Kaempferol

Pharmacology & Research

Kaempferol is a common dietary flavonol — structurally quercetin minus one hydroxyl — found across most edible plants. It has an unusual evidence profile for a molecule this well known: there are no randomised controlled trials of isolated kaempferol for any indication. What exists is (1) dietary epidemiology — cohort studies associating higher kaempferol intake with lower risk of certain cancers and cardiovascular death — and (2) a large preclinical (cell and animal) literature on its anticancer and anti-inflammatory mechanisms. Neither is the same as a demonstrated effect of taking the compound, and both are undercut by the fact that also limits quercetin: kaempferol is poorly absorbed (oral bioavailability ~2%), circulating almost entirely as conjugated metabolites at sub-micromolar levels far below the concentrations used in the cell studies ^{16,17,18Reference 16Barve A et al. · 2009AnimalMetabolism, oral bioavailability and pharmacokinetics of chemopreventive kaempferol in rats (~2% oral bioavailability)View study →Reference 17DuPont MS et al. · 2004Absorption of kaempferol from endive, a source of kaempferol-3-glucuronide, in humans (Cmax ~0.1 µM)View study →Reference 18Dabeek WM · 2019ReviewDietary quercetin and kaempferol: bioavailability and potential cardiovascular-related bioactivity in humans — reviewView study →}. Read what follows as association and mechanism, not efficacy.

1. Cancer risk (epidemiology)

Kaempferol’s best human evidence — and it is still only associational. In the Nurses’ Health Study prospective cohort (66,940 women), higher intake of kaempferol and luteolin was associated with lower ovarian cancer risk, strongest for serous tumours ^{1Reference 1Gates MA et al. · 2007A prospective study of dietary flavonoid intake and incidence of epithelial ovarian cancerView study →}, and pooled meta-analyses of flavonoid subclasses corroborate a modest inverse flavonol–ovarian association ^{2,3Reference 2Hua X et al. · 2016Meta-analysisAssociation among dietary flavonoids, flavonoid subclasses and ovarian cancer risk — a meta-analysisView study →Reference 3Naghshi S et al. · 2016Systematic reviewOvarian cancer risk and non-isoflavone flavonoids intake — a systematic review of epidemiological studiesView study →}. A meta-analysis of epidemiological studies also linked higher dietary flavonol intake to reduced gastric cancer risk ^{4Reference 4Xie Y et al. · 2016Meta-analysisDietary flavonols intake and risk of esophageal and gastric cancer — a meta-analysis of epidemiological studiesView study →}, consistent with broader flavonoid-food cohort work ^{5Reference 5Cutler GJ et al. · 2008Dietary flavonoid intake and risk of cancer in postmenopausal women (Iowa Women’s Health Study)View study →}.

Gap: these are associations for dietary flavonol intake estimated from food-frequency questionnaires, not administered kaempferol; effect sizes are modest (relative risks ~0.75–0.90), kaempferol-specific estimates are imprecise, and residual confounding from overall vegetable/fruit intake is unresolved. No trial has tested whether raising kaempferol intake changes cancer incidence ^{1,4Reference 1Gates MA et al. · 2007A prospective study of dietary flavonoid intake and incidence of epithelial ovarian cancerView study →Reference 4Xie Y et al. · 2016Meta-analysisDietary flavonols intake and risk of esophageal and gastric cancer — a meta-analysis of epidemiological studiesView study →}.

2. Cardiovascular & mortality

A meta-analysis of prospective cohorts found higher total flavonoid intake associated with lower cardiovascular and all-cause mortality — but the flavonol subclass specifically did not reach significance in that pooling, an honest weakness ^{6Reference 6Kim Y · 2017Meta-analysisFlavonoid intake and mortality from cardiovascular disease and all causes — a meta-analysis of prospective cohort studiesView study →}. Larger syntheses and a 2024 umbrella review report inverse associations for total flavonoids and several subclasses with mortality, with kaempferol among the compounds linked to lower CVD risk in some cohorts ^{7,8Reference 7Grosso G et al. · 2020Meta-analysisA greater flavonoid intake is associated with lower total and cause-specific mortality — a meta-analysis of cohort studiesView study →Reference 8Zhao Y et al. · 2024Meta-analysisDietary flavonoids consumption and health — an umbrella review of meta-analysesView study →}.

