Quercetin

Quercetin at a Glance

Quercetin is the most widely distributed flavonol in the human diet — the yellow pigment of onion skin and caper buds, and a constituent of most medicinal plants. In food and in plants it exists almost entirely as glycosides, sugar-attached forms such as rutin and isoquercitrin, rather than as the free molecule sold in capsules.

Its defining practical property is poor and erratic absorption. The sugar attached to it largely decides how much gets in, which is why quercetin from onions behaves differently from quercetin from a supplement, and why in-vitro concentrations rarely correspond to anything achievable in blood.

Where the human evidence is strongest is cardiovascular: blood pressure, with metabolic markers behind it. The antiviral interest that grew around it during the COVID-19 period rests on a different and much thinner footing.

What It's Used For

Quercetin is the most widely distributed flavonol in the plant kingdom — the yellow pigment behind onion skin, caper buds and countless herb extracts. It is one of the most heavily supplemented and studied plant molecules, yet its clinical story is modest and, above all, governed by one fact: the aglycone is poorly and erratically absorbed, circulates almost entirely as conjugated metabolites, and reaches plasma levels far below those used in most cell studies ^{18,19,20Reference 18Hollman PC et al. · 1997Relative bioavailability of the antioxidant flavonoid quercetin from various foods in manView study →Reference 19Graefe EU et al. · 2001Pharmacokinetics and bioavailability of quercetin glycosides in humansView study →Reference 20Mohos V et al. · 2020Inhibitory effects of quercetin and its main methyl, sulfate, and glucuronic acid conjugates on cytochrome P450 enzymes, and on OATP, BCRP and MRP2 transportersView study →}.

Read the human evidence with that in mind — the effects that survive meta-analysis are small and dose-gated.

Evidence by IndicationStrength of support · Beta

01Blood pressure & cardiovascularPromising68%Meta-analyses of RCTs; real but ~3 mmHg and only ≥500 mg/day ^{1,2,3Reference 1Serban MC et al. · 2016Meta-analysisEffects of quercetin on blood pressure: a systematic review and meta-analysis of randomized controlled trials (7 RCTs, n≈587)View study →Reference 2Huang H et al. · 2020Meta-analysisEffect of quercetin supplementation on plasma lipid profiles, blood pressure, and glucose levels — systematic review and meta-analysisView study →Reference 3Arabi SM et al. · 2023Meta-analysisThe effects of quercetin supplementation on cardiometabolic outcomes — an umbrella review of meta-analyses of randomised controlled trialsView study →}

02Metabolic markersPromising52%Several meta-analyses that disagree; subgroup/dose-dependent ^{3,4,5,6Reference 3Arabi SM et al. · 2023Meta-analysisThe effects of quercetin supplementation on cardiometabolic outcomes — an umbrella review of meta-analyses of randomised controlled trialsView study →Reference 4Ostadmohammadi V et al. · 2019Meta-analysisEffects of quercetin supplementation on glycemic control among patients with metabolic syndrome and related disorders — systematic review and meta-analysis of RCTsView study →Reference 5Sahebkar A · 2017Meta-analysisEffects of quercetin supplementation on lipid profile — systematic review and meta-analysis of randomised controlled trialsView study →Reference 6Tabrizi R et al. · 2020Meta-analysisThe effects of quercetin supplementation on lipid profiles and inflammatory markers among patients with metabolic syndrome and related disorders — systematic review and meta-analysis of RCTsView study →}

03Uric acid & goutShaky42%One good small crossover RCT + strong xanthine-oxidase mechanism ^{9Reference 9Shi Y · 2016RCTQuercetin lowers plasma uric acid in pre-hyperuricaemic males — randomised, double-blinded, placebo-controlled, cross-over trial (n=22)View study →}

04Antiviral & COVID-19Shaky30%RCTs exist but small, open-label, often phytosome not aglycone ^{10,11,12Reference 10Di Pierro F et al. · 2021RCTPotential clinical benefits of quercetin in the early stage of COVID-19 — second, pilot, randomised, controlled, open-label clinical trialView study →Reference 11Ziaei S et al. · 2023Meta-analysisThe effect of quercetin supplementation on clinical outcomes in COVID-19 patients — systematic review and meta-analysisView study →Reference 12Cheema HA et al. · 2023Meta-analysisQuercetin for the treatment of COVID-19 patients — systematic review and meta-analysisView study →}

