IngredientsMyricetin (systematic name: 3,5,7,3′,4′,5′-hexahydroxyflavone) is one of the natural flavonols found in fruits, vegetables, tea, and medicinal plants. It carries the chemical formula C₁₅H₁₀O₈ and a relative molecular mass of 318.24. Its backbone consists of three rings — two benzene rings and one heterocyclic ring — and is distinguished by six hydroxyl (–OH) groups attached to the rings at specific positions. The significant antioxidant activity of myricetin is attributed in particular to the presence of three hydroxyl groups on ring B, compared to other flavonoids.
Myricetin is structurally similar to fisetin, luteolin, and quercetin and is reported to have many of the same functions as these other members of the flavonol class of flavonoids. Despite its considerable biological activity, myricetin has limited solubility in water (~0.45 mg/mL at 25 °C) and is more soluble in organic solvents such as ethanol or DMSO.
Myricetin can be found glycosylated, in which form it is called myricitrin. Myricitrin is converted to myricetin by intestinal microflora; myricetin also occurs ubiquitously in plants and is consumed in fruits, vegetables, and beverages.
The plant families Myricaceae, Polygonaceae, Primulaceae, Pinaceae, and Anacardiaceae are among the richest sources of myricetin. The discovery of myricetin as an isolated compound dates to the late 19th century, when chemists isolated it from the bark of Myrica gale (sweet gale), and the name "myricetin" directly references that plant genus.
Common dietary sources include vegetables (including tomatoes), fruits (including oranges), nuts, berries, tea, and red wine. More specifically:
The concentration of myricetin in plant foods can vary due to factors such as genetic makeup, environmental conditions, ripeness, and processing methods, which can reduce amounts significantly. Reported average intake of myricetin per day varies depending on diet, but has been shown in the Netherlands to average 23 mg/day. The Flemish Dietetic Association database determined an average daily intake of myricetin of 2.2 ± 2.5 mg.
Myricetin and its glycosides are found in several foodstuffs, including fruits, vegetables, honey, red wine, and tea; the aglycone is also contained by dietary supplements, with a typical recommended daily dose of 100 mg. There is currently no established Recommended Daily Allowance (RDA) for myricetin. As a supplement, myricetin is sold in capsule and powder forms, with the aglycone (free form) being the most commonly used. Researchers have also investigated encapsulated delivery systems to address its poor water solubility; myricetin encapsulated by poly lactic-co-glycolic acid (PLGA), an FDA-approved material used as drug carriers, has been synthesized and its antitumor activity evaluated in vivo. The use of myricetin as a preserving agent to extend the shelf life of foods containing oils and fats is attributed to the compound's ability to protect lipids against oxidation.
Historically, myricetin-rich botanicals such as Myrica species and certain berries have been used in traditional medicine systems for their purported health-promoting properties, including anti-inflammatory and antioxidant activities.
In traditional diets, many cultures prized myricetin-rich ingredients. Northern European folk herbalists used Myrica gale (bog myrtle) as a digestive aid. Bayberry root bark, which contains significant myricetin, was used in decoctions to treat fevers, diarrhea, and sore throats.
Myricetin has been used as a form of traditional medicine for diabetes in Northern Brazil. The compound is well known in Traditional Chinese Medicine, being employed in remedies to eliminate the hangover produced after ingesting large amounts of alcohol through spirits.
Traditional cuisines, especially in Mediterranean and South Asian regions, have long used myricetin-rich herbs and fruits, such as bay leaves in stews and parsley in salads. The Indian globe thistle has long-documented antiulcer applications in traditional practice, and the flavonoids kaempferol and myricetin present in such plants are utilized to help heal gastric ulcers, with these polyphenolic compounds also possessing anti-Helicobacter pylori activity.
It was not until the 1990s that high-performance liquid chromatography (HPLC) allowed precise quantification of myricetin across many foods, providing a scientific framework to re-examine these traditional uses.