Gap: associational and subclass-inconsistent, confounded by the healthy-diet patterns that accompany high flavonoid intake. No interventional confirmation exists for the isolate ^{6,8Reference 6Kim Y · 2017Meta-analysisFlavonoid intake and mortality from cardiovascular disease and all causes — a meta-analysis of prospective cohort studiesView study →Reference 8Zhao Y et al. · 2024Meta-analysisDietary flavonoids consumption and health — an umbrella review of meta-analysesView study →}.

3. Anti-inflammatory & metabolic

Mechanistically rich but entirely cell and animal. Kaempferol activates Nrf2 and inhibits NF-κB in rodent organ-injury models — protecting against cadmium-induced liver and kidney damage ^{9,10Reference 9Alalaiwe A et al. · 2022Kaempferol prevents cadmium-chloride-induced liver damage by upregulating Nrf2 and suppressing NF-κBView study →Reference 10Alshehri AS et al. · 2022The ameliorative effect of kaempferol against CdCl2-mediated renal damage entails activation of Nrf2 and inhibition of NF-κBView study →} — and attenuated angiotensin-II-induced cardiac remodelling and hyperglycaemia-induced cardiac injury in rodents, via reduced inflammation and oxidative stress ^{11,12Reference 11Feng H et al. · 2019Kaempferol prevents against angiotensin-II-induced cardiac remodelling by attenuating inflammation and oxidative stressView study →Reference 12Chen X et al. · 2018Kaempferol attenuates hyperglycemia-induced cardiac injuries by inhibiting inflammatory responses and oxidative stressView study →}.

Gap: no human dosing at all, and kaempferol’s ~2% bioavailability means these in-vivo potencies may not translate. This is preclinical signal, not clinical effect ^{9,12Reference 9Alalaiwe A et al. · 2022Kaempferol prevents cadmium-chloride-induced liver damage by upregulating Nrf2 and suppressing NF-κBView study →Reference 12Chen X et al. · 2018Kaempferol attenuates hyperglycemia-induced cardiac injuries by inhibiting inflammatory responses and oxidative stressView study →}.

4. Anticancer activity

A strong, consistent laboratory signal — pro-apoptotic, cell-cycle arrest, anti-angiogenic — reviewed comprehensively ^{13Reference 13Chen AY · 2013ReviewA review of the dietary flavonoid kaempferol on human health and cancer chemopreventionView study →}; for example, kaempferol inhibited gastric-cancer growth in vitro and in xenograft mice ^{14Reference 14Song H et al. · 2015In vitroKaempferol inhibits gastric cancer tumour growth — an in vitro and in vivo studyView study →}.

Gap: this is mechanism, not clinical effect. Direct human anticancer efficacy of isolated kaempferol is 0% — there is none. Do not read the laboratory potency as a treatment claim ^{13Reference 13Chen AY · 2013ReviewA review of the dietary flavonoid kaempferol on human health and cancer chemopreventionView study →}.

Mechanisms

Target / pathway	Nature of evidence	Relevant to
Nrf2 activation / antioxidant (↑ HO-1, phase-II enzymes)	rodent organ-injury models	anti-inflammatory & metabolic, anticancer
NF-κB inhibition (↓ pro-inflammatory cytokines)	animal / in vitro	anti-inflammatory & metabolic
Pro-apoptotic / cell-cycle arrest / anti-angiogenic	in vitro + xenograft	anticancer
MAO-A inhibition (selective, sub-µM in isolated enzyme)	in-vitro enzymology	neuroprotective / mood (hypothetical)
Estrogen / ERR / AhR & progestin-receptor modulation	in vitro / animal	hormone-related cancers, safety

Almost all of these are demonstrated at 10–100 µM of free aglycone in vitro — well above the ~0.1 µM free plasma levels kaempferol reaches in people (see Pharmacokinetics), so mechanism-to-clinic extrapolation should be cautious.