05Allergy & mast-cell stabilizationShaky25%Strong in-vitro mechanism; human trials thin and use derivatives ^{13,14Reference 13Weng Z et al. · 2012Quercetin is more effective than cromolyn in blocking human mast cell cytokine release and inhibits contact dermatitis and photosensitivity in humansView study →Reference 14Hirano T et al. · 2009Preventive effect of enzymatically modified isoquercitrin on ocular symptoms of Japanese cedar pollinosis (a quercetin glycoside derivative)View study →}

06Exercise performanceShaky22%Well-studied → reliably trivial (meta-analysis) ^{16Reference 16Pelletier DM et al. · 2013Meta-analysisEffects of quercetin supplementation on endurance performance and maximal oxygen consumption — meta-analysis (7 studies, n=288)View study →}

Mechanisms

Most of these are demonstrated at in-vitro concentrations (10–100 µmol/L of free aglycone) well above what oral dosing achieves in blood — see Pharmacokinetics below.

Pharmacokinetics

Quercetin’s defining pharmacological fact is poor, glycoside-dependent oral bioavailability — and the sugar attached to the molecule matters more than the dose. In the classic human comparison, the same nominal quercetin dose was absorbed best from onion glucosides (set at 100%), reaching only ~24% from the pure aglycone and ~17% from rutin (quercetin-3-O-rutinoside) ^{18Reference 18Hollman PC et al. · 1997Relative bioavailability of the antioxidant flavonoid quercetin from various foods in manView study →}. The reason is the absorption site: glucosides are cleaved and taken up high in the small intestine (a fast, ~1 h peak), whereas rutin’s rhamnose–glucose disaccharide resists small-intestinal enzymes and must reach the colon to be freed by gut bacteria — giving a delayed, blunted, highly variable peak ^{18,19Reference 18Hollman PC et al. · 1997Relative bioavailability of the antioxidant flavonoid quercetin from various foods in manView study →Reference 19Graefe EU et al. · 2001Pharmacokinetics and bioavailability of quercetin glycosides in humansView study →}. So “quercetin” is not one drug: isoquercitrin behaves nothing like rutin.

Whatever is absorbed is immediately conjugated, so free aglycone is essentially undetectable in blood — circulating quercetin is a mix of glucuronides, sulfates and the methylated metabolite isorhamnetin ^{19,20Reference 19Graefe EU et al. · 2001Pharmacokinetics and bioavailability of quercetin glycosides in humansView study →Reference 20Mohos V et al. · 2020Inhibitory effects of quercetin and its main methyl, sulfate, and glucuronic acid conjugates on cytochrome P450 enzymes, and on OATP, BCRP and MRP2 transportersView study →}. The conjugates clear slowly (terminal half-lives ~11–28 h), so plasma accumulates modestly with daily dosing, but total concentrations stay low — typically well under 1–2 µmol/L even after gram-level doses ^{19Reference 19Graefe EU et al. · 2001Pharmacokinetics and bioavailability of quercetin glycosides in humansView study →}. This is the crux of quercetin’s in-vitro-vs-in-vivo gap: much of its published bioactivity uses 10–100 µmol/L of free aglycone, one to two orders of magnitude above achievable plasma levels and in a form that barely exists in the body ^{20Reference 20Mohos V et al. · 2020Inhibitory effects of quercetin and its main methyl, sulfate, and glucuronic acid conjugates on cytochrome P450 enzymes, and on OATP, BCRP and MRP2 transportersView study →}.

Clinical trials

Quercetin has been tested in dozens of small investigator-led RCTs — chiefly in blood pressure, metabolic markers and, recently, COVID-19 — but as a cheap, off-patent food molecule it attracts little registered industry trial activity, and several “quercetin” trials actually use branded phytosome or glycoside formulations.

Last checked: July 2026.

Monoamine oxidase (MAO) inhibition

Quercetin is one of the better-characterized flavonoid monoamine-oxidase inhibitors — a moderate, MAO-A-preferring inhibitor with a reported IC50 around 11 µM against MAO-A ^{17Reference 17Herraiz T · 2018Monoamine oxidase-A inhibition and associated antioxidant activity in plant extracts with potential antidepressant actionsView study →}. This is sometimes invoked to explain the mood effects of quercetin-rich plants, but it is far weaker than the β-carboline inhibitors and, given quercetin’s low systemic and brain exposure, is more a footnote than a primary mechanism. See the natural MAO inhibitors guide for the full comparison.

