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Kaempferol is one of the bioflavonoids that is present in high levels in cruciferous vegetables, and may mediate some of the bioactivities of these plants. It appears to hold anti-cancer potential.

Our evidence-based analysis on kaempferol features 25 unique references to scientific papers.

Research analysis led by and reviewed by the Examine team.
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Research Breakdown on Kaempferol

1Sources and Structure


Kaempferol, as a polyphenol, is present in many compounds. Common sources include:

  • Apples

  • Citris Fruits

  • Grapes and red wine

  • Onions and leeks

  • Tea (camellia sinensis)

  • Ginkgo Bilboa and St.Johns Wort

  • Nymphaea odorata[1]

  • Alpinia officinarum hance, or Galangal Extract[2]

  • Hedyotis verticillata (Source of kaempferitrin, kaempferol's rhamnoside sugar form)

  • Red beans and pinto beans (husk)[3] generally the species of bean Phaseolus Vulgaris.[4]



The bioavailability of an oral load of kaempferol appears to be about 2% relative to an IV injection,[5] with most detectable molecules becoming quercetin, conjugated kaempferol, or isorhamnetin (3-O' methylated Quercetin).

About 3-4% of an oral dose of kaempferol (after 100mg/kg ingestion) appears to be excreted in the urine as free kaempferol.[5] The majority of the urinary metabolites appear to be glucuronides.


After a 1mg/kg bodyweight dose of Kaempferol in rats, a Cmax of 2.04+/-0.8nM was reached in serum after 30 minutes.[6] Higher doses have a slightly delated max peak at 60-90 minutes.[5] Approximately half of orally ingested Kaempferol is removed from the serum 4 hours after ingestion, and no free Kaempferol can be detected 6 hours even after a 250mg/kg bodyweight dose.[5]

In bone cells, the Cmax of Kaempferol is 0.684nM after 90 minutes.[6]

Chronic feeding (at 5mg/kg bodyweight) results in levels of 0.311nM after 4 weeks and 0.838nM after 12 weeks in rats.[6]

2.3Interactions with P450

The liver appears to be more readily active on kaempferol than do the intestines, as assessed by a higher Vmax.[5] This was paired with a lower Km for hepatic microsomes relative to intestinal, suggesting more importance for the liver in the P450 metabolism of kaempferol.

Metabolic clearance via UDPGA conjugation appears to happen more readily than does Phase I oxidation.[5] When kaempferol undergoes Phase I oxidation, it becomes Quercetin,[7][5] and when it gets conjugated kaempferol becomes primarily Kaempferol-7O-glucuronide[8][9] although up to four glucuronides have been noted, including Astragalin (Kaempferol-3O-glucoside).[5] Glucuronidation is primarily undertaken by UGT1A3 and UGT1A9.[8]



Kaempferol possesses the ability to block the enzyme NAPDH oxidase (NOX), and act as a neuroprotectant against degeneration processes mediated by the NOX enzyme, [10] such as 4-HNE, a product created from lipid peroxidation of cellular membranes[10] and Advanced Glycemic End-products at an oral dose of 2-4mg/kg bodyweight in rats.[11]

4Interactions with Glucose Metabolism

4.1Glucose Uptake

Kaempferol, possibly through the metabolite kaempferol 3-neohesperidoside, may increase glucose uptake into myocytes via processes mediated by phosphatidylinositol 3-kinase (PI3K) and protein kinase C (PKC) pathways[12][13] and has been suspected as being as potent as insulin in this regard.[14]

5Skeletal and Joint Health


Similar to myricetin, Kaempferol prevents against oxidation in in vitro bone cells and may exert anti-osteoporotic effects.[15]

6Fat Mass and Obesity


Kaempferol's inhibitory activity on Fatty Acid Synthase(FASN), the sole enzyme responsible for de novo lipogenesis, is via acting as an inhibitor of the FASN cascade, which uses the two substrate malonyl-CoA and acetyl-Coa along with NAPDH to ultimately produce palmitate.[16] Out of tested polyphenols, Kaempferol's inhibition of FASN was more potent than that of Green Tea Catechins, Apigenin and Taxifolin but less than that of quercetin and luteolin, of which the latter was the most inhibitory.[16]

