• ChemFaces is a professional high-purity natural products manufacturer.
  • Product Intended Use
  • 1. Reference standards
  • 2. Pharmacological research
  • 3. Inhibitors
  • Home
  • Natural Products
  • Bioactive
  • Screening Libraries
  • Hot Products
  • Plant Catalog
  • Customer Support
  • Product Use Citation
  • About Us
  • Contact Us
  • Natural Products
    Biochanin A
    CAS No. 491-80-5 Price $40 / 20mg
    Catalog No.CFN99734Purity>=98%
    Molecular Weight284.26Type of CompoundFlavonoids
    FormulaC16H12O5Physical DescriptionYellow cryst.
    Download Manual    COA    MSDSSimilar structuralComparison (Web)
    How to Order
    Orders via your E-mail:

    1. Product number / Name / CAS No.
    2. Delivery address
    3. Ordering/billing address
    4. Contact information
    Sent to Email: info@chemfaces.com
    Contact Us
    Order & Inquiry & Tech Support

    Tel: (0086)-27-84237683
    Fax: (0086)-27-84254680
    E-mail: manager@chemfaces.com
    Address: No. 83, CheCheng Rd., WETDZ, Wuhan, Hubei 430056, PRC
    Delivery time
    Delivery & Payment method

    1. Usually delivery time: Next day delivery by 9:00 a.m. Order now

    2. We accept: Wire transfer & Credit card & Paypal & Western Union
    * Packaging according to customer requirements(5mg, 10mg, 20mg and more). We shipped via FedEx, DHL, UPS, EMS and others courier.
    Our products had been exported to the following research institutions and universities, And still growing.
  • Shanghai Institute of Organic Ch... (China)
  • Universidad Miguel Hernández (Spain)
  • Universidad de Buenos Aires (Argentina)
  • Institute of Tropical Disease Un... (Indonesia)
  • Aarhus University (Denmark)
  • Calcutta University (India)
  • Guangzhou Institutes of Biomedic... (China)
  • Michigan State University (USA)
  • The Ohio State University (USA)
  • China Medical University (Taiwan)
  • Kamphaengphet Rajabhat University (Thailand)
  • More...
  • Package
    Featured Products
    Gnetin D

    Catalog No: CFN92423
    CAS No: 84870-53-1
    Price: $468/5mg

    Catalog No: CFN98509
    CAS No: 5928-25-6
    Price: $228/20mg

    Catalog No: CFN90458
    CAS No: 66791-77-3
    Price: $288/20mg
    Mulberroside F

    Catalog No: CFN90794
    CAS No: 193483-95-3
    Price: $398/10mg
    Dihydrocucurbitacin B

    Catalog No: CFN92140
    CAS No: 13201-14-4
    Price: $418/5mg
    Biological Activity
    Description: Biochanin A, an O-methylated natural isoflavonoid classified as phytoestrogen, is a naturally occurring fatty acid amide hydrolase (FAAH) inhibitor, which inhibits FAAH with IC50s of 1.8, 1.4 and 2.4 μM for mouse, rat, and human FAAH, respectively. Biochanin A has hypoglycemic, antilipemic,anti-tumorigenesis, anti-oxidation, and anti-inflammatory properties, it also has neuroprotective effects in cerebral ischemia/reperfusion by inhibiting inflammatory response and the inactivation of p38 signaling pathway. Biochanin A could inhibit Methicillin-resistant Staphylococcus aureus efflux system through reducing pathogen' s expression of nor A and norA protein.
    Targets: TNF-α | IL Receptor | p38MAPK | LDL | Bcl-2/Bax | P-gp | EGFR | NO | NOS | IkB | NF-kB | IKK | FAAH
    In vitro:
    Wei Sheng Wu Xue Bao. 2014 Oct 4;54(10):1204-11.
    [Inhibitory effects of biochanin A on the efflux pump of methicillin-resistant Staphylococcus aureus (MRSA)].[Pubmed: 25803898]