Isolate vs. Plant Studies

Quercetin sits at an unusual crossroads: its human trials genuinely test the isolated molecule (or a supplement of it), yet its plant occurrence is almost entirely as something else. Two cautions follow.

First, the supplement is often not the plain aglycone. Several headline human trials — the allergy and COVID-19 studies especially — used better-absorbed derivatives (enzymatically-modified isoquercitrin) or a phytosome formulation rather than plain quercetin ^{10,14,15Reference 10Di Pierro F et al. · 2021RCTPotential clinical benefits of quercetin in the early stage of COVID-19 — second, pilot, randomised, controlled, open-label clinical trialView study →Reference 14Hirano T et al. · 2009Preventive effect of enzymatically modified isoquercitrin on ocular symptoms of Japanese cedar pollinosis (a quercetin glycoside derivative)View study →Reference 15Yamada S et al. · 2022RCTEffects of repeated oral intake of a quercetin-containing supplement on allergic reaction — randomised, placebo-controlled, double-blind parallel-group studyView study →}. Their results describe those specific preparations, not necessarily generic quercetin powder.

A worked example of what that concentration buys. In murine cutaneous leishmaniasis, orally administered quercetin glycosides at 16 mg/kg/day matched the crude Kalanchoe pinnata aqueous extract at 320 mg/kg/day — controlling lesion growth and significantly reducing parasite load at a twentieth of the dose. Free quercetin at the same 16 mg/kg did the same, and plasma analysis of the extract-treated mice found quercetin and quercetin glucuronides to be the main circulating metabolites of the plant’s glycosides ^{29Reference 29Muzitano MF et al. · 2009AnimalOral metabolism and efficacy of Kalanchoe pinnata flavonoids in a murine model of cutaneous leishmaniasis — mouse in vivo animal modelView study →}. That is the isolate-versus-extract trade in one number: a 20-fold concentration of activity into a defined molecule, and the loss of everything else the extract contained.

Second, in plants quercetin is stored as glycosides, not free aglycone — rutin, isoquercitrin, quercitrin, hyperoside, spiraeoside — which absorb very differently ^{18,19Reference 18Hollman PC et al. · 1997Relative bioavailability of the antioxidant flavonoid quercetin from various foods in manView study →Reference 19Graefe EU et al. · 2001Pharmacokinetics and bioavailability of quercetin glycosides in humansView study →}. So a herb’s “quercetin content” is really its quercetin-yielding glycoside pool, and a whole-plant antioxidant effect can’t be assumed to be free quercetin. Across this database quercetin is named in the antioxidant flavonoid fraction of many herbs — bearberry, ginkgo, raspberry leaf, hibiscus, horsetail and others — almost always as part of a mixed extract and frequently as glycosides. A few monographs attribute specific activity to quercetin isolated from the plant (for example anti-psoriatic / antiproliferative activity from Smilax rhizome, or cytokine suppression by isolated quercetin), but most “quercetin” herb claims are whole-plant attributions. Read the supplement trials as evidence for the molecule (in a stated form), and the herb chemistry as evidence for the plants.

Prevalence in Nature

Quercetin is among the most ubiquitous of all plant flavonols, turning up across most flowering-plant lineages rather than a few families ^{21,22Reference 21Dabeek WM · 2019Dietary quercetin and kaempferol: bioavailability and potential cardiovascular-related bioactivity in humansView study →Reference 22Vollmannová A et al. · 2024ReviewQuercetin as one of the most abundant represented biological valuable plant components with remarkable chemoprotective effects — review (occurrence, biosynthesis, manufacture)View study →}. The densest dietary sources cluster in a handful: capers (Capparis spinosa) by a wide margin, onion skin (Allium cepa), kale and other Brassica, leafy Apiaceae (dill, lovage), apple peel, Vaccinium berries (cranberry, lingonberry, blueberry), elderberry, buckwheat and tea ^{22,23Reference 22Vollmannová A et al. · 2024ReviewQuercetin as one of the most abundant represented biological valuable plant components with remarkable chemoprotective effects — review (occurrence, biosynthesis, manufacture)View study →Reference 23U.S · 2018Department of Agriculture, Agricultural Research ServiceView study →}. It concentrates in the metabolically exposed, UV-stressed organs — leaves, flower buds, fruit skins and outer scales — rather than in flesh or roots (see the Content-by-Source chart) ^{23Reference 23U.S · 2018Department of Agriculture, Agricultural Research ServiceView study →}.

