Myricetin

Myricetin at a Glance

Myricetin is a widely distributed dietary flavonol found in berries, walnuts, tea and red wine.

Its chemistry is the reason it behaves differently from its relatives. Myricetin carries a pyrogallol B-ring — three adjacent hydroxyls where quercetin has two — which makes it a notably strong antioxidant at low concentrations and, at high ones, a pro-oxidant and genotoxin. The same feature drives both behaviours, so the direction depends on dose.

There are no trials of the isolated molecule in humans; its human evidence is dietary-intake epidemiology, which is mixed, with the laboratory work concentrated on metabolic and anticancer activity.

What It's Used For

Myricetin is one of the most broadly distributed dietary flavonols — the “pyrogallol” flavonol, defined by three adjacent hydroxyls on its B-ring (positions 3′,4′,5′). That one structural feature is the whole story: it makes myricetin an unusually strong metal-chelator and radical scavenger, and it is also what lets the molecule auto-oxidize, generate hydrogen peroxide and damage DNA at higher concentrations ^{1,11Reference 1Semwal DK et al. · 2016Myricetin — a dietary molecule with diverse biological activitiesView study →Reference 11Hirao Y et al. · 2023Myricetin causes site-specific DNA damage via reactive oxygen species generation by redox interactions with copper ionsView study →}.

So the honest framing is a double-edge, not a simple “antioxidant.” Its human evidence is thin — there are no trials of isolated myricetin in people — and rests on dietary epidemiology, which is mixed ^{2,3Reference 2Zamora-Ros R et al. · 2014Dietary intakes of individual flavanols and flavonols are inversely associated with incident type 2 diabetes in European populationsView study →Reference 3Song Y et al. · 2005ObservationalAssociations of dietary flavonoids with risk of type 2 diabetes, and markers of insulin resistance and systemic inflammation in women — a prospective study and cross-sectional analysisView study →}.

Everything mechanistic (anticancer, antiviral, anti-inflammatory) is preclinical ^{1Reference 1Semwal DK et al. · 2016Myricetin — a dietary molecule with diverse biological activitiesView study →}.

No human isolate trials.Every claim below is either dietary epidemiology (a food pattern, not the pure compound) or laboratory/animal work.

Type-2 diabetes — genuinely mixed:a large European prospective analysis found higher flavonol/myricetin intake inversely associated with incident diabetes ^{2Reference 2Zamora-Ros R et al. · 2014Dietary intakes of individual flavanols and flavonols are inversely associated with incident type 2 diabetes in European populationsView study →}, but an equally large US women’s cohort found no association ^{3Reference 3Song Y et al. · 2005ObservationalAssociations of dietary flavonoids with risk of type 2 diabetes, and markers of insulin resistance and systemic inflammation in women — a prospective study and cross-sectional analysisView study →}.

The antioxidant story has a pro-oxidant twin:the pyrogallol B-ring scavenges radicals and, at higher concentration and with copper/iron, generates H₂O₂ and site-specific DNA damage — and can act as a topoisomerase-II poison ^{10,11Reference 10Bandele OJ et al. · 2008Dietary polyphenols as topoisomerase II poisons — B-ring and C-ring substituents determine the mechanism of enzyme-mediated DNA cleavage enhancementView study →Reference 11Hirao Y et al. · 2023Myricetin causes site-specific DNA damage via reactive oxygen species generation by redox interactions with copper ionsView study →}.

Anticancer is preclinical and pro-oxidant-driven:myricetin kills cancer cells in vitro by that same H₂O₂ chemistry ^{6Reference 6Knickle A et al. · 2018Myricetin-induced apoptosis of triple-negative breast cancer cells is mediated by the iron-dependent generation of reactive oxygen species from hydrogen peroxideView study →} — but the human cancer epidemiology is null ^{5Reference 5Wang L et al. · 2009Dietary intake of selected flavonols, flavones and flavonoid-rich foods and risk of cancer in middle-aged and older womenView study →}.

Antiviral is enzyme-level:it inhibits SARS-CoV/SARS-CoV-2 helicase and main protease in the low-µM range in vitro ^{7,8Reference 7Yu MS et al. · 2012Identification of myricetin and scutellarein as novel chemical inhibitors of the SARS coronavirus helicase, nsP13View study →Reference 8Xiao T et al. · 2021Myricetin inhibits SARS-CoV-2 viral replication by targeting Mpro and ameliorates pulmonary inflammationView study →} — concentrations its poor oral absorption doesn’t reach.