Pharmacokinetics

Kaempferol is a textbook poorly-bioavailable flavonol, and its pharmacokinetics mirror quercetin’s. In a controlled rat study, oral kaempferol reached the circulation with an absolute bioavailability of only ~2%, peaking at ~1–2 h with a terminal half-life of ~3–4 h — the low figure driven by extensive first-pass metabolism in the gut wall and liver, not by poor uptake ^{16Reference 16Barve A et al. · 2009AnimalMetabolism, oral bioavailability and pharmacokinetics of chemopreventive kaempferol in rats (~2% oral bioavailability)View study →}. What circulates is not free aglycone but phase-II conjugates (glucuronides, sulfates, methylated forms) ^{16,18Reference 16Barve A et al. · 2009AnimalMetabolism, oral bioavailability and pharmacokinetics of chemopreventive kaempferol in rats (~2% oral bioavailability)View study →Reference 18Dabeek WM · 2019ReviewDietary quercetin and kaempferol: bioavailability and potential cardiovascular-related bioactivity in humans — reviewView study →}.

Form matters, because kaempferol occurs in food almost entirely as glycosides — astragalin (3-glucoside), nicotiflorin (3-rutinoside), kaempferitrin, and others — and the attached sugar dictates where it can be freed for absorption: glucosides are cleaved in the small intestine, whereas rutinosides and rhamnosides must reach the colon for bacterial glycosidases to release the aglycone ^{18Reference 18Dabeek WM · 2019ReviewDietary quercetin and kaempferol: bioavailability and potential cardiovascular-related bioactivity in humans — reviewView study →}. This shows in humans: after a ~9 mg dose from endive (which supplies kaempferol-3-glucuronide), peak plasma concentration was only ~0.1 µM at a Tmax of ~5.8 h, and kaempferol-3-glucuronide was the predominant species in plasma and urine ^{17Reference 17DuPont MS et al. · 2004Absorption of kaempferol from endive, a source of kaempferol-3-glucuronide, in humans (Cmax ~0.1 µM)View study →}. That sets up the crucial gap — mechanistic studies use 10–100 µM, but achievable free-aglycone levels sit near 0.1 µM, so laboratory potencies routinely cannot be reproduced at realistic exposures ^{16,17Reference 16Barve A et al. · 2009AnimalMetabolism, oral bioavailability and pharmacokinetics of chemopreventive kaempferol in rats (~2% oral bioavailability)View study →Reference 17DuPont MS et al. · 2004Absorption of kaempferol from endive, a source of kaempferol-3-glucuronide, in humans (Cmax ~0.1 µM)View study →}. Kaempferol is also metabolically interconverted: human liver microsomes hydroxylate it at the 3′-position to yield quercetin (mainly via CYP1A2/2C9), the one-hydroxyl difference between the two flavonols ^{19,20Reference 19Otake Y · 2002Oxidation of the flavonoids galangin and kaempferide by human liver microsomes and CYP1A1, CYP1A2, and CYP2C9 (kaempferol ↔ quercetin interconversion)View study →Reference 20Breinholt VM et al. · 2002In vitroIn vitro investigation of cytochrome P450-mediated metabolism of dietary flavonoidsView study →}.

Clinical trials

Kaempferol has no completed efficacy trials as an isolated molecule — a defining fact of its evidence base. The only controlled human study is a short safety trial; everything else is dietary-intake epidemiology (which tests food patterns, not the compound) or preclinical.

Efficacy trials (isolate)	Safety trials	Planned	Preclinical
None	1 (4-week, 50 mg/day)	—	Extensive

Last checked: July 2026.

