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    CAS No. 520-18-3 Price $30 / 20mg
    Catalog No.CFN98838Purity>=98%
    Molecular Weight286.2 Type of CompoundFlavonoids
    FormulaC15H10O6Physical DescriptionYellow powder
    Download Manual    COA    MSDSSimilar structuralComparison (Web)
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    Biological Activity
    Description: 1. Kaempferol activates LXR-β and suppresses SREBP-1 to enhance symptoms in metabolic syndrome.
    2. Kaempferol exerts a potent inhibitory effect on in vitro bone resorption.
    3. Kaempferol has anti-inflammatory action, can prevent and treat inflammatory diseases such as rheumatoid arthritis, systemic lupus erythematosus, and ankylosing spondylitis.
    4. Kaempferol has therapeutic potential for the prevention and treatment of thrombovascular diseases, can enhance relaxations caused by endothelium-derived and exogenous NO as well as those due to endothelium-dependent hyperpolarization.
    5. Kaempferol can inhibit cancer cell invasion through blocking the PKCδ/MAPK/AP-1 cascade and subsequent MMP-9 expression and its activity, may act as a therapeutic potential candidate for cancer metastasis.
    6. Kaempferol is an autophagic enhancer, has a more general protection in Parkinson's disease, can mediate antiapoptotic and antioxidant effects is the enhancement of mitochondrial turnover by autophagy.
    Targets: ROS | AP-1 | MMP(e.g.TIMP) | PKC | NO | Autophagy
    In vitro:
    Free Radic Biol Med. 2015 Jun;83:41-53.
    Kaempferol suppresses collagen-induced platelet activation by inhibiting NADPH oxidase and protecting SHP-2 from oxidative inactivation.[Pubmed: 25645952]
    Reactive oxygen species (ROS) generated upon collagen stimulation act as second messengers to propagate various platelet-activating events. Among the ROS-generating enzymes, NADPH oxidase (NOX) plays a prominent role in platelet activation. Thus, NOX has been suggested as a novel target for anti-platelet drug development. Although Kaempferol has been identified as a NOX inhibitor, the influence of Kaempferol on the activation of platelets and the underlying mechanism have never been investigated. Here, we studied the effects of Kaempferol on NOX activation, ROS-dependent signaling pathways, and functional responses in collagen-stimulated platelets.
    Superoxide anion generation stimulated by collagen was significantly inhibited by Kaempferol in a concentration-dependent manner. More importantly, Kaempferol directly bound p47(phox), a major regulatory subunit of NOX, and significantly inhibited collagen-induced phosphorylation of p47(phox) and NOX activation. In accordance with the inhibition of NOX, ROS-dependent inactivation of SH2 domain-containing protein tyrosine phosphatase-2 (SHP-2) was potently protected by Kaempferol. Subsequently, the specific tyrosine phosphorylation of key components (Syk, Vav1, Btk, and PLCγ2) of collagen receptor signaling pathways was suppressed by Kaempferol. Kaempferol also attenuated downstream responses, including cytosolic calcium elevation, P-selectin surface exposure, and integrin-αIIbβ3 activation. Ultimately, Kaempferol inhibited platelet aggregation and adhesion in response to collagen in vitro and prolonged in vivo thrombotic response in carotid arteries of mice.
    This study shows that Kaempferol impairs collagen-induced platelet activation through inhibition of NOX-derived ROS production and subsequent oxidative inactivation of SHP-2. This effect suggests that Kaempferol has therapeutic potential for the prevention and treatment of thrombovascular diseases.
    Int Immunopharmacol. 2015 Apr 11.
    Kaempferol enhances the suppressive function of Treg cells by inhibiting FOXP3 phosphorylation.[Pubmed: 25870037]
    Kaempferol is a natural flavonoid found in many vegetables and fruits. Epidemiologic studies have described that Kaempferol intake could reduce risk of cancer, especially lung, gastric, pancreatic and ovarian cancers. Recent studies have shown that Kaempferol could also be beneficial to the body to defend against inflammation, and infection by bacteria and viruses; however, the molecular mechanism of its immunoregulatory function remains largely unknown.