    To study the inhibitory effect of Biochanin A on efflux system of Methicillin-resistant Staphylococcus aureus (MRSA). Biochanin A alone had no inhibitory effect on MRSA41577, but it showed synergy effect with ciprofloxacin in inhibition MRSA41577 in which 40pg/mL Biochanin A decreased the minimum inhibitory concentration (MIC) value of ciprofloxacin from 64 microg/mL to 8 microgg/mL. Biochanin A significantly increased the accumulation of ciprofloxacin in MRSA41577 in a time-dependent manner. At 15 min, Biochanin A increased ciprofloxacin in MRSA41577 by 83%, which is similar to that of reserpine (positive control). Further mechanism studies indicated that Biochanin A could reduce the expression of nor A in ciprofloxacin-treated MRSA41577. After incubated with Biochanin A and ciprofloxacin for 16 h, the relative expression of nor A of MRSA41577 was reduced by 65%. SDS-PAGE analysis showed that the total protein profiles of MRSA41577 were significantly changed after treatment with Biochanin A for 16h, in which both norA protein and efflux system ABC transporter ATP-binding protein were significantly decreased.
    Biochanin A could inhibit Methicillin-resistant Staphylococcus aureus efflux system through reducing pathogen' s expression of nor A and norA protein.
    Eur J Pharmacol. 2011 Feb 25;653(1-3):8-15.
    Biochanin-A, an isoflavon, showed anti-proliferative and anti-inflammatory activities through the inhibition of iNOS expression, p38-MAPK and ATF-2 phosphorylation and blocking NFκB nuclear translocation.[Pubmed: 21147093 ]
    Biochanin A, an isoflavone, existing in red clover, cabbage and alfalfa, has an inhibitory and apoptogenic effect on certain cancer cells. However, the actual mechanism by which this compound inhibits proliferation and induces apoptosis in cancer cells and the mechanism of its anti-inflammatory activities have not been well characterized. In this study, we have investigated the anti-inflammatory and anti-proliferative activity of Biochanin A.
    The effects of Biochanin A on RAW 264.7, HT-29 cell lines and mouse peritoneal macrophages have been investigated in vitro. Cell proliferation and anti-inflammatory effects were analyzed by 3-(4-5-dimethylthiozol-2-yl)2-5-diphenyl-tetrazolium bromide (MTT) assay, (3)H-thymidine incorporation assay, Western blot, cytokines estimation, Luciferase assay, Electrophoretic mobility shift assay (EMSA) and Kinase assay. Present investigation demonstrated that, Biochanin A inhibited lipopolysacharide (LPS)-induced nitric oxide(NO) production in macrophage and showed dose dependent inhibition of inducible nitric oxide synthase (iNOS) expression. The induction of NF-κB binding activity by LPS was inhibited markedly by co-incubation with different doses of Biochanin A. Biochanin A inhibited the LPS-induced IkB kinase (IKK) activity and nuclear factor kappa beta (NF-κB) activation associated with the inhibition of iNOS expression. LPS-induced phosphorylation of IκBα and p38 MAPK was blocked by Biochanin A and it inhibited IL-6, IL-1β and TNF-α production in RAW264.7 cells indicating its anti-inflammatory activity in association with anti-proliferation.
    Biochanin A is important for the prevention of phosphorylation and degradation of IκBα, thereby blocking NF-κB activation, which in turn leads to decreased expression of the iNOS, thus preventing proliferation and inflammation.
    In vivo:
    Iran Red Crescent Med J. 2014 Sep 5;16(9):e15424.
    Effect of biochanin a on serum visfatin level of streptozocin-induced diabetic rats.[Pubmed: 25593725]
    Bioflavonoids are well known for their multi directional biologic activity including antidiabetic effect. It has been demonstrated that flavonoids can act as insulin secretagogue or insulin mimetic agents. This experimental study was designed in Arak University of Medical Sciences, Arak, Iran, to investigate the effects of Biochanin A (a bioflavonoid) on fasting blood glucose (FBG), body weight, glycosylated hemoglobin (HbA1c), lipid profile, serum enzymes, and visfatin of streptozocin-induced diabetic rats.
    We used 24 male Wistar rats and randomly allocated them to four groups of six rats. One group was randomly assigned as control and diabetes was induced in three other groups by administration of streptozocin (35 mg/kg of body weight) intraperitoneally. The groups received the following treatments: group 1 (control), 5% DMSO; group 2 (diabetic control), 0.5% DMSO; and group 3 and 4, respectively 10 and 15 mg/kg Biochanin A for 30 days. Body weight and biochemical parameters including FBG, HbA1c, lipid profile, aspartate aminotransferase (AST), alanine aminotransferase (ALT), alkaline phosphatase (ALP), and visfatin were measured in all rats. FBG level was significantly reduced in treated diabetic rats (139.8 ± 9.3 and 206 ± 11 mg/dL in groups 3 and 4, respectively) in comparison to the diabetic control (295.1 ± 14 mg/dL) (P < 0.05). Administration of Biochanin A significantly decreased HbA1c in group 3 (6.66 ± 0.33) and group 4 (7.11 ± 0.31) in comparison to the diabetic control group (8.26 ± 0.44) (P < 0.05). Levels of serum visfatin were improved to near normal levels in the treated rats (249 ± 35.5 and 161.33 ± 13.07 in groups 3 and 4, respectively) in comparison to the diabetic control (302.17 ± 19.4) (P < 0.05). Furthermore, Biochanin A showed a protective effect against weight loss in diabetic rats (P < 0.05). In treated rats, serum total cholesterol, triglyceride, and low-density lipoprotein cholesterol (LDL-c) were significantly decreased and high-density lipoprotein (HDL-c) was increased in comparison with the diabetic control group. In addition, Biochanin A restored the altered plasma enzymes (AST, ALT, and ALP) activities to near normal. Histopathologic examination of the pancreas also indicated that Biochanin A had protective effects on β-cells in streptozocin-induced diabetic rats.
    This study demonstrated that Biochanin A possessed hypoglycemic and antilipemic activities and could increase visfatin expression, which suggests its beneficial effect in the treatment of diabetes.
    Biochanin A Description
    Source: The herbs of Trifolium pretense 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.
    Recent ChemFaces New Products and Compounds
    Bryonamide B