Myricetin is well-known for its strong antioxidant qualities and is essential for neutralizing free radicals, and preventing oxidative stress and possible cell damage. Flavonoids including myricetin are able to scavenge reactive oxygen species (ROS) and can chelate intracellular transition metal ions that ultimately produce ROS. Myricetin can induce the enzyme glutathione S-transferase (GST), which has been suggested to protect cells against oxidative stress by scavenging free radicals; in vitro studies have shown that myricetin significantly increased GST activity.
In cell-based studies, myricetin increased the level of the anti-apoptotic factor Bcl-2 and decreased levels of pro-apoptotic factors Bax, active caspase-9 and caspase-3, while inhibiting the release of cytochrome c from mitochondria to cytosol in oxidatively stressed cells.
A dual, context-dependent character has been documented: multiple studies have demonstrated that myricetin can also act as a pro-oxidant due to its tendency to undergo autoxidation depending upon its environment; when in the presence of cyanide, autoxidation is favored, resulting in superoxide, a byproduct characteristic of causing cellular damage. The pro-oxidative effect is attributed to the catechol groups in its structure, which form semi-quinone radicals that are further oxidized when both hydroxyl groups on the B and C rings form a quinone.
Research findings suggest that myricetin may inhibit inflammatory response through the regulation of both MyD88-dependent and -independent pathways in TLR signaling. Specifically, in animal models of middle cerebral artery occlusion, myricetin has been shown to reduce ischemic brain injury by targeting mitogen-activated protein kinases (MAPK), NF-κB/p65, and AKT signaling pathways.
Myricetin and its derivatives are known for radical scavenging, immunomodulating and anti-inflammatory activities by interfering with the NF-κB signaling pathway. In models of myocardial dysfunction, myricetin has been shown to suppress inflammatory cytokines and reduce mortality rate. Myricetin has also been found to reduce platelet aggregation.
Laboratory research has demonstrated that myricetin attenuates LPS-induced heart injuries by inhibiting oxidative stress and NF-κB/p65 activity, and that its antioxidant activity may be associated with enhancing the Nrf2/HO-1 pathway in the diabetic mouse heart, though myricetin has also been found to inhibit NF-κB activity independently of Nrf2. Mechanistically, myricetin blocks NF-κB signaling by activation of Nrf2 in IL-1β-stimulated cells.
Myricetin has been demonstrated to modulate cell pathways essential for supporting tumor cell survival, including the PI3K/Akt pathway, Nrf2 signaling, canonical and non-canonical Wnt pathway, mTOR pathway, Ras/Raf pathway, and JAK/STAT pathway. Myricetin plays a role in cancer prevention through the inhibition of inflammatory markers such as inducible nitric oxide synthase (iNOS) and cyclooxygenase-2 (COX-2).
Research has confirmed that myricetin prevents pancreatic beta-cell dysfunction by inhibiting cyclin-dependent kinase 5 (CDK5) and oxidative stress, improving insulin secretion, beta-cell survival, and glucose-stimulated insulin release, which may protect against beta-cell failure in hyperglycaemic conditions. It has been concluded that myricetin prevents the diabetes-associated decrease in expression of Nrf2 and inhibits the IκB/NF-κB (P65) signaling pathway.
Myricetin is a natural flavonoid with powerful antioxidant and anti-inflammatory potential. The vital role of this flavonoid in the prevention and treatment of various diseases is evidenced by its ability to reduce inflammation and oxidative stress, maintain tissue architecture, and modulate cell signaling pathways.
Evidence strength: The antioxidant and anti-inflammatory activities of myricetin are among its most thoroughly documented properties; however, few clinical trials have been performed using myricetin as a nutraceutical; the majority of evidence derives from preclinical pharmacological studies. Human evidence for isolated anti-inflammatory endpoints remains limited.
Researchers have explored the therapeutic potential of myricetin for cardiovascular protection, among other areas. The consumption of myricetin along with other flavonoids by menopausal women resulted in a reduced risk of coronary heart disease (CHD). The study also reported a decrease in serum triglycerides (TG), LDL cholesterol, and apolipoproteins.