    Through screening a small molecule library of traditional Chinese medicine (TCM), we identified that Kaempferol could enhance the suppressive function of regulatory T cells (Tregs). Kaempferol was found to increase FOXP3 expression level in Treg cells and prevent pathological symptoms of collagen-induced arthritis in a rat animal model. Kaempferol could also reduce PIM1-mediated FOXP3 phosphorylation at S422.
    Our study reveals a molecular mechanism that underlies the anti-inflammatory action of Kaempferol for the prevention and treatment of inflammatory diseases such as rheumatoid arthritis, systemic lupus erythematosus, and ankylosing spondylitis.
    Br J Pharmacol. 2015 Jun;172(12):3003-14.
    Kaempferol enhances endothelium-dependent relaxation in the porcine coronary artery through activation of large-conductance Ca(2+) -activated K(+) channels.[Pubmed: 25652142]
    BACKGROUND AND PURPOSE: Kaempferol, a plant flavonoid present in normal human diet, can modulate vasomotor tone.EXPERIMENTAL APPROACH: The effect of Kaempferol on the relaxation of porcine coronary arteries to endothelium-dependent Kaempferol, a plant flavonoid present in normal human diet, can modulate vasomotor tone. The present study aimed to elucidate the signalling pathway through which this flavonoid enhanced relaxation of vascular smooth muscle.
    The effect of Kaempferol on the relaxation of porcine coronary arteries to endothelium-dependent (bradykinin) and -independent (sodium nitroprusside) relaxing agents was studied in an in vitro organ chamber setup. The whole-cell patch-clamp technique was used to determine the effect of Kaempferol on potassium channels in porcine coronary artery smooth muscle cells (PCASMCs). At a concentration without direct effect on vascular tone, Kaempferol (3 × 10(-6) M) enhanced relaxations produced by bradykinin and sodium nitroprusside. The potentiation by Kaempferol of the bradykinin-induced relaxation was not affected by N(ω)-nitro-L-arginine methyl ester, an inhibitor of NO synthase (10(-4) M) or TRAM-34 plus UCL 1684, inhibitors of intermediate- and small-conductance calcium-activated potassium channels, respectively (10(-6) M each), but was abolished by tetraethylammonium chloride, a non-selective inhibitor of calcium-activated potassium channels (10(-3) M), and iberiotoxin, a selective inhibitor of large-conductance calcium-activated potassium channel (KCa 1.1; 10(-7) M). Iberiotoxin also inhibited the potentiation by Kaempferol of sodium nitroprusside-induced relaxations. Kaempferol stimulated an outward-rectifying current in PCASMCs, which was abolished by iberiotoxin.
    The present results suggest that, in smooth muscle cells of the porcine coronary artery, Kaempferol enhanced relaxations caused by endothelium-derived and exogenous NO as well as those due to endothelium-dependent hyperpolarization. This vascular effect of Kaempferol involved the activation of KCa 1.1 channels.
    In vivo:
    J Nutr Biochem. 2015 Aug;26(8):868-75.
    Kaempferol ameliorates symptoms of metabolic syndrome by regulating activities of liver X receptor-β.[Pubmed: 25959373]
    Kaempferol is a dietary flavonol previously shown to regulate cellular lipid and glucose metabolism. However, its molecular mechanisms of action and target proteins have remained elusive, probably due to the involvement of multiple proteins.
    This study investigated the molecular targets of Kaempferol. Ligand binding of Kaempferol to liver X receptors (LXRs) was quantified by time-resolved fluorescence resonance energy transfer and surface plasmon resonance analyses. Kaempferol directly binds to and induces the transactivation of LXRs, with stronger specificity for the β-subtype (EC50 = 0.33 μM). The oral administration of Kaempferol in apolipoprotein-E-deficient mice (150 mg/day/kg body weight) significantly reduced plasma glucose and increased high-density lipoprotein cholesterol levels and insulin sensitivity compared with the vehicle-fed control. Kaempferol also reduced plasma triglyceride concentrations and did not cause liver steatosis, a common side effect of potent LXR activation. In immunoblotting analysis, Kaempferol reduced the nuclear accumulation of sterol regulatory element-binding protein-1 (SREBP-1).
