This page on Kaempferol is currently marked as in-progress. We are still compiling research.
You can help contribute by:
Kaempferol is one of the many flavonoids found in foods alongside others like luteolin and Quercetin. It is showing promise in and of itself in being an anti-obesity agent and anti-cancer agent.
Research on kaempferol is scarce in humans in supplemental form, but in vitro research seems promising.
Follow this Page for updates
Kaempferol, as a polyphenol, is present in many compounds. Common sources include:
The bioavailability of an oral load of kaempferol appears to be about 2% relative to an IV injection, 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. 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. Higher doses have a slightly delated max peak at 60-90 minutes. 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.
In bone cells, the Cmax of Kaempferol is 0.684nM after 90 minutes.
Chronic feeding (at 5mg/kg bodyweight) results in levels of 0.311nM after 4 weeks and 0.838nM after 12 weeks in rats.
The liver appears to be more readily active on kaempferol than do the intestines, as assessed by a higher Vmax. 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. When kaempferol undergoes Phase I oxidation, it becomes Quercetin, and when it gets conjugated kaempferol becomes primarily Kaempferol-7O-glucuronide although up to four glucuronides have been noted, including Astragalin (Kaempferol-3O-glucoside). Glucuronidation is primarily undertaken by UGT1A3 and UGT1A9.
Kaempferol possesses the ability to block the enzyme NAPDH oxidase (NOX), and act as a neuroprotectant against degeneration processes mediated by the NOX enzyme,  such as 4-HNE, a product created from lipid peroxidation of cellular membranes and Advanced Glycemic End-products at an oral dose of 2-4mg/kg bodyweight in rats.
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 and has been suspected as being as potent as insulin in this regard.
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. 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.
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. 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.
Possible inhibition of PPARγ induced by other agonists thereof
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. It works with insulin, and has no effect without insulin stimulation.
Kaempferol appears to have some affinity for the alpha subset of the estrogen receptor (ERα) with an IC50 of 8.2µM 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 which appears to be comparable or slightly less than some other flavonoids (8-prenylnaringenin and Apigenin) and significantly less than the Soy Isoflavones genistein (0.025-0.09), daidzein (0.1-1.20) and the S-equol metabolite (16-110pM).
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)
When in the hull of red and pinto beans, free kaempferol (but not the glycoside) seems to inhibit iron absorption. 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.
(Common misspellings for Kaempferol include kampherol, kampferol, kaempherol)
(Common phrases used by users for this page include red bean medicine interactions, kaempytarl, kaempferol supplements, kaempferol glucose structure, kaemferol fatty acid, beninger cw)