In animal models, different concentrations of myricetin improved cardiac function, significantly reduced the levels of myocardial injury markers, alleviated myocardial ultrastructural damage, reduced the area of ischemia/hypoxia, and increased the content of CX43. A recent finding reported that myricetin improves cardiac function in diabetic cardiomyopathy mice by decreasing interstitial fibrosis and cardiomyocyte hypertrophy.
Evidence strength: Preclinical (in vitro and animal) evidence for cardiovascular effects is substantial. The human data on CHD and lipid profiles come from observational or small supplementation studies and should be interpreted cautiously. Controlled clinical trials in cardiovascular populations are lacking.
Myricetin has been used as a form of traditional medicine for diabetes in Northern Brazil and is hypothesized by the Finnish Mobile Clinic Health Examination Survey to potentially be correlated with a lower risk of Type 2 diabetes in individuals whose diets included higher than average amounts of myricetin. However, since studies in the United States, such as the Women's Health Study, do not confirm these results, there is doubt as to whether the difference in risk can actually be attributed to myricetin and is not the result of confounding variables such as racial background or dietary inconsistencies between participants.
In a clinical trial spanning four weeks, blueberin and myricetin were administered at a quantity of 250 mg blueberry leaves and 50 mg myricetin (300 mg together) daily. This placebo-controlled trial revealed that the combination successfully reduced plasma sugar levels in type-2 diabetic patients, with plasma sugar levels falling from 143 ± 5.2 mg/L to 104 ± 5.7 mg/L.
In vitro model studies found that myricetin protected endothelial cells from high glucose-induced oxidative stress by enhancing antioxidant capacity and reducing markers of apoptosis, suggesting potential to promote cardiovascular health in diabetes.
Evidence strength: The clinical trial combining myricetin with blueberin is small and uses a combined preparation, making it impossible to isolate myricetin's specific contribution. Epidemiological data are mixed across populations. Animal and cell-culture data are extensive but do not directly translate to clinical conclusions. While hyperglycemic levels were significantly normalized in some T2DM patient studies, these clinical trials cannot be considered sufficient.
According to a clinical survey, the consumption of myricetin can lead to a low incidence of prostate cancer risk. Another clinical trial on lung cancer reported that the regular consumption of myricetin was associated with a decreased incidence of lung cancer.
In preclinical research, myricetin was identified as a potent α-ketoglutarate-type inhibitor that blocks the demethylation activity by KDM4 enzymes and significantly reduced the proliferation of both androgen-dependent and androgen-independent castration-resistant prostate cancer (CRPC) cells.
Myricetin's role in cancer prevention has been noted through modulation of angiogenesis, inflammation, cell cycle arrest, and induction of apoptosis, as well as through inhibition of inflammatory markers such as iNOS and COX-2. Moreover, myricetin increases the chemotherapeutic potential of other anticancer drugs through modulation of cell signaling molecule activity.
Evidence strength: The bulk of anticancer evidence comes from in vitro cell line studies and animal xenograft models. The prostate and lung cancer human data are epidemiological (dietary survey-based) rather than interventional, meaning causation cannot be established. The clinical trial studies on myricetin are limited. No large-scale randomized controlled trials (RCTs) in oncology have been published.
A growing body of evidence has reported that myricetin supplementation displays therapeutic activities in numerous nervous system disorders, such as cerebral ischemia, Alzheimer's disease, Parkinson's disease, epilepsy, and glioblastoma. Myricetin supplementation can also protect against pathological changes and behavioral impairment induced by multiple sclerosis and chronic stress. Mechanistic studies have shown that inhibition of oxidative stress, cellular apoptosis, and neuroinflammatory response are common mechanisms for the neuroprotective actions of myricetin.
Regarding Alzheimer's disease: one prospective study reported that the onset of Alzheimer's disease is inversely associated with dietary intake of myricetin, and higher dietary intake may be associated with a decreased risk of approximately 38% of developing Alzheimer's disease dementia. In preclinical research, myricetin treatment improved learning memory and ameliorated tau phosphorylation and reduced pre- and postsynaptic proteins in Aβ42 oligomer-treated neuronal cells and triple-transgenic (3×Tg) mice.