Evidence by IndicationStrength of support · Beta

Support is an experimental score I’m building — a composite weighted by study type (human > animal > in vitro > review) and study volume, tempered for isolate-vs-source match and bioavailability. It’s a beta: a fast way to rank strength of evidence at a glance, not a validated metric. Scores here are held low because there is no isolated-myricetin human trial — the “Rests on” column names what each really tested. Each application links to its write-up.

Myricetin’s best-known “human” association is diabetes, and it is genuinely unresolved. In the EPIC-InterAct case-cohort — the large prospective European analysis — higher intake of flavonols (myricetin among them) was inversely associated with incident type-2 diabetes ^{2Reference 2Zamora-Ros R et al. · 2014Dietary intakes of individual flavanols and flavonols are inversely associated with incident type 2 diabetes in European populationsView study →}.

But the Women’s Health Study (≈38,000 US women) found no significant association between flavonol/myricetin intake and diabetes risk ^{3Reference 3Song Y et al. · 2005ObservationalAssociations of dietary flavonoids with risk of type 2 diabetes, and markers of insulin resistance and systemic inflammation in women — a prospective study and cross-sectional analysisView study →}.

Both are large, prospective and well-conducted; they disagree. Preclinically myricetin improves insulin signaling and glucose uptake in rodent models ^{1,4Reference 1Semwal DK et al. · 2016Myricetin — a dietary molecule with diverse biological activitiesView study →Reference 4Ong KC · 1997Biological effects of myricetinView study →}, which is the mechanistic rationale — but no one has tested the isolated compound in a human trial.

Gap: this is dietary-intake epidemiology (people eating myricetin-containing foods, which also carry quercetin, fiber, etc.), not a trial of myricetin; the two best cohorts contradict each other; and there is zero interventional human evidence. Score held to reflect the conflict ^{2,3Reference 2Zamora-Ros R et al. · 2014Dietary intakes of individual flavanols and flavonols are inversely associated with incident type 2 diabetes in European populationsView study →Reference 3Song Y et al. · 2005ObservationalAssociations of dietary flavonoids with risk of type 2 diabetes, and markers of insulin resistance and systemic inflammation in women — a prospective study and cross-sectional analysisView study →}.

Mechanisms

Target / pathway	Effect	Relevant to	Evidence
Radical scavenging + Fe/Cu chelation (pyrogallol B-ring)	antioxidant at low concentration	general	in vitro
Auto-oxidation → H₂O₂; Cu/Fe-mediated ROS	pro-oxidant, DNA-damaging at high concentration	safetyanticancer	in vitro ^{6,11Reference 6Knickle A et al. · 2018Myricetin-induced apoptosis of triple-negative breast cancer cells is mediated by the iron-dependent generation of reactive oxygen species from hydrogen peroxideView study →Reference 11Hirao Y et al. · 2023Myricetin causes site-specific DNA damage via reactive oxygen species generation by redox interactions with copper ionsView study →}
Topoisomerase-II poisoning	strand breaks (genotoxic)	safety	in vitro ^{10,12Reference 10Bandele OJ et al. · 2008Dietary polyphenols as topoisomerase II poisons — B-ring and C-ring substituents determine the mechanism of enzyme-mediated DNA cleavage enhancementView study →Reference 12Constantinou A et al. · 1995Flavonoids as DNA topoisomerase antagonists and poisons — structure-activity relationshipsView study →}
↑ insulin signaling / GLUT4 glucose uptake	glucose lowering	diabetes	animal ^{1,4Reference 1Semwal DK et al. · 2016Myricetin — a dietary molecule with diverse biological activitiesView study →Reference 4Ong KC · 1997Biological effects of myricetinView study →}
Viral enzyme inhibition (helicase, Mpro, RT)	antiviral	antiviral	in vitro/mouse ^{7,8Reference 7Yu MS et al. · 2012Identification of myricetin and scutellarein as novel chemical inhibitors of the SARS coronavirus helicase, nsP13View study →Reference 8Xiao T et al. · 2021Myricetin inhibits SARS-CoV-2 viral replication by targeting Mpro and ameliorates pulmonary inflammationView study →}