    Catalog No: CFN91057
    CAS No: 5942-25-6
    Price: $218/5mg
    6''-O-acetylsaikosaponin A

    Catalog No: CFN95086
    CAS No: 64340-46-1
    Price: $268/10mg

    Catalog No: CFN92029
    CAS No: 52012-29-0
    Price: $288/20mg

    Catalog No: CFN95099
    CAS No: 116383-31-4
    Price: $288/20mg
    Glyasperin C

    Catalog No: CFN95065
    CAS No: 142474-53-1
    Price: $333/5mg
    Neochlorogenic acid

    Catalog No: CFN97472
    CAS No: 906-33-2
    Price: $138/20mg
    Tenuifoliside A

    Catalog No: CFN90770
    CAS No: 139726-35-5
    Price: $278/20mg
    Chrysin 6-C-arabinoside 8-C-glucos...

    Catalog No: CFN92284
    CAS No: 185145-33-9
    Price: $368/5mg
    Recently, ChemFaces products have been cited in many studies from excellent and top scientific journals

    Cell. 2018 Jan 11;172(1-2):249-261.e12.
    doi: 10.1016/j.cell.2017.12.019.

    PMID: 29328914

    Mol Cell. 2017 Nov 16;68(4):673-685.e6.
    doi: 10.1016/j.molcel.2017.10.022.

    PMID: 29149595

    Scientific Reports 2017 Dec 11;7(1):17332.
    doi: 10.1038/s41598-017-17427-6.