Regarding Parkinson's disease: myricetin has been reported to have biological functions of anti-oxidation, anti-apoptosis, anti-inflammation and iron-chelation. In a study investigating the neuroprotective effect of myricetin on MPP⁺-treated dopaminergic cells, myricetin treatment significantly attenuated MPP⁺-induced cell loss and nuclear condensation, suppressed intracellular ROS production, restored mitochondrial transmembrane potential, increased Bcl-2/Bax ratio, and decreased caspase-3 activation.
Due to the pleiotropic properties of myricetin, including anti-amyloid, anti-phosphorylation of tau protein, anti-inflammatory, anti-oxidant and autophagic effects, as well as its ability to increase acetylcholine, myricetin is considered a promising candidate for treatment after ischemia-related brain neurodegeneration.
Evidence strength: Neuroprotective evidence is almost entirely preclinical (cell and animal models). Preclinical activities on Alzheimer, Parkinson, and Huntington diseases, and even in amyotrophic lateral sclerosis, have been demonstrated. The one human study showing an inverse association between dietary myricetin intake and Alzheimer's risk is observational and cannot demonstrate causation. No clinical intervention trials in neurodegenerative disease have been reported.
Animal studies have examined the role of myricetin in a diet-induced non-alcoholic steatohepatitis (NASH) model. Myricetin was shown to restore the activity of antioxidant enzymes, reduce lipid peroxidation, decrease xanthine oxidase activity, and modulate levels of molecular inflammation markers (NF-κB, Nrf-2, TNF-α, and IL-6).
Evidence strength: Hepatoprotective effects are supported primarily by animal and in vitro data. No dedicated clinical trials in human liver disease have been published for myricetin as an isolated compound.
It has been revealed that myricetin exhibits anti-microbial properties due to obstructive virulence factors, preventing biofilm formation and disrupting membrane integrity. Myricetin is commonly found in plants and its antimicrobial and antioxidant activities are well demonstrated in the literature.
Evidence strength: Antimicrobial data are predominantly in vitro. No human clinical trials evaluating myricetin as an antimicrobial agent have been identified.
Bone health has been demonstrated to be improved by myricetin in preclinical research, showing the ability to counter osteoporosis. Myricetin enhances the osteogenic differentiation of human periodontal ligament stem cells (hPDLSCs) by enhancing the regulation of the ALP, BMP-2/Smad, and ERK/JNK/p38 MAPK signaling pathways.
Evidence strength: Preliminary; data derive from in vitro and animal studies. No clinical trials in osteoporosis or bone density endpoints have been reported.
Oral bioavailability of myricetin is only about 9.62% and 9.74%, respectively, at two oral doses of 50 and 100 mg/kg, indicating a poor absorbing property. Maximum plasma concentration (Cmax) and area under the curve (AUC) of myricetin increased after oral administration proportional to the dose, indicating absorption by passive diffusion in vivo. A longer time to achieve maximum concentration (Tmax) of 6.4 hours is consistent with its low aqueous solubility.
Like other flavonoids, myricetin has low oral bioavailability of less than 10% in rats. Peak plasma concentrations of myricetin and its (sulfate and glucuronide) metabolites were together approximately 8 μM after per os treatment of rats with 100 mg/kg of myricetin.
One of the challenges associated with the therapeutic application of myricetin is its limited water solubility, which hampers its bioavailability and subsequent efficacy. Researchers have investigated strategies to improve this, including amorphous solid dispersions and nanoformulations. Amorphous solid dispersions with polyvinylpyrrolidone showed significantly improved solubility, dissolution rate, and in vitro neuroprotective activities compared to the pure compound.
Dietary supplement preparations of myricetin aglycone typically carry a recommended daily dose of 100 mg. The appropriate dosage of myricetin can vary based on factors such as the specific health condition being addressed, individual health status, and concentration of the supplement; generally, doses in research studies range from 100 to 600 mg per day.