Pharmacokinetics

Myricetin is poorly and erratically absorbed, and its own chemistry works against it. In food it is stored mostly as glycosides that must be hydrolyzed before uptake, and the free aglycone is chemically fragile — the electron-rich pyrogallol B-ring auto-oxidizes readily in neutral/alkaline, aerobic conditions, so a fraction degrades before or during absorption ^{1Reference 1Semwal DK et al. · 2016Myricetin — a dietary molecule with diverse biological activitiesView study →}. What is absorbed is heavily conjugated: a rat pharmacokinetic study using enzymatic deconjugation measured an absolute oral bioavailability of only ~9.6% and confirmed extensive glucuronidation and sulfation ^{9Reference 9Dang Y et al. · 2014AnimalQuantitative determination of myricetin in rat plasma by UPLC-MS/MS and its absolute bioavailabilityView study →}. As with the other flavonols, this means the circulation carries myricetin conjugates rather than much free aglycone, and the low-micromolar concentrations that drive its in-vitro mechanisms are difficult to reach in tissue from oral intake — the central reason its potent laboratory activity has not translated. (The headline ~9.6% figure is a rat value; there is no clean human bioavailability trial ^{9Reference 9Dang Y et al. · 2014AnimalQuantitative determination of myricetin in rat plasma by UPLC-MS/MS and its absolute bioavailabilityView study →}.)

Clinical trials

None of isolated myricetin. The human evidence is entirely observational dietary epidemiology, and it does not agree with itself:

Human diabetes evidence	Human cancer evidence	Isolate trials
EPIC-InterAct: inverse ^{2Reference 2Zamora-Ros R et al. · 2014Dietary intakes of individual flavanols and flavonols are inversely associated with incident type 2 diabetes in European populationsView study →} · Women’s Health Study: null ^{3Reference 3Song Y et al. · 2005ObservationalAssociations of dietary flavonoids with risk of type 2 diabetes, and markers of insulin resistance and systemic inflammation in women — a prospective study and cross-sectional analysisView study →}	Women’s Health Study: null ^{5Reference 5Wang L et al. · 2009Dietary intake of selected flavonols, flavones and flavonoid-rich foods and risk of cancer in middle-aged and older womenView study →}	None

Last checked: July 2026.

Isolate vs. Plant Studies

Myricetin is a textbook case for reading flavonol claims skeptically. The human data are dietary, not molecular: the diabetes and cancer associations come from food-frequency questionnaires, where myricetin travels with quercetin, kaempferol, fiber, vitamin C and everything else in berries and greens — so a signal can’t be assigned to myricetin, and here the two largest cohorts even disagree on diabetes ^{2,3,5Reference 2Zamora-Ros R et al. · 2014Dietary intakes of individual flavanols and flavonols are inversely associated with incident type 2 diabetes in European populationsView study →Reference 3Song Y et al. · 2005ObservationalAssociations of dietary flavonoids with risk of type 2 diabetes, and markers of insulin resistance and systemic inflammation in women — a prospective study and cross-sectional analysisView study →Reference 5Wang L et al. · 2009Dietary intake of selected flavonols, flavones and flavonoid-rich foods and risk of cancer in middle-aged and older womenView study →}. The “antioxidant” label oversimplifies: the same pyrogallol B-ring that scavenges radicals also makes myricetin a pro-oxidant and genotoxin at high concentration — the mechanism behind both its in-vitro anticancer activity and its safety flags is one and the same ^{6,11Reference 6Knickle A et al. · 2018Myricetin-induced apoptosis of triple-negative breast cancer cells is mediated by the iron-dependent generation of reactive oxygen species from hydrogen peroxideView study →Reference 11Hirao Y et al. · 2023Myricetin causes site-specific DNA damage via reactive oxygen species generation by redox interactions with copper ionsView study →}. And potency in a dish ≠ effect in a person: its low-µM antiviral and pro-apoptotic actions sit far above the exposure its ~9.6% (rat) bioavailability delivers ^{9Reference 9Dang Y et al. · 2014AnimalQuantitative determination of myricetin in rat plasma by UPLC-MS/MS and its absolute bioavailabilityView study →}. Within this database myricetin appears at occurrence level across many herbs (e.g. bearberry/uva-ursi, red clover); those are “contains myricetin among many flavonoids” hits, not evidence that myricetin drives the herb’s effect. (Note: earlier accounts listed walnuts as a source — USDA analysis puts walnut myricetin at 0.00, so that claim has been removed.)