Crucially, in living tissue quercetin is stored as glycosides, not the free aglycone: rutin (quercetin-3-O-rutinoside), isoquercitrin (3-O-glucoside), quercitrin (3-O-rhamnoside), hyperoside (3-O-galactoside) and onion’s spiraeoside (4’-O-glucoside). The food-table figures are “total quercetin” measured after acid hydrolysis of these conjugates — the plant’s quercetin-yielding potential, not its free-aglycone content ^{21,22Reference 21Dabeek WM · 2019Dietary quercetin and kaempferol: bioavailability and potential cardiovascular-related bioactivity in humansView study →Reference 22Vollmannová A et al. · 2024ReviewQuercetin as one of the most abundant represented biological valuable plant components with remarkable chemoprotective effects — review (occurrence, biosynthesis, manufacture)View study →}.

Biosynthetically it is a flavonol built through the phenylpropanoid → flavonoid pathway: phenylalanine is converted (via PAL / C4H / 4CL) to p-coumaroyl-CoA, which chalcone synthase condenses with malonyl-CoA to naringenin; flavanone 3-hydroxylase and flavonoid 3’-hydroxylase then give dihydroquercetin (taxifolin), and flavonol synthase desaturates it to quercetin ^{22Reference 22Vollmannová A et al. · 2024ReviewQuercetin as one of the most abundant represented biological valuable plant components with remarkable chemoprotective effects — review (occurrence, biosynthesis, manufacture)View study →}. The pathway is strongly up-regulated by UV-B and other stress, consistent with quercetin’s role as a plant sunscreen and antioxidant — hence its accumulation in sun-exposed peels and outer leaves. There is essentially no natural non-plant source: animals and ordinary bacteria do not make it, and it is absent from meat, dairy and eggs; the only non-botanical “source” is engineered microbial fermentation in the lab ^{22Reference 22Vollmannová A et al. · 2024ReviewQuercetin as one of the most abundant represented biological valuable plant components with remarkable chemoprotective effects — review (occurrence, biosynthesis, manufacture)View study →}.

Discovery & Synthesis

Quercetin takes its name from the oak: from quercetum (“oak forest”), itself from the genus Quercus. The name has been in use since about 1857, applied to the yellow flavonol pigment characterized from plants in the mid-nineteenth century. Nineteenth-century flavonoid nomenclature was tangled, though — quercetin, quercitrin and rutin were described and renamed by several chemists across the 1840s–60s — and no single primary publication or first isolator can be reliably pinned, so the etymology and approximate date are solid but the “who” is not ^{22Reference 22Vollmannová A et al. · 2024ReviewQuercetin as one of the most abundant represented biological valuable plant components with remarkable chemoprotective effects — review (occurrence, biosynthesis, manufacture)View study →}.

Commercially, quercetin is almost never made by total synthesis (laboratory routes to the flavonol skeleton exist but are not cost-competitive). Instead it is produced by acid hydrolysis of rutin: rutin is boiled with dilute acid, cleaving its rhamnose–glucose sugar to free the quercetin aglycone. The rutin feedstock is extracted in bulk from the flower buds of the Japanese pagoda tree (Sophora japonica, ~15–20% rutin by dry weight — the dominant global source) and the Brazilian legume fava d’anta (Dimorphandra mollis) ^{22Reference 22Vollmannová A et al. · 2024ReviewQuercetin as one of the most abundant represented biological valuable plant components with remarkable chemoprotective effects — review (occurrence, biosynthesis, manufacture)View study →}.

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

Toxicity & Safety

Oral quercetin is generally well tolerated: human trials have used up to ~1 g/day for weeks to months with adverse effects usually limited to mild GI upset, headache or tingling — and its poor absorption is, ironically, part of that safety margin. The most-cited toxicity signal is route-specific and does not apply to supplements: a 1996 Phase I oncology trial gave quercetin by intravenous bolus and hit dose-limiting renal toxicity at 1700 mg/m², with a measurable acute drop in glomerular filtration even at the recommended dose ^{24Reference 24Ferry DR et al. · 1996Clinical trialPhase I clinical trial of the flavonoid quercetin — pharmacokinetics and evidence for in vivo tyrosine kinase inhibition (intravenous; dose-limiting nephrotoxicity)View study →}. That is IV dosing that bypasses the gut and reaches plasma levels unattainable by mouth — not evidence that oral quercetin harms the kidneys.