    PMID: 29230013

    Molecules. 2017 Oct 27;22(11). pii: E1829.
    doi: 10.3390/molecules22111829.

    PMID: 29077044

    J Cell Biochem. 2018 Feb;119(2):2231-2239.
    doi: 10.1002/jcb.26385.

    PMID: 28857247

    Phytomedicine. 2018 Feb 1;40:37-47.
    doi: 10.1016/j.phymed.2017.12.030.

    PMID: 29496173
    Calculate Dilution Ratios(Only for Reference)
    1 mg 5 mg 10 mg 20 mg 25 mg
    1 mM 3.5179 mL 17.5895 mL 35.1791 mL 70.3581 mL 87.9477 mL
    5 mM 0.7036 mL 3.5179 mL 7.0358 mL 14.0716 mL 17.5895 mL
    10 mM 0.3518 mL 1.759 mL 3.5179 mL 7.0358 mL 8.7948 mL
    50 mM 0.0704 mL 0.3518 mL 0.7036 mL 1.4072 mL 1.759 mL
    100 mM 0.0352 mL 0.1759 mL 0.3518 mL 0.7036 mL 0.8795 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:
    J Pharmacol Exp Ther. 2003 Mar;304(3):1258-67.
    Effects of the flavonoids biochanin A, morin, phloretin, and silymarin on P-glycoprotein-mediated transport.[Pubmed: 12604704 ]
    Flavonoids are constituents of fruits, vegetables, and plant-derived beverages, as well as components in herbal-containing dietary supplements. The objective of this investigation was to characterize the effect of flavonoids on P-glycoprotein (P-gp)-mediated cellular efflux and to determine the molecular mechanism(s) of the flavonoid-drug interaction.
    Studies were conducted in the sensitive and multidrug resistant human breast cancer cell lines MCF-7 and MDA435/LCC6 and examined the effects of the flavonoids Biochanin A, morin, phloretin, and silymarin on daunomycin (DNM) accumulation and doxorubicin cytotoxicity. The potential mechanism(s) involved in the interaction was evaluated by determining flavonoid effects on 1) P-gp ATPase activity, 2) [(3)H]azidopine photoaffinity labeling of P-gp, and 3) cellular P-gp levels. The flavonoids increased [(3)H]DNM accumulation in P-gp positive cells, but not P-gp negative cells, and these effects were both flavonoid concentration- and P-gp expression level-dependent. Biochanin A and silymarin potentiated doxorubicin cytotoxicity in P-gp positive cells. Biochanin A and phloretin stimulated, whereas morin and silymarin inhibited P-gp ATPase activity, confirming that these flavonoids interact with P-gp. Morin and silymarin significantly inhibited [(3)H]azidopine photoaffinity labeling of P-gp, suggesting a direct interaction with P-gp substrate binding. A 24-h preincubation with all flavonoids, followed by flavonoid removal, did not alter cellular P-gp level in P-gp positive cells.
    Biochanin A, morin, phloretin, and silymarin all inhibited P-gp-mediated cellular efflux and the mechanism of the interaction involved, at least in part, a direct interaction. The findings of this study indicate a potential for significant flavonoid-drug interactions with P-gp substrates.
    Prostate. 1993;22(4):335-45.
    Genistein and biochanin A inhibit the growth of human prostate cancer cells but not epidermal growth factor receptor tyrosine autophosphorylation.[Pubmed: 8497428]
    The effect of the isoflavones, genistein, daidzein, and Biochanin A on the growth of the LNCaP and DU-145 human prostate cancer cell lines has been examined.
    Genistein and Biochanin A, but not daidzein, inhibit both serum and EGF-stimulated growth of LNCaP and DU-145 cells (IC50 values from 8.0 to 27 micrograms/ml for serum and 4.3 to 15 micrograms/ml for EGF), but have no significant effect of the EGF receptor tyrosine autophosphorylation. In contrast, tyrphostin 25, a specific EGF receptor tyrosine kinase inhibitor, inhibits EGF-stimulated growth and EGF receptor tyrosine autophosphorylation in these whole cells, but does not inhibit serum-stimulated growth.