Prevalence in Nature

Myricetin is a widely but unevenly distributed flavonol, usually present as glycosides (myricitrin and other myricetin glycosides) and released on hydrolysis ^{1Reference 1Semwal DK et al. · 2016Myricetin — a dietary molecule with diverse biological activitiesView study →}. It is not concentrated in one signature food the way some flavonoids are; instead it turns up across herbs, leafy vegetables, berries, tea and wine. By USDA analysis the richest common sources are fennel bulb (~19.8 mg/100 g) and parsley (~14.8 mg/100 g, lower-confidence data), followed by the berries — cranberry (~7.6), wild blueberry (~7.3) and black currant (~6.2 mg/100 g) — and leafy greens such as dock/sorrel (~5.7) and sweet-potato leaf (~2.9) ^{13,14Reference 13Häkkinen SH et al. · 1999Content of the flavonols quercetin, myricetin and kaempferol in 25 edible berriesView study →Reference 14Haytowitz DB et al. · 2018USDA Database for the Flavonoid Content of Selected Foods, Release 3.3View study →}. Beverages contribute modestly per serving but add up: red wine and brewed black tea each supply roughly 0.4–0.5 mg/100 mL ^{14Reference 14Haytowitz DB et al. · 2018USDA Database for the Flavonoid Content of Selected Foods, Release 3.3View study →}. Two data-integrity notes matter here: a viral figure of “cranberry 6600 mg/100 g” is a ~1000× unit error — the real value is single-digit (~7.6) — and walnuts contain essentially none (USDA: 0.00), despite older listings ^{13,14Reference 13Häkkinen SH et al. · 1999Content of the flavonols quercetin, myricetin and kaempferol in 25 edible berriesView study →Reference 14Haytowitz DB et al. · 2018USDA Database for the Flavonoid Content of Selected Foods, Release 3.3View study →}. There are no meaningful non-plant sources.

Biosynthetically myricetin sits at the most-hydroxylated end of the common flavonol series. The enzyme flavonoid 3′,5′-hydroxylase (F3′5′H) adds hydroxyls at the 3′ and 5′ positions of the B-ring, converting the mono-/di-hydroxylated flavonols into the trihydroxy (pyrogallol) pattern: kaempferol → quercetin → myricetin corresponds to 1 → 2 → 3 B-ring hydroxyls ^{15Reference 15Liu Y et al. · 2022Hydroxylation decoration patterns of flavonoids in horticultural crops — chemistry, bioactivity and biosynthesisView study →}. The same F3′5′H branch that yields myricetin also feeds the delphinidin/blue-anthocyanin and prodelphinidin lines, which is why myricetin-rich plants (currants, certain grapes) tend also to be rich in the blue-purple pigments.

Discovery & Synthesis

Myricetin takes its name from the plant genus Myrica — the bayberries or wax myrtles — and is reported to have been first isolated from the bark of Myrica nagi. That naming-and-first-isolation history is documented only in secondary/review literature rather than a primary indexed paper, so it should be treated as reported rather than firmly sourced ^{1Reference 1Semwal DK et al. · 2016Myricetin — a dietary molecule with diverse biological activitiesView study →}. Chemically myricetin is 3,3′,4′,5,5′,7-hexahydroxyflavone — the flavonol carrying six hydroxyl groups, three of them the adjacent 3′,4′,5′ pyrogallol cluster on the B-ring that defines its behavior. It is the B-ring 5′-hydroxy homologue of quercetin (which lacks the 5′-OH) and, two hydroxyls up, of kaempferol; reducing the C-ring 2,3-double bond gives the related dihydromyricetin (ampelopsin).

Isolated myricetin is a yellow solid that is notably unstable in solution — the pyrogallol B-ring oxidizes in air, especially at neutral-to-alkaline pH, which complicates both its formulation and the interpretation of assays where the “myricetin” tested may be partly oxidation products ^{1,11Reference 1Semwal DK et al. · 2016Myricetin — a dietary molecule with diverse biological activitiesView study →Reference 11Hirao Y et al. · 2023Myricetin causes site-specific DNA damage via reactive oxygen species generation by redox interactions with copper ionsView study →}. Commercial material is obtained by extraction from plant sources (e.g. bayberry bark, or other myricetin-rich botanicals) and by enzymatic/acid hydrolysis of its glycosides; laboratory total syntheses of the flavonol skeleton exist but plant extraction dominates supply.

Patents: not yet researched (future patent-loop pass).