Monoamine oxidase (MAO) inhibition

Kaempferol is one of the more active dietary flavonols against monoamine oxidase — reported as a selective, MAO-A-preferring inhibitor with sub-micromolar potency in isolated-enzyme work (an IC50 on the order of ~0.7 µM against MAO-A, much weaker on MAO-B) ^{15Reference 15Sinreih M et al. · 2016Kaempferol as a selective human MAO-A inhibitor — analytical detection and enzyme assayView study →}. As with the other flavonoids this is a genuine but modest activity next to the β-carboline inhibitors, and given kaempferol’s very low systemic and brain exposure it is best read as an in-vitro property, not an established clinical effect. See the natural MAO inhibitors guide for context.

Isolate vs. Plant Studies

Kaempferol’s evidence is almost never about the pure molecule, in three overlapping senses.

First, the human evidence is about diet, not the compound. The cancer and mortality findings estimate dietary kaempferol intake from food-frequency questionnaires across whole diets ^{1,6Reference 1Gates MA et al. · 2007A prospective study of dietary flavonoid intake and incidence of epithelial ovarian cancerView study →Reference 6Kim Y · 2017Meta-analysisFlavonoid intake and mortality from cardiovascular disease and all causes — a meta-analysis of prospective cohort studiesView study →} — a proxy several steps removed from a measured dose of kaempferol, and one that co-varies with overall fruit and vegetable intake. No one has given people the isolated molecule and measured an outcome.

Second, in plants kaempferol is stored as glycosides, not the free aglycone — astragalin, nicotiflorin, kaempferitrin, afzelin — which absorb differently and are what a “kaempferol-containing” herb actually delivers ^{18Reference 18Dabeek WM · 2019ReviewDietary quercetin and kaempferol: bioavailability and potential cardiovascular-related bioactivity in humans — reviewView study →}. Across this database kaempferol is named in the antioxidant flavonoid fraction of many herbs — ginkgo, hibiscus, horsetail, raspberry leaf, amaranth and others — almost always as a contributor to a whole-extract effect rather than an isolated-compound result, and frequently as a glycoside. Two repo findings that are isolate-level actually concern distinct glycoside molecules, not the aglycone: kaempferitrin (kaempferol-3,7-dirhamnoside) showed antitumour activity in an epazote study, and a kaempferol rhamnoside (afzelin) was a hepatoprotective isolate from chanca-piedra — worth their own entries, not merged into kaempferol.

Third, the preclinical mechanism uses concentrations the body doesn’t reach ^{16,17Reference 16Barve A et al. · 2009AnimalMetabolism, oral bioavailability and pharmacokinetics of chemopreventive kaempferol in rats (~2% oral bioavailability)View study →Reference 17DuPont MS et al. · 2004Absorption of kaempferol from endive, a source of kaempferol-3-glucuronide, in humans (Cmax ~0.1 µM)View study →}. So a whole-plant antioxidant effect, a dietary-intake association, and a 50 µM cell result are three different things — read each on its own terms.

Prevalence in Nature

Kaempferol is one of the most widely distributed flavonols in the plant kingdom, spanning hundreds of species and many families — prominently Brassicaceae (kale, broccoli, arugula, cress, mustard), Capparaceae (capers), Alliaceae (chives, leek), Apiaceae (dill, fennel), Asteraceae (endive, chicory), Amaranthaceae (spinach, chard), Iridaceae (saffron) and Theaceae (tea), plus many medicinal genera (Ginkgo, Sophora, Tilia, Equisetum) ^{28Reference 28Calderón-Montaño JM et al. · 2011ReviewA review on the dietary flavonoid kaempferol (distribution, glycosides, occurrence, name)View study →}. It accumulates in leaves, flowers, flower buds and pollen, where flavonols act as UV screens and antioxidants — and, crucially, it occurs overwhelmingly as glycosides, not free aglycone: astragalin (3-glucoside), trifolin (3-galactoside), nicotiflorin (3-rutinoside), afzelin (3-rhamnoside) and kaempferitrin (3,7-dirhamnoside). Food-composition figures are measured after acid hydrolysis, so tabulated “kaempferol” values are total aglycone released from those glycosides ^{18Reference 18Dabeek WM · 2019ReviewDietary quercetin and kaempferol: bioavailability and potential cardiovascular-related bioactivity in humans — reviewView study →}.