The interactions matter more than the side effects, because quercetin is a promiscuous modulator of drug-handling enzymes and transporters. It inhibits CYP3A4 and P-glycoprotein and can disturb cyclosporine exposure — a real concern for transplant patients on that narrow-margin immunosuppressant ^{25,26Reference 25Choi JS et al. · 2004Effect of quercetin on the pharmacokinetics of oral cyclosporineView study →Reference 26Yu CP et al. · 2011Quercetin and rutin reduced the bioavailability of cyclosporine from Neoral, an immunosuppressant, through activating P-glycoprotein and CYP 3A4View study →}. A week of quercetin raised exposure to fexofenadine (a P-glycoprotein / OATP substrate) by roughly 50% in healthy volunteers ^{27Reference 27Kim KA et al. · 2009Short-term effect of quercetin on the pharmacokinetics of fexofenadine, a substrate of P-glycoprotein, in healthy volunteersView study →}. It displaces warfarin from serum albumin and inhibits CYP2C9, so caution and monitoring are prudent with anticoagulants ^{28Reference 28Poór M et al. · 2017Interaction of quercetin and its metabolites with warfarin — displacement of warfarin from serum albumin and inhibition of CYP2C9 enzymeView study →}, and its circulating conjugates themselves inhibit several CYPs plus the OATP, BCRP and MRP2 transporters ^{20Reference 20Mohos V et al. · 2020Inhibitory effects of quercetin and its main methyl, sulfate, and glucuronic acid conjugates on cytochrome P450 enzymes, and on OATP, BCRP and MRP2 transportersView study →}. A long-standing in-vitro caution — that high-dose flavonoids might antagonize fluoroquinolone antibiotics at their shared topoisomerase / gyrase target — remains theoretical rather than a documented clinical failure. Reasonable caution therefore applies to anyone on immunosuppressants, anticoagulants or multiple CYP3A4 / P-gp / OATP-substrate drugs, and to those with significant renal impairment.

Dosage

Human trials have most often used 500–1,000 mg/day of quercetin (usually the aglycone, sometimes a phytosome or glycoside form), and the recurring lesson is a dose threshold: blood-pressure, glucose and uric-acid effects appear only at ≥500 mg/day ^{1,4,9Reference 1Serban MC et al. · 2016Meta-analysisEffects of quercetin on blood pressure: a systematic review and meta-analysis of randomized controlled trials (7 RCTs, n≈587)View study →Reference 4Ostadmohammadi V et al. · 2019Meta-analysisEffects of quercetin supplementation on glycemic control among patients with metabolic syndrome and related disorders — systematic review and meta-analysis of RCTsView study →Reference 9Shi Y · 2016RCTQuercetin lowers plasma uric acid in pre-hyperuricaemic males — randomised, double-blinded, placebo-controlled, cross-over trial (n=22)View study →}. Divided or with-food dosing is common because absorption is low and glycoside-dependent.

These are doses used in research and are not a personal recommendation — appropriateness depends on the individual, their medications (see interactions above) and professional guidance. Note that better-absorbed forms (isoquercitrin, phytosome) are not interchangeable milligram-for-milligram with plain quercetin.