Toxicity & Safety

At the levels supplied by a normal diet, myricetin is a well-tolerated food constituent with a low toxicity profile — it has been eaten in berries, vegetables, tea and wine for as long as people have eaten those foods. The important caveat is specifically about concentrated, high-dose supplemental intake, where its defining chemistry cuts the other way.

The pyrogallol B-ring is pro-oxidant and genotoxic at high concentration. In cell-free and cellular systems myricetin auto-oxidizes to generate hydrogen peroxide and, in the presence of copper (or iron) ions, causes site-specific oxidative DNA damage ^{11Reference 11Hirao Y et al. · 2023Myricetin causes site-specific DNA damage via reactive oxygen species generation by redox interactions with copper ionsView study →}. It also acts as a topoisomerase-II poison — stabilizing the enzyme–DNA cleavage complex to produce DNA strand breaks — an activity tied directly to its B-ring hydroxylation pattern ^{10,12Reference 10Bandele OJ et al. · 2008Dietary polyphenols as topoisomerase II poisons — B-ring and C-ring substituents determine the mechanism of enzyme-mediated DNA cleavage enhancementView study →Reference 12Constantinou A et al. · 1995Flavonoids as DNA topoisomerase antagonists and poisons — structure-activity relationshipsView study →}. This is the same chemistry that makes it kill cancer cells in vitro ^{6Reference 6Knickle A et al. · 2018Myricetin-induced apoptosis of triple-negative breast cancer cells is mediated by the iron-dependent generation of reactive oxygen species from hydrogen peroxideView study →}; it is a genuine double-edge, and the reason that “more is better” does not follow for a supposedly antioxidant flavonol. Topoisomerase-II poisons are also of theoretical concern for the rare infant leukemias linked to maternal dietary bioflavonoids, which is a further reason to avoid concentrated supplements around pregnancy.

Because there are no human safety trials of isolated myricetin, the upper bound of safe supplemental intake is simply not characterized ^{1Reference 1Semwal DK et al. · 2016Myricetin — a dietary molecule with diverse biological activitiesView study →}. Like many flavonoids it can also inhibit drug-metabolizing enzymes and transporters in laboratory systems, so interactions with medications are plausible though not clinically quantified. The sensible reading: dietary myricetin is fine and probably beneficial; concentrated high-dose supplements are not well-characterized and carry a real, mechanism-based genotoxicity concern.

Dosage

There is no established dose of myricetin, because no human trial has ever tested the isolated compound. Typical dietary intakes of myricetin are on the order of a few milligrams per day, obtained from berries, leafy greens, herbs, tea and wine ^{14Reference 14Haytowitz DB et al. · 2018USDA Database for the Flavonoid Content of Selected Foods, Release 3.3View study →}. Supplement products exist but rest on animal and in-vitro data, not human dosing studies, and the pro-oxidant/genotoxicity signal at high concentration is a specific reason not to extrapolate upward from food to high-dose capsules ^{10,11Reference 10Bandele OJ et al. · 2008Dietary polyphenols as topoisomerase II poisons — B-ring and C-ring substituents determine the mechanism of enzyme-mediated DNA cleavage enhancementView study →Reference 11Hirao Y et al. · 2023Myricetin causes site-specific DNA damage via reactive oxygen species generation by redox interactions with copper ionsView study →}.

Context	Basis	Notes
Dietary intake	Food surveys	A few mg/day from berries, greens, herbs, tea, wine ^{14Reference 14Haytowitz DB et al. · 2018USDA Database for the Flavonoid Content of Selected Foods, Release 3.3View study →}
Supplemental	No human trials	Any dose is extrapolated from animal/in-vitro work; genotoxicity caveat applies ^{10,11Reference 10Bandele OJ et al. · 2008Dietary polyphenols as topoisomerase II poisons — B-ring and C-ring substituents determine the mechanism of enzyme-mediated DNA cleavage enhancementView study →Reference 11Hirao Y et al. · 2023Myricetin causes site-specific DNA damage via reactive oxygen species generation by redox interactions with copper ionsView study →}

These are descriptive figures, not a recommendation — the honest position is that isolated-myricetin dosing in humans is unstudied.

