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    Butein (NSC-652892; CCG208298; CS-5675; AC 1NQY7L)
    Butein (NSC-652892; CCG208298; CS-5675; AC 1NQY7L)

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    This product is for research use only, not for human use. We do not sell to patients.
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    InvivoChem Cat #: V0550
    CAS #: 487-52-5Purity ≥98%

    Description: Butein (NSC 652892; CCG-208298; CS5675; AC1NQY7L) is a naturally occuring plant polyphenol and chalconoid isolated from Rhus verniciflua with a broad spectrum of pharmacological effects such as antiinflammatory, antioxidative, aldose reductase and advanced glycation endproducts inhibitory and anticancer activities. It is a chalcone of the chalconoid found in Toxicodendron vernicifluum, Dahlia, Butea and Coreopsis. Butein is able to inhibit the activation of protein tyrosine kinase, NF-κB and STAT3, it also inhibits EGFR. 

    References: Biochem Biophys Res Commun. 1998;245(2):435-8; Clin Cancer Res. 2011;17(6):1425-39; Planta Med.2003;69(11):990-4.

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    olecular Weight (MW)272.25
    CAS No.487-52-5
    Storage-20℃ for 3 years in powder form
    -80℃ for 2 years in solvent
    Solubility (In vitro)DMSO: 55 mg/mL (202.0 mM)
    Water: <1 mg/mL
    Ethanol: 55 mg/mL (202.0 mM)
    Other info

    Chemical Name: (E)-1-(2,4-dihydroxyphenyl)-3-(3,4-dihydroxyphenyl)prop-2-en-1-one


    InChi Code: InChI=1S/C15H12O5/c16-10-3-4-11(14(19)8-10)12(17)5-1-9-2-6-13(18)15(20)7-9/h1-8,16,18-20H/b5-1+

    SMILES Code: O=C(C1=CC=C(O)C=C1O)/C=C/C2=CC=C(O)C(O)=C2


    Butein; CCG208298; CCG 208298; CS-5675; NSC 652892; CCG-208298; CS5675; AC1NQY7L; AC1N-QY7L; AC1N QY7L; CS-5675; NSC-652892; NSC652892; 

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    In Vitro

    In vitro activity: Butein inhibits the epidermal growth factor (EGF)-stimulated auto-phosphotyrosine level of EGF receptor in HepG2 cells, and also inhibits tyrosine-specific protein kinase activities of EGF receptor and p60c-src with IC50 of 65 μM in vitro. The inhibition is competitive to ATP and non-competitive to the phosphate acceptor, poly (Glu, Ala, Tyr) 6:3:1 for EGF receptor tyrosine kinase. In contrast, Butein non-significantly inhibits the activities of serine- and threonine-specific protein kinases such as PKC or PKA. Butein inhibits Nuclear Factor(NF)-κB and NF-κB-regulated gene expression through direct inhibition of IκBα Kinase β on Cysteine 179 Residue. Butein (10 μM) inhibits over 90% iNOS and COX-2 expression, as well as nitrite and TNF-α production in LPS-stimulated RAW 264.7 cells. Butein (10 μM) inhibits LPS-induced DNA binding activity of NF-κB, which is mediated through inhibition of the degradation of inhibitory factor-κB and phosphorylation of Erk1/2 MAP kinase, as well as increases binding of the osteopontin a vb3 integrin receptor. Butein (20 μM) treatment induces morphologic changes of bladder cancer cells BLS(M) from elongated morphology to rounded epithelial-like cells, accompanied by downregulation of vimentin, and gaining of E-cadherin compared to untreated control cells, indicating the reversal of mesenchymal-like phenotype. Butein (20 μM) suppresses motility and invasion capacity of BLS(M) cells, and reverts EMT-like phenotype induced by TNF-α, through the ERK1/2 and NF-κB signaling pathways. Butein inhibits the constitutive activation of STAT3 in HepG2 cells in a dose-dependent manner, with maximum inhibition occurring at 50 μM, mediated through the inhibition of activation of upstream kinases c-Src and Janus-activated kinase2. Butein (50 μM) also could completely inhibit IL-6-induced STAT3 phosphorylation in SNU-387 cells. Butein downregulates the expression of cyclin D1, Bcl-2, Bcl-xL, survivin, and VEGF, markers of STAT3 activation. Butein (50 μM) significantly enhance the apoptotic effects of doxorubicin from 18% to 55% and of paclitaxel from 15% to 42%. Butein is as a powerful antioxidant against lipid and LDL peroxidation. Butein inhibits iron-induced lipid peroxidation in rat brain homogenate with an IC50 of 3.3 μM. Butein is as potent α-tocopherol in reducing the stable free radical diphenyl-2-picrylhydrazyl (DPPH) with IC0.2 of 9.2 μM. Butein also inhibits the activity of xanthine oxidase with an IC50 of 5.9 μM. Butein scavenges the peroxyl radical derived from 2,2-azobis(2-amidinopropane) dihydrochloride (AAPH) in aqueous phase. Furthermore, Butein inhibits copper-catalyzed oxidation of human low-density lipoprotein (LDL) in a concentration-dependent manner. Butein is a chelator of ferrous and copper ions.

    Kinase Assay: Butein inhibited the activation of AKT, extracellular signal-regulated kinase (ERKs) and p38 kinases in the presence of cisplatin.

    Cell Assay: The cells (5× 103/mL, Human hepatoma cells HepG2) are incubated in triplicate in a 96-well plate in the presence or absence of indicated concentration of Butein in a final volume of 0.2 mL for different time intervals at 37 ℃. Thereafter, 20 μL MTT solution (5 mg/mL in PBS) is added to each well. After a 2-hour incubation at 37 ℃, 0.1 mL lysis buffer (20% SDS, 50% dimethylformamide) is added, incubation is continued overnight at 37 ℃, and then the optical density at 570 nm is measured by plate reader.

    In VivoButein at 2 mg/kg induces significant inhibition of hepatocellular tumor growth compared with the corn oil-treated controls. At necropsy on day 22 after initial treatment, there is more than 2-fold decrease in tumor growth in the Butein-treated group (mean relativetumor burden, 3.90) compared with the control group (8.46), associated with reduced constitutive p-STAT3 (9% vs 81% of vehicle group), Bcl-2 levels (26% vs 96% of vehicle group), and increased caspase-3 level (98% vs 21% of vehicle group) in HCC tumor tissues. Butein shows antifibrogenic activity. Butein (25 mg/kg/day) reduces serum AST and ALT activation to 35% and 69%, respectively, of control CCl4-induced rat levels. Butein (25 mg/kg/day) reduces liver hydroxyproline contents and TBAR4 concentration to 54% and 54%, respectively. α1(I) collagen and TIMP-1 expression in Butein-treated rats is 28% and 20.3% compared with the values for the respective CCl4-treated control.
    Animal modelHuman hepatocellular carcinoma xenografts HepG2
    Formulation & DosageDissolved in 200 μL corn oil;  2 mg/kg; i.p. injection.

    Biochem Biophys Res Commun. 1998 Apr 17;245(2):435-8; Clin Cancer Res. 2011 Mar 15;17(6):1425-39; Planta Med. 2003 Nov;69(11):990-4.

    These protocols are for reference only. InvivoChem does not independently validate these methods.


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