    Our results show that the suppression of SREBP-1 activity and the selectivity for LXR-β over LXR-α by Kaempferol contribute to the reductions of plasma and hepatic triglyceride concentrations in mice fed Kaempferol. They also suggest that Kaempferol activates LXR-β and suppresses SREBP-1 to enhance symptoms in metabolic syndrome.
    Kaempferol Description
    Source: The roots of Kaempferia galangal L.
    Solvent: Chloroform, Dichloromethane, Ethyl Acetate, DMSO, Acetone, etc.
    Storage: Providing storage is as stated on the product vial and the vial is kept tightly sealed, the product can be stored for up to 24 months(2-8C).

    Wherever possible, you should prepare and use solutions on the same day. However, if you need to make up stock solutions in advance, we recommend that you store the solution as aliquots in tightly sealed vials at -20C. Generally, these will be useable for up to two weeks. Before use, and prior to opening the vial we recommend that you allow your product to equilibrate to room temperature for at least 1 hour.

    Need more advice on solubility, usage and handling? Please email to: service@chemfaces.com

    After receiving: The packaging of the product may have turned upside down during transportation, resulting in the natural compounds adhering to the neck or cap of the vial. take the vial out of its packaging and gently shake to let the compounds fall to the bottom of the vial. for liquid products, centrifuge at 200-500 RPM to gather the liquid at the bottom of the vial. try to avoid loss or contamination during handling.
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    Calculate Dilution Ratios(Only for Reference)
    1 mg 5 mg 10 mg 20 mg 25 mg
    1 mM 3.4941 mL 17.4703 mL 34.9406 mL 69.8812 mL 87.3515 mL
    5 mM 0.6988 mL 3.4941 mL 6.9881 mL 13.9762 mL 17.4703 mL
    10 mM 0.3494 mL 1.747 mL 3.4941 mL 6.9881 mL 8.7352 mL
    50 mM 0.0699 mL 0.3494 mL 0.6988 mL 1.3976 mL 1.747 mL
    100 mM 0.0349 mL 0.1747 mL 0.3494 mL 0.6988 mL 0.8735 mL
    * Note: If you are in the process of experiment, it's need to make the dilution ratios of the samples. The dilution data of the sheet for your reference. Normally, it's can get a better solubility within lower of Concentrations.
    Kinase Assay:
    Biochem Cell Biol. 2015 Feb;93(1):16-27.
    Inhibitory effects of kaempferol on the invasion of human breast carcinoma cells by downregulating the expression and activity of matrix metalloproteinase-9.[Pubmed: 25453494]
    Matrix metalloproteinases (MMPs) have been regarded as major critical molecules assisting tumor cells during metastasis, for excessive ECM (ECM) degradation, and cancer cell invasion.
    In the present study, in vitro and in vivo assays were employed to examine the inhibitory effects of Kaempferol, a natural polyphenol of flavonoid family, on tumor metastasis. Data showed that Kaempferol could inhibit adhesion, migration, and invasion of MDA-MB-231 human breast carcinoma cells. Moreover, Kaempferol led to the reduced activity and expression of MMP-2 and MMP-9, which were detected by gelatin zymography, real-time PCR, and western blot analysis, respectively. Further elucidation of the mechanism revealed that Kaempferol treatment inhibited the activation of transcription factor activator protein-1 (AP-1) and MAPK signaling pathway. Moreover, Kaempferol repressed phorbol-12-myristate-13-acetate (PMA)-induced MMP-9 expression and activity through suppressing the translocation of protein kinase Cδ (PKCδ) and MAPK signaling pathway. Our results also indicated that Kaempferol could block the lung metastasis of B16F10 murine melanoma cells as well as the expression of MMP-9 in vivo.