Kaempferol may inhibit they fatty acid synthase enzyme associated with production of fatty acids from glucose

Kaempferol (as well as Quercetin) are able to inhibit PPARγ activation of adipogenesis by rosiglitazone and other endogenous ligands by having high affinity to the receptor but low potency to activate it.[17] Kaempferol appeared to activate PPARγ at most of 45% relative to rosiglitazone whilst Quercetin maxed at 20%, and neither induced adipocyte differentiation at concentrations ranging from 5-50µM.

Over the long term, Kaempferol may reduce adipocyte formation by causing its stem cell (bone marrow cells) to favor osteogenesis (bone forming) rather than fat cell forming.[6]

Possible inhibition of PPARγ induced by other agonists thereof

6.2Glucose Uptake

Kaempferol is able to increase glucose uptake into a lab model of immortal adipocytes (3T3-L1), which suggests it may be able to reduce serum glucose levels and act as an anti-diabetic agent.[17] It works with insulin, and has no effect without insulin stimulation.

7Interactions with Hormones


Kaempferol appears to have some affinity for the alpha subset of the estrogen receptor (ERα) with an IC50 of 8.2µM[18] and also appears to have affinity for the beta subset of the estrogen receptor (ERβ) with an IC50 in the range of 50pM to 50µM[18][19] which appears to be comparable or slightly less than some other flavonoids (8-prenylnaringenin[20] and apigenin[19]) and significantly less than the soy isoflavones genistein (0.025-0.09), daidzein (0.1-1.20) and the S-equol metabolite (16-110pM).[21]

8Interactions with Cancer Metabolism


Vicariously through its inhibitory effects on the FASN enzyme, Kaempferol shows promise in being able to inhibit certain types of cancer from developing. This is suspected to be due to a correlation between FASN activity being upregulated in cancer cells (due to a possible need for excess fatty acids for cell membrance production) and an apparent cytotoxic effect noted in cancer cells (but not normal cells) when the FASN precursor, Malonyl-CoA, hits supra-physiological levels. (Although other mechanisms are still under investigation)[22][23]

9Nutrient-Nutrient Interactions


When in the hull of red and pinto beans, free kaempferol (but not the glycoside) seems to inhibit iron absorption.[3] The addition of Ascorbic Acid (Vitamin C) did not increase bioavailability, and the inhibitory effect of kaempferol ranged from 15.5%-62.8% with concentrations of 40-1000uM, with inhibition potential as low as 0.37mM.[24]

Quercetin appeared to have a larger inhibition effect than did Kaempferol.[3] These inhibitory effects may be related to Kaempferol and Quercetin's ability to chelate metals by forming complexes.

The above interactions are behind the general idea of white beans, or foods low in flavonoid content, in having more bioavailable iron despite lower iron contents.[3][25]