References

Semwal DK, Semwal RB, Combrinck S, Viljoen A. (2016). Myricetin — a dietary molecule with diverse biological activities. Nutrients, 8(2), 90. https://pubmed.ncbi.nlm.nih.gov/26891321/
Zamora-Ros R, Forouhi NG, Sharp SJ, et al. (2014). Dietary intakes of individual flavanols and flavonols are inversely associated with incident type 2 diabetes in European populations. The Journal of Nutrition, 144(3), 335–343. https://pubmed.ncbi.nlm.nih.gov/24368432/
Song Y, Manson JE, Buring JE, Sesso HD, Liu S. (2005). Associations of dietary flavonoids with risk of type 2 diabetes, and markers of insulin resistance and systemic inflammation in women — a prospective study and cross-sectional analysis. Journal of the American College of Nutrition, 24(5), 376–384. https://pubmed.ncbi.nlm.nih.gov/16192263/
Ong KC, Khoo HE. (1997). Biological effects of myricetin. General Pharmacology, 29(2), 121–126. https://pubmed.ncbi.nlm.nih.gov/9251891/
Wang L, Lee IM, Zhang SM, Blumberg JB, Buring JE, Sesso HD. (2009). Dietary intake of selected flavonols, flavones and flavonoid-rich foods and risk of cancer in middle-aged and older women. The American Journal of Clinical Nutrition, 89(3), 905–912. https://pubmed.ncbi.nlm.nih.gov/19158208/
Knickle A, Fernando W, Greenshields AL, Rupasinghe HPV, Hoskin DW. (2018). Myricetin-induced apoptosis of triple-negative breast cancer cells is mediated by the iron-dependent generation of reactive oxygen species from hydrogen peroxide. Food and Chemical Toxicology, 118, 154–167. https://pubmed.ncbi.nlm.nih.gov/29742465/
Yu MS, Lee J, Lee JM, et al. (2012). Identification of myricetin and scutellarein as novel chemical inhibitors of the SARS coronavirus helicase, nsP13. Bioorganic & Medicinal Chemistry Letters, 22(12), 4049–4054. https://pubmed.ncbi.nlm.nih.gov/22578462/
Xiao T, Cui M, Zheng C, et al. (2021). Myricetin inhibits SARS-CoV-2 viral replication by targeting Mpro and ameliorates pulmonary inflammation. Frontiers in Pharmacology, 12, 669642. https://pubmed.ncbi.nlm.nih.gov/34220507/
Dang Y, Lin G, Xie Y, et al. (2014). Quantitative determination of myricetin in rat plasma by UPLC-MS/MS and its absolute bioavailability. Drug Research, 64(10), 516–522. https://pubmed.ncbi.nlm.nih.gov/24357136/
Bandele OJ, Clawson SJ, Osheroff N. (2008). Dietary polyphenols as topoisomerase II poisons — B-ring and C-ring substituents determine the mechanism of enzyme-mediated DNA cleavage enhancement. Chemical Research in Toxicology, 21(6), 1253–1260. https://pubmed.ncbi.nlm.nih.gov/18461976/
Hirao Y, Kobayashi H, Mori Y, et al. (2023). Myricetin causes site-specific DNA damage via reactive oxygen species generation by redox interactions with copper ions. Mutation Research — Genetic Toxicology and Environmental Mutagenesis, 891, 503694. https://pubmed.ncbi.nlm.nih.gov/37770136/
Constantinou A, Mehta R, Runyan C, Rao K, Vaughan A, Moon R. (1995). Flavonoids as DNA topoisomerase antagonists and poisons — structure-activity relationships. Journal of Natural Products, 58(2), 217–225. https://pubmed.ncbi.nlm.nih.gov/7769390/
Häkkinen SH, Kärenlampi SO, Heinonen IM, Mykkänen HM, Törrönen AR. (1999). Content of the flavonols quercetin, myricetin and kaempferol in 25 edible berries. Journal of Agricultural and Food Chemistry, 47(6), 2274–2279. https://pubmed.ncbi.nlm.nih.gov/10794622/
Haytowitz DB, Wu X, Bhagwat S. (2018). USDA Database for the Flavonoid Content of Selected Foods, Release 3.3. U.S. Department of Agriculture, Agricultural Research Service. [Database — no PMID.] https://www.ars.usda.gov/nutrientdata
Liu Y, Qian J, Li J, et al. (2022). Hydroxylation decoration patterns of flavonoids in horticultural crops — chemistry, bioactivity and biosynthesis. Horticulture Research, 9, uhab068. https://pubmed.ncbi.nlm.nih.gov/35048127/