References

1. Serban MC, Sahebkar A, Zanchetti A, Mikhailidis DP, Howard G, Antal D, et al. (2016). Effects of quercetin on blood pressure: a systematic review and meta-analysis of randomized controlled trials (7 RCTs, n≈587). Journal of the American Heart Association, 5(7), e002713. https://pubmed.ncbi.nlm.nih.gov/27405810/
2. Huang H, Liao D, Dong Y, Pu R. (2020). Effect of quercetin supplementation on plasma lipid profiles, blood pressure, and glucose levels — systematic review and meta-analysis. Nutrition Reviews, 78(8), 615–626. https://pubmed.ncbi.nlm.nih.gov/31940027/
3. Arabi SM, Shahraki Jazinaki M, Chambari M, et al. (2023). The effects of quercetin supplementation on cardiometabolic outcomes — an umbrella review of meta-analyses of randomised controlled trials. Phytotherapy Research. https://pubmed.ncbi.nlm.nih.gov/37654199/
4. Ostadmohammadi V, Milajerdi A, Ayati E, Kolahdooz F, Asemi Z. (2019). Effects of quercetin supplementation on glycemic control among patients with metabolic syndrome and related disorders — systematic review and meta-analysis of RCTs. Phytotherapy Research, 33(5), 1330–1340. https://pubmed.ncbi.nlm.nih.gov/30848564/
5. Sahebkar A. (2017). Effects of quercetin supplementation on lipid profile — systematic review and meta-analysis of randomised controlled trials. Critical Reviews in Food Science and Nutrition, 57(4), 666–676. https://pubmed.ncbi.nlm.nih.gov/25897620/
6. Tabrizi R, Tamtaji OR, Mirhosseini N, Lankarani KB, Akbari M, Dadgostar E, et al. (2020). The effects of quercetin supplementation on lipid profiles and inflammatory markers among patients with metabolic syndrome and related disorders — systematic review and meta-analysis of RCTs. Critical Reviews in Food Science and Nutrition, 60(11), 1855–1868. https://pubmed.ncbi.nlm.nih.gov/31017459/
7. Mohammadi-Sartang M, Mazloom Z, Sherafatmanesh S, Ghorbani M, Firoozi D. (2017). Effects of supplementation with quercetin on plasma C-reactive protein concentrations — systematic review and meta-analysis of randomised controlled trials. European Journal of Clinical Nutrition, 71(9), 1033–1039. https://pubmed.ncbi.nlm.nih.gov/28537580/
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9. Shi Y, Williamson G. (2016). Quercetin lowers plasma uric acid in pre-hyperuricaemic males — randomised, double-blinded, placebo-controlled, cross-over trial (n=22). British Journal of Nutrition, 115(5), 800–806. https://pubmed.ncbi.nlm.nih.gov/26785820/
10. Di Pierro F, Iqtadar S, Khan A, Ullah Mumtaz S, Masud Chaudhry M, Bertuccioli A, et al. (2021). Potential clinical benefits of quercetin in the early stage of COVID-19 — second, pilot, randomised, controlled, open-label clinical trial. International Journal of General Medicine, 14, 2807–2816. https://pubmed.ncbi.nlm.nih.gov/34194240/
11. Ziaei S, Alimohammadi-Kamalabadi M, Hasani M, et al. (2023). The effect of quercetin supplementation on clinical outcomes in COVID-19 patients — systematic review and meta-analysis. Food Science & Nutrition. https://pubmed.ncbi.nlm.nih.gov/38107099/
12. Cheema HA, Sohail A, Fatima A, et al. (2023). Quercetin for the treatment of COVID-19 patients — systematic review and meta-analysis. Reviews in Medical Virology. https://pubmed.ncbi.nlm.nih.gov/36779438/
13. Weng Z, Zhang B, Asadi S, Sismanopoulos N, Butcher A, Fu X, et al. (2012). Quercetin is more effective than cromolyn in blocking human mast cell cytokine release and inhibits contact dermatitis and photosensitivity in humans. PLoS ONE, 7(3), e33805. https://pubmed.ncbi.nlm.nih.gov/22470478/
14. Hirano T, Kawai M, Arimitsu J, et al. (2009). Preventive effect of enzymatically modified isoquercitrin on ocular symptoms of Japanese cedar pollinosis (a quercetin glycoside derivative). Allergology International, 58(3), 419–424. https://pubmed.ncbi.nlm.nih.gov/19454839/
15. Yamada S, Shirai M, Inaba Y, et al. (2022). Effects of repeated oral intake of a quercetin-containing supplement on allergic reaction — randomised, placebo-controlled, double-blind parallel-group study. European Review for Medical and Pharmacological Sciences, 26(12). https://pubmed.ncbi.nlm.nih.gov/35776034/