    Taken together, these results demonstrated that Kaempferol could inhibit cancer cell invasion through blocking the PKCδ/MAPK/AP-1 cascade and subsequent MMP-9 expression and its activity. Therefore, Kaempferol might act as a therapeutic potential candidate for cancer metastasis.
    Cell Research:
    Neurobiol Aging. 2012 Apr;33(4):767-85.
    Neuroprotection of kaempferol by autophagy in models of rotenone-mediated acute toxicity: possible implications for Parkinson's disease.[Pubmed: 20594614 ]
    This study aims to elucidate the processes underlying neuroprotection of Kaempferol in models of rotenone-induced acute toxicity.
    We demonstrate that Kaempferol, but not quercetin, myricetin or resveratrol, protects SH-SY5Y cells and primary neurons from rotenone toxicity, as a reduction of caspases cleavage and apoptotic nuclei are observed. Reactive oxygen species (ROS) levels and mitochondrial carbonyls decrease significantly. Mitochondrial network, transmembrane potential and oxygen consumption are also deeply preserved. We demonstrate that the main event responsible for the Kaempferol-mediated antiapoptotic and antioxidant effects is the enhancement of mitochondrial turnover by autophagy. Indeed, fluorescence and electron microscopy analyses show an increase of the mitochondrial fission rate and mitochondria-containing autophagosomes. Moreover, the autophagosome-bound microtubule-associated protein light chain-3 (LC3-II) increases during Kaempferol treatment and chemical/genetic inhibitors of autophagy abolish Kaempferol protective effects. Autophagy affords protection also toward other mitochondrial toxins (1-methyl-4-phenyilpiridinium, paraquat) used to reproduce the typical features of Parkinson's disease (PD), but is inefficient against apoptotic stimuli not directly affecting mitochondria (H(2)O(2), 6-hydroxydopamine, staurosporine). Striatal glutamatergic response of rat brain slices is also preserved by Kaempferol, suggesting a more general protection of Kaempferol in Parkinson's disease.
    Overall, the data provide further evidence for Kaempferol to be identified as an autophagic enhancer with potential therapeutic capacity.
    Biochem Pharmacol. 2003 Jan 1;65(1):35-42.
    Potent inhibitory effect of naturally occurring flavonoids quercetin and kaempferol on in vitro osteoclastic bone resorption.[Pubmed: 12473376]
    Several recent studies have suggested that flavonols, a class of phytochemicals with many biological activities, might exert a protective effect against post-menopausal bone loss.
    In the present study, we investigated the effects of quercetin and Kaempferol, two of the major naturally occurring flavonols on the in vitro bone resorbing activity of osteoclasts. Our results indicate that both compounds, at concentrations ranging from 0.1 to 100 microM reduce bone resorption in a time and dose-dependent manner. Significant inhibitory effects were observed at concentrations as low as 0.1 microM especially with Kaempferol. The IC(50)s, or concentration inhibitory of 50% of basal resorption, calculated for quercetin and Kaempferol were 1.6 and 5.3 microM, respectively. Using highly purified rabbit osteoclasts, we showed that both flavonols directly induce apoptosis of mature osteoclasts in the same dose-range effective for inhibiting bone resorption. When osteoclasts were treated with 50 microM of quercetin and Kaempferol, intracellular reactive oxygen species levels decreased significantly by 75 and 25%, respectively, indicating these molecules keep their antioxidant properties at this concentration. However, at concentrations below 50 microM, neither quercetin nor Kaempferol exerted antiradical action, suggesting that antioxidant properties cannot fully explain the inhibitory effect on bone resorption. Finally, we report that Kaempferol-, but not the quercetin-induced inhibition of bone resorption was partially abolished by the presence of the pure anti-estrogen ICI 182780 suggesting that Kaempferol's estrogenic effect could be involved in the inhibition of bone resorption.
    The present study demonstrates that flavonols widely distributed in human diet such as quercetin and Kaempferol, exert a potent inhibitory effect on in vitro bone resorption.