PMC10743569/
  21. https://www.frontiersin.org/journals/chemistry/articles/10.3389/fchem.2019.00697/full
  22. https://www.lifespan.io/topic/fisetin-benefits-side-effects/
  23. https://www.researchgate.net/publication/365084491_Synthese_des_Fisetins
  24. https://onlinelibrary.wiley.com/doi/full/10.1002/efd2.3
  25. https://www.chemicalbook.com/article/the-source-and-biological-activity-of-fisetin.htm
  26. https://www.businesswire.com/news/home/20250413308210/en/BeFisetin-Announced-the-Global-No.1-All-Natural-Fisetin-With-SA-GRAS-Status
  27. https://pmc.ncbi.nlm.nih.gov/articles/PMC6261287/
  28. https://www.researchgate.net/publication/308671217_Fisetin_and_Its_Role_in_Chronic_Diseases
  29. https://www.sciencedirect.com/science/article/abs/pii/S1011134415003346
  30. https://www.researchgate.net/publication/305952978_Extraction_Isolation_and_Quantification_of_Bioactive_Compound_Fisetin_and_its_Product_Formulation
  31. https://www.fengchengroup.com/additive-and-herbal-extracts/herbal-extracts/fisetin-528-48-3-from-cotinus-coggygria-bark.html
  32. https://doi.org/10.1016/j.ymben.2015.07.002
  33. https://link.springer.com/article/10.1007/s44372-024-00063-6
  34. https://www.sciencedirect.com/science/article/pii/S0960852417309306
  35. https://onlinelibrary.wiley.com/doi/10.1002/ame2.12476
  36. https://pmc.ncbi.nlm.nih.gov/articles/PMC9574875/
  37. https://pubmed.ncbi.nlm.nih.gov/19090755/
  38. https://www.researchgate.net/publication/51570205_Fisetin_disposition_and_metabolism_in_mice_Identification_of_geraldol_as_an_active_metabolite
  39. https://pubmed.ncbi.nlm.nih.gov/29862816/
  40. https://pubmed.ncbi.nlm.nih.gov/30781396/
  41. https://pubmed.ncbi.nlm.nih.gov/38310454/
  42. https://pubmed.ncbi.nlm.nih.gov/29792955/
  43. https://pubmed.ncbi.nlm.nih.gov/26590114/
  44. https://pubmed.ncbi.nlm.nih.gov/28213268/
  45. https://pubmed.ncbi.nlm.nih.gov/33616827/
  46. https://pubmed.ncbi.nlm.nih.gov/31540162/
  47. https://pubmed.ncbi.nlm.nih.gov/22842629/
  48. https://pubmed.ncbi.nlm.nih.gov/22261340/
  49. https://pubmed.ncbi.nlm.nih.gov/25286082/
  50. https://www.mdpi.com/1420-3049/27/3/738
  51. https://febs.onlinelibrary.wiley.com/doi/10.1111/febs.16350
  52. https://pubmed.ncbi.nlm.nih.gov/36010664/
  53. https://pmc.ncbi.nlm.nih.gov/articles/PMC3788058/
  54. https://pubmed.ncbi.nlm.nih.gov/37990267/
  55. https://pubmed.ncbi.nlm.nih.gov/38815408/
  56. https://journals.lww.com/aptb/fulltext/2021/11010/pharmacological_aspects_of_fisetin.1.aspx
  57. https://pmc.ncbi.nlm.nih.gov/articles/PMC11047672/
  58. https://www.frontiersin.org/journals/pharmacology/articles/10.3389/fphar.2022.1015835/full
  59. https://pmc.ncbi.nlm.nih.gov/articles/PMC8057890/
  60. https://www.nature.com/articles/s41598-021-87257-0
  61. https://pubmed.ncbi.nlm.nih.gov/37098680/
  62. https://www.sciencedirect.com/science/article/abs/pii/S0300908419301725
  63. https://pmc.ncbi.nlm.nih.gov/articles/PMC11260082/
  64. https://pubmed.ncbi.nlm.nih.gov/27107205/
  65. https://pmc.ncbi.nlm.nih.gov/articles/PMC10412067/
  66. https://doi.org/10.1007/s00280-010-1505-8
  67. https://pubmed.ncbi.nlm.nih.gov/26944285/
  68. https://pmc.ncbi.nlm.nih.gov/articles/PMC5527824/
  69. https://www.ebiomedicine.com/article/S2352-3964(18)30373-6/fulltext
  70. https://pmc.ncbi.nlm.nih.gov/articles/PMC12341784/
  71. https://pubmed.ncbi.nlm.nih.gov/30279143/
  72. https://pmc.ncbi.nlm.nih.gov/articles/PMC5861950/
  73. https://pmc.ncbi.nlm.nih.gov/articles/PMC8816314/
  74. https://pmc.ncbi.nlm.nih.gov/articles/PMC9714549/
  75. https://pmc.ncbi.nlm.nih.gov/articles/PMC5666800/
  76. https://clinicaltrials.gov/study/NCT03675724
  77. https://pmc.ncbi.nlm.nih.gov/articles/PMC10050516/
  78. https://www.clinicaltrials.gov/study/NCT05595499
  79. https://www.clinicaltrials.gov/study/NCT06431932
  80. https://clinicaltrials.gov/study/NCT06133634
  81. https://www.clinicaltrials.gov/study/NCT03675724
  82. https://www.nad.com/news/fisetin-fights-frailty-new-study-shows-supplment-preserves-strength
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