  1. ^ Zhang Z, et al. Phenolic compounds from Nymphaea odorata. J Nat Prod. (2003)
  2. ^ Li BH, Tian WX. Presence of fatty acid synthase inhibitors in the rhizome of Alpinia officinarum hance. J Enzyme Inhib Med Chem. (2003)
  3. ^ a b c d Hu Y, et al. Kaempferol in red and pinto bean seed (Phaseolus vulgaris L.) coats inhibits iron bioavailability using an in vitro digestion/human Caco-2 cell model. J Agric Food Chem. (2006)
  4. ^ Beninger CW, Hosfield GL, Nair MG. Flavonol glycosides from the seed coat of a new manteca-type dry bean (Phaseolus vulgaris L.. J Agric Food Chem. (1999)
  5. ^ a b c d e f g h Barve A, et al. Metabolism, oral bioavailability and pharmacokinetics of chemopreventive kaempferol in rats. Biopharm Drug Dispos. (2009)
  6. ^ a b c d Trivedi R, et al. Kaempferol has osteogenic effect in ovariectomized adult Sprague-Dawley rats. Mol Cell Endocrinol. (2008)
  7. ^ Nielsen SE, et al. In vitro biotransformation of flavonoids by rat liver microsomes. Xenobiotica. (1998)
  8. ^ a b Chen Y, et al. Glucuronidation of flavonoids by recombinant UGT1A3 and UGT1A9. Biochem Pharmacol. (2008)
  9. ^ Yodogawa S, et al. Glucurono- and sulfo-conjugation of kaempferol in rat liver subcellular preparations and cultured hepatocytes. Biol Pharm Bull. (2003)
  10. ^ a b Jang YJ, et al. Kaempferol attenuates 4-hydroxynonenal-induced apoptosis in PC12 cells by directly inhibiting NADPH oxidase. J Pharmacol Exp Ther. (2011)
  11. ^ Kim JM, et al. Kaempferol modulates pro-inflammatory NF-kappaB activation by suppressing advanced glycation endproducts-induced NADPH oxidase. Age (Dordr). (2010)
  12. ^ Zanatta L, et al. Insulinomimetic effect of kaempferol 3-neohesperidoside on the rat soleus muscle. J Nat Prod. (2008)
  13. ^ Cazarolli LH, et al. Signaling pathways of kaempferol-3-neohesperidoside in glycogen synthesis in rat soleus muscle. Biochimie. (2009)
  14. ^ Jorge AP, et al. Insulinomimetic effects of kaempferitrin on glycaemia and on 14C-glucose uptake in rat soleus muscle. Chem Biol Interact. (2004)
  15. ^ Suh KS, et al. Kaempferol attenuates 2-deoxy-d-ribose-induced oxidative cell damage in MC3T3-E1 osteoblastic cells. Biol Pharm Bull. (2009)
  16. ^ a b Brusselmans K, et al. Induction of cancer cell apoptosis by flavonoids is associated with their ability to inhibit fatty acid synthase activity. J Biol Chem. (2005)
  17. ^ a b Fang XK, Gao J, Zhu DN. Kaempferol and quercetin isolated from Euonymus alatus improve glucose uptake of 3T3-L1 cells without adipogenesis activity. Life Sci. (2008)
  18. ^ a b The Flavonoid Kaempferol Is Responsible for the Majority of Estrogenic Activity in Red Wine.
  19. ^ a b Han DH, et al. Relationship between estrogen receptor-binding and estrogenic activities of environmental estrogens and suppression by flavonoids. Biosci Biotechnol Biochem. (2002)
  20. ^ Milligan SR, et al. Identification of a potent phytoestrogen in hops (Humulus lupulus L.) and beer. J Clin Endocrinol Metab. (1999)
  21. ^ Hajirahimkhan A, Dietz BM, Bolton JL. Botanical modulation of menopausal symptoms: mechanisms of action. Planta Med. (2013)
  22. ^ Lupu R, Menendez JA. Pharmacological inhibitors of Fatty Acid Synthase (FASN)--catalyzed endogenous fatty acid biogenesis: a new family of anti-cancer agents. Curr Pharm Biotechnol. (2006)
  23. ^ Marfe G, et al. Kaempferol induces apoptosis in two different cell lines via Akt inactivation, Bax and SIRT3 activation, and mitochondrial dysfunction. J Cell Biochem. (2009)
  24. ^ Laparra JM, Glahn RP, Miller DD. Bioaccessibility of phenols in common beans ( Phaseolus vulgaris L.) and iron (Fe) availability to Caco-2 cells. J Agric Food Chem. (2008)
  25. ^ Lung'aho MG, Glahn RP. Use of white beans instead of red beans may improve iron bioavailability from a Tanzanian complementary food mixture. Int J Vitam Nutr Res. (2010)