Concentrations span roughly three orders of magnitude. The richest sources are capers and saffron (both very high — but note capers are raw flower buds and saffron is a dried spice, so those figures aren’t directly comparable to the fresh greens), followed by cruciferous and leafy greens (arugula, spinach, kale, mustard), culinary herbs (dill, chives), beans, broccoli and tea — see the Content-by-Source chart ^{30Reference 30U.S et al. · 2011U.S. Department of Agriculture, Agricultural Research Service. USDA Database for the Flavonoid Content of Selected Foods, Release 3 (2011) — kaempferol, mg/100 g. https://www.ars.usda.gov/arsuserfiles/80400525/data/flav/flav_r03.pdfView study →}.

Biosynthetically, kaempferol is a phenylpropanoid → flavonoid end-product: naringenin is hydroxylated by flavanone 3-hydroxylase to dihydrokaempferol, which flavonol synthase desaturates to kaempferol ^{29Reference 29Winkel-Shirley B · 2001Flavonoid biosynthesis — a colourful model for genetics, biochemistry, cell biology and biotechnology (CHS/F3H/FLS/F3′H pathway)View study →}. The key branch point is the B-ring: if flavonoid 3′-hydroxylase (F3′H) adds a second hydroxyl, the product is quercetin instead — so a tissue’s kaempferol:quercetin ratio is a readout of F3′H activity, and the two flavonols are routinely co-produced ^{29Reference 29Winkel-Shirley B · 2001Flavonoid biosynthesis — a colourful model for genetics, biochemistry, cell biology and biotechnology (CHS/F3H/FLS/F3′H pathway)View study →}. There is essentially no non-plant source: animals and ordinary bacteria do not make it (engineered microbes can, but that is lab production, not a dietary reservoir).

Discovery & Synthesis

Kaempferol is an eponym honouring the German physician-naturalist Engelbert Kaempfer (1651–1716), who carried botanical knowledge from Japan and Persia to Europe; Linnaeus named the ginger-family genus Kaempferia after him, and the flavonol — abundant in Kaempferia galanga alongside its methylated cousin kaempferide — took the stem “kaempfer-” plus the “-ol” phenol suffix ^{28Reference 28Calderón-Montaño JM et al. · 2011ReviewA review on the dietary flavonoid kaempferol (distribution, glycosides, occurrence, name)View study →}. Secondary sources consistently report a first isolation in 1902, from larkspur (Delphinium consolida), by A. G. Perkin and E. J. Wilkinson; this is chronologically plausible (Perkin was the leading flavonol chemist of the era) but predates the modern literature index and could not be verified against a primary source, so treat the date as commonly-cited rather than settled.

Structurally kaempferol is 3,4′,5,7-tetrahydroxyflavone — quercetin minus one B-ring hydroxyl (quercetin has an extra 3′-OH), the same difference that lets liver enzymes convert kaempferol into quercetin ^{19Reference 19Otake Y · 2002Oxidation of the flavonoids galangin and kaempferide by human liver microsomes and CYP1A1, CYP1A2, and CYP2C9 (kaempferol ↔ quercetin interconversion)View study →}. Commercially it is not made by total synthesis: the routine routes are extraction from flavonol-rich plant biomass (tea seed, Ginkgo, Sophora, capers) — usually followed by enzymatic hydrolysis of its glycosides to free the scarce aglycone — with engineered-microbe biosynthesis emerging as a still-pre-commercial alternative ^{28Reference 28Calderón-Montaño JM et al. · 2011ReviewA review on the dietary flavonoid kaempferol (distribution, glycosides, occurrence, name)View study →}.