    These data suggest that the mechanism of action of genistein and Biochanin A does not depend on inhibition of EGF receptor tyrosine autophosphorylation, but on a more distal event in the EGF receptor-mediated signal transduction cascade.
    Cell Research:
    Cell Physiol Biochem. 2015;35(2):639-46.
    Biochanin A promotes proliferation that involves a feedback loop of microRNA-375 and estrogen receptor alpha in breast cancer cells.[Pubmed: 25613180]
    Biochanin A and formononetin are O-methylated isoflavones that are isolated from the root of Astragalus membranaceus, and have antitumorigenic effects. Our previous studies found that formononetin triggered growth-inhibitory and apoptotic activities in MCF-7 breast cancer cells. We performed in vivo and in vitro studies to further investigate the potential effect of Biochanin A in promoting cell proliferation in estrogen receptor (ER)-positive cells, and to elucidate underlying mechanisms.
    ERα-positive breast cancer cells (T47D, MCF-7) were treated with Biochanin A. The MTT assay and flow cytometry were used to assess cell proliferation and apoptosis. mRNA levels of ERα, Bcl-2, and miR-375 were quantified using real-time polymerase chain reaction. Compared with the control, low Biochanin A concentrations (2-6 μM) stimulated ERα-positive cell proliferation (T47D, MCF-7). The more sensitive T47D cells were used to study the relevant signaling pathway. After treatment with Biochanin A, ERα, miR-375, and Bcl-2 expression was significantly upregulated. Additionally, in the in vivo studies, uterine weight in ovariectomized mice treated with Biochanin A increased significantly.
    This study demonstrated that Biochanin A promoted ERα-positive cell proliferation through miR-375 activation and this mechanism is possibly involving in a miR-375 and ERα feedback loop.
    Animal Research:
    J Neurol Sci. 2015 Jan 15;348(1-2):121-5.
    Biochanin A protects against focal cerebral ischemia/reperfusion in rats via inhibition of p38-mediated inflammatory responses.[Pubmed: 25466482]
    Biochanin A, an O-methylated natural isoflavonoid classified as phytoestrogen, has been reported to show anti-tumorigenesis, anti-oxidation, and anti-inflammatory properties. However, little is known about the effects of Biochanin A on cerebral ischemia/reperfusion.
    In this study, the neuroprotective and anti-inflammatory effects of Biochanin A against ischemia/reperfusion injury, as well as the related molecular mechanisms, were investigated in rat models. Male Sprague-Dawley rats were subjected to middle cerebral artery occlusion (MCAO) for 2h, followed by 24h of reperfusion. Then neurological deficits, infarct volume and brain edema were evaluated. The MPO activity and TNF-α and IL-1β levels in ischemic boundary zone were determined by a spectrophotometer and the enzyme-linked immunosorbent assay (ELISA). The expressions of TNF-α, IL-1β, and phosphorylation of p38 were measured by RT-PCR or Western blotting. Consequently, our findings showed that Biochanin A treatment for 14 days had significantly reduced infarct volume and brain edema, and improved neurological deficits in focal cerebral ischemia/reperfusion rats. The MPO activity and TNF-α and IL-1β levels were greatly increased after ischemia/reperfusion injury, while treatment with Biochanin A dramatically suppressed these inflammatory processes. Furthermore, Biochanin A attenuated the increase in p-p38 level in the ischemia/reperfusion brain tissue.
    Taken together, Biochanin A has been shown to have neuroprotective effects in cerebral ischemia/reperfusion, and the mechanisms may correlate with inhibiting inflammatory response, as well as the inactivation of p38 signaling pathway.