In animal research, specific dosages used include:
In the only human placebo-controlled trial specifically reported in the literature: blueberin and myricetin were administered at a quantity of 250 mg blueberry leaves and 50 mg myricetin (300 mg combined) on a daily basis over four weeks.
While human clinical research on myricetin is still limited, a few small-scale studies have explored its bioavailability and safety in humans, generally reporting good tolerance. While myricetin from food sources is well-tolerated, high-dose supplements may present potential side effects, including mild digestive discomfort such as nausea or diarrhea, particularly when taken on an empty stomach. Allergic reactions, though rare, are also possible.
In a bacterial reverse mutation assay, myricetin tested positive for frameshift mutations under metabolic activation conditions. Myricetin has been shown to exert both anti- and pro-oxidant effects, as well as exhibit mutagenic and anti-mutagenic potential, suggesting a possible dual role in mutagenesis and carcinogenesis.
Both myricitrin and myricetin induced micronuclei in human TK6 cells in the absence of metabolic activation (−S9). In vivo mouse testing yielded an equivocal result for myricetin with respect to genotoxicity. It is important to note that these findings are primarily from in vitro bacterial and cell assays, and their relevance to dietary or supplemental intake in humans remains unclear.
Myricetin has been reported to interfere with several cytochrome P450 enzymes, including CYP3A4, CYP2D6, CYP2C9, CYP2B6, and CYP1A2, which can modulate the pharmacokinetics of a range of drugs. The inhibition of cytochrome P450 enzymes (drug-metabolizing cytochromes) and P-glycoproteins (drug efflux pumps) is a recognized mechanism of myricetin.
A specific example involves the antihypertensive drug losartan: losartan's peak plasma content increased by 31.8–50.2% and the area under the plasma concentration-time curve by 31.4–61.1% when myricetin (2 or 8 mg/kg) was present; myricetin also caused a 20% reduction in the metabolite-parent AUC ratio, providing evidence that myricetin inhibits the CYP-mediated metabolism of losartan to its active metabolite.
For the cardiovascular drug carvedilol: the enhanced oral bioavailability of carvedilol following myricetin co-administration may result from inhibition of CYP2C9- or CYP2D6-mediated metabolism and P-glycoprotein-mediated efflux of carvedilol in the small intestine and/or liver.
Myricetin is known to have anti-platelet properties, among its other physiological activities. This theoretically raises the possibility of interaction with anticoagulant or antiplatelet medications, though direct human data on this interaction are not yet established.
Further acute and chronic toxicological data on vital organs are of extreme importance. It is strongly recommended that randomized, double-blinded clinical trials be urgently conducted. Only after such research and in-depth analysis will myricetin be more fully characterized as a clinical tool for human disease.
Several flavonoids have been recognized as nutraceuticals, and myricetin is a prominent example. Myricetin is commonly found in plants and its antimicrobial and antioxidant activities are well demonstrated. One of its beneficial biological effects is neuroprotective activity, showing preclinical activities on Alzheimer, Parkinson, and Huntington diseases, and even in amyotrophic lateral sclerosis. Myricetin has also revealed antidiabetic, anticancer, immunomodulatory, cardiovascular, analgesic, and antihypertensive activities. However, few clinical trials have been performed using myricetin as a nutraceutical.
Reviews of the current body of literature seek to increase the understanding of myricetin's pharmacological potential in various diseases and highlight its effective mechanisms of action, while consistently noting that further wide-ranging research, as well as more randomized and controlled clinical trial studies, should be executed to determine its therapeutic value, safety, and usefulness against various human diseases.
Health conditions that Myricetin may help support.
Myricetin, a flavonol in berries, red wine, and tea, inhibited IgE- and PMACI-mediated histamine release and intracellular calcium elevation in RBL-2H3 mast cells in a peer-reviewed comparative study. It suppressed TNF-α and IL-6 production and blocked NF-κB activation. It is described in primary literature as a particularly effective mast cell stabilizer.
Body systems that Myricetin may help support.
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