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

Toxicity & Safety

As a widely eaten dietary flavonol (kale, capers, tea, broccoli, beans), kaempferol is regarded as low-toxicity, and ordinary food intake carries no established hazard. Isolated-kaempferol human safety data are sparse but not absent: a randomised, double-blind, placebo-controlled trial found 50 mg/day of the aglycone for 4 weeks (roughly five times typical dietary intake) produced no adverse events and no clinically significant changes in blood pressure or blood/urine parameters in healthy adults ^{21Reference 21Akiyama M et al. · 2023RCTA randomised, placebo-controlled trial evaluating the safety of excessive administration of kaempferol aglycone (50 mg/day, 4 weeks)View study →}. Beyond that short, low-dose study, long-term and high-dose safety in humans is uncharacterised.

The interaction signals are mostly in-vitro and unlikely to matter from food, but worth noting for concentrated supplements. Kaempferol is metabolised by, and inhibits, several CYP enzymes (CYP1A2/2C9/3A4) in the tens-of-micromolar range ^{19,20Reference 19Otake Y · 2002Oxidation of the flavonoids galangin and kaempferide by human liver microsomes and CYP1A1, CYP1A2, and CYP2C9 (kaempferol ↔ quercetin interconversion)View study →Reference 20Breinholt VM et al. · 2002In vitroIn vitro investigation of cytochrome P450-mediated metabolism of dietary flavonoidsView study →}, and it inhibits the efflux transporters P-glycoprotein and BCRP/ABCG2 in vitro ^{26,27Reference 26Limtrakul P et al. · 2005Inhibition of P-glycoprotein function and expression by kaempferol and quercetinView study →Reference 27Imai Y et al. · 2004Phytoestrogens/flavonoids reverse breast cancer resistance protein (BCRP/ABCG2)-mediated multidrug resistanceView study →} — a plausible (if unproven) interaction with narrow-therapeutic-index substrates of those systems, chiefly at the gut wall where enterocyte concentrations can exceed plasma levels. The more distinctive flag is endocrine activity: kaempferol is a phytoestrogen with biphasic estrogenic effects, an inverse agonist of estrogen-related receptors ERRα/γ ^{22Reference 22Wang J et al. · 2009Kaempferol is an estrogen-related receptor α and γ inverse agonistView study →}, a phytoprogestin with progestogenic effects and uterine gene regulation in animals ^{23,24Reference 23Toh MF et al. · 2014AnimalKaempferol exhibits progestogenic effects in ovariectomised ratsView study →Reference 24Bergsten TM et al. · 2023Kaempferol, a phytoprogestin, induces a subset of progesterone-regulated genes in the uterusView study →}, and an aryl-hydrocarbon-receptor antagonist ^{25Reference 25Macpherson L · 2010Inhibition of aryl-hydrocarbon-receptor-dependent transcription by resveratrol or kaempferol is independent of estrogen receptor α expression in human breast cancer cellsView study →}. These argue for caution in hormone-sensitive conditions and with hormonal therapies.

Dosage

There is no evidence-based dose for kaempferol, because no trial has tested it for efficacy. The only human dosing data are a safety trial (50 mg/day of the aglycone for 4 weeks, well tolerated) ^{21Reference 21Akiyama M et al. · 2023RCTA randomised, placebo-controlled trial evaluating the safety of excessive administration of kaempferol aglycone (50 mg/day, 4 weeks)View study →} and typical dietary intakes, which are on the order of a few to ~30 mg/day depending on vegetable and tea consumption. Because absorption is low and glycoside-dependent, even those amounts produce only sub-micromolar plasma levels ^{17Reference 17DuPont MS et al. · 2004Absorption of kaempferol from endive, a source of kaempferol-3-glucuronide, in humans (Cmax ~0.1 µM)View study →}.

These figures are descriptive, not a recommendation — no dose has been shown to do anything in a human trial. Anyone considering a concentrated supplement should note the endocrine and transporter signals above and seek professional guidance.

References