16. Pelletier DM, Lacerte G, Goulet ED. (2013). Effects of quercetin supplementation on endurance performance and maximal oxygen consumption — meta-analysis (7 studies, n=288). International Journal of Sport Nutrition and Exercise Metabolism, 23(1), 73–82. https://pubmed.ncbi.nlm.nih.gov/22805526/
17. Herraiz T, Guillén H. (2018). Monoamine oxidase-A inhibition and associated antioxidant activity in plant extracts with potential antidepressant actions. BioMed Research International, 2018, 4810394. https://pubmed.ncbi.nlm.nih.gov/29568754/
18. Hollman PC, van Trijp JM, Buysman MN, van der Gaag MS, Mengelers MJ, de Vries JH, Katan MB. (1997). Relative bioavailability of the antioxidant flavonoid quercetin from various foods in man. FEBS Letters, 418(1–2), 152–156. https://pubmed.ncbi.nlm.nih.gov/9414116/
19. Graefe EU, Wittig J, Mueller S, Riethling AK, Uehleke B, Drewelow B, et al. (2001). Pharmacokinetics and bioavailability of quercetin glycosides in humans. Journal of Clinical Pharmacology, 41(5), 492–499. https://pubmed.ncbi.nlm.nih.gov/11361045/
20. Mohos V, Fliszár-Nyúl E, Ungvári O, Kuffa K, Needs PW, Kroon PA, et al. (2020). Inhibitory effects of quercetin and its main methyl, sulfate, and glucuronic acid conjugates on cytochrome P450 enzymes, and on OATP, BCRP and MRP2 transporters. Nutrients, 12(8), 2306. https://pubmed.ncbi.nlm.nih.gov/32751996/
21. Dabeek WM, Marra MV. (2019). Dietary quercetin and kaempferol: bioavailability and potential cardiovascular-related bioactivity in humans. Nutrients, 11(10), 2288. https://pubmed.ncbi.nlm.nih.gov/31557798/
22. Vollmannová A, Bojňanská T, Musilová J, et al. (2024). Quercetin as one of the most abundant represented biological valuable plant components with remarkable chemoprotective effects — review (occurrence, biosynthesis, manufacture). Heliyon, 10(13), e33342. https://pubmed.ncbi.nlm.nih.gov/39021910/
23. U.S. Department of Agriculture, Agricultural Research Service. USDA Database for the Flavonoid Content of Selected Foods, Release 3.3 (March 2018) — total quercetin, mg/100 g. https://www.ars.usda.gov/ARSUserFiles/80400535/Data/Flav/Flav3.3.pdf
24. Ferry DR, Smith A, Malkhandi J, Fyfe DW, deTakats PG, Anderson D, et al. (1996). Phase I clinical trial of the flavonoid quercetin — pharmacokinetics and evidence for in vivo tyrosine kinase inhibition (intravenous; dose-limiting nephrotoxicity). Clinical Cancer Research, 2(4), 659–668. https://pubmed.ncbi.nlm.nih.gov/9816216/
25. Choi JS, Choi BC, Choi KE (2004). Effect of quercetin on the pharmacokinetics of oral cyclosporine. American Journal of Health-System Pharmacy, 61(22), 2406–2409. https://pubmed.ncbi.nlm.nih.gov/15581264/
26. Yu CP, Wu PP, Hou YC, Lin SP, Tsai SY, Chen CT, Chao PD. (2011). Quercetin and rutin reduced the bioavailability of cyclosporine from Neoral, an immunosuppressant, through activating P-glycoprotein and CYP 3A4. Journal of Agricultural and Food Chemistry, 59(9), 4644–4648. https://pubmed.ncbi.nlm.nih.gov/21466223/
27. Kim KA, Park PW, Park JY. (2009). Short-term effect of quercetin on the pharmacokinetics of fexofenadine, a substrate of P-glycoprotein, in healthy volunteers. European Journal of Clinical Pharmacology, 65(6), 609–614. https://pubmed.ncbi.nlm.nih.gov/19221726/
28. Poór M, Boda G, Needs PW, Kroon PA, Lemli B, Bencsik T. (2017). Interaction of quercetin and its metabolites with warfarin — displacement of warfarin from serum albumin and inhibition of CYP2C9 enzyme. Biomedicine & Pharmacotherapy, 88, 574–581. https://pubmed.ncbi.nlm.nih.gov/28135601/
29. Muzitano MF, Falcão CA, Cruz EA, Bergonzi MC, Bilia AR, Vincieri FF, Rossi-Bergmann B, Costa SS (2009). Oral metabolism and efficacy of Kalanchoe pinnata flavonoids in a murine model of cutaneous leishmaniasis — mouse in vivo animal model. Planta Medica. https://pubmed.ncbi.nlm.nih.gov/19085683/

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