Butein

Catalog No.S8036 Batch:S803601

Technical Data

Formula	C₁₅H₁₂O₅
Molecular Weight	272.25	CAS No.	487-52-5
Solubility (25°C)*	In vitro	DMSO	55 mg/mL (202.02 mM)
		Ethanol	55 mg/mL (202.02 mM)
		Water	Insoluble
* <1 mg/ml means slightly soluble or insoluble. * Please note that Selleck tests the solubility of all compounds in-house, and the actual solubility may differ slightly from published values. This is normal and is due to slight batch-to-batch variations. * Room temperature shipping (Stability testing shows this product can be shipped without any cooling measures.)

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Biological Activity

Description

Butein, a plant polyphenol isolated from Rhus verniciflua, is able to inhibit the activation of protein tyrosine kinase, NF-κB and STAT3, also inhibits EGFR.

Targets

EGFR ^[1]

In vitro

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 p60^c-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. ^[1] Butein inhibits Nuclear Factor(NF)-κB and NF-κB-regulated gene expression through direct inhibition of IκBα Kinase β on Cysteine 179 Residue. ^[2] 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. ^[3] 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. ^[4] 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%. ^[5] 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. ^[6]

In vivo

Butein 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. ^[5] 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. ^[7]

Protocol (from reference)

Cell Assay:^{^[5]}	Cell lines Human hepatoma cells HepG2 Concentrations ~50 μM Incubation Time 1 days Method The cells (5× 10³/mL) 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.
Animal Study:^{^[5]}	Animal Models Human hepatocellular carcinoma xenografts HepG2 Dosages 2 mg/kg Administration intraperitoneal injection, 5 doses per week for 3 consecutive weeks

Cell Assay:^{^[5]}

Cell lines
Human hepatoma cells HepG2
Concentrations
~50 μM
Incubation Time
1 days
Method
The cells (5× 10³/mL) 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.

Animal Study:^{^[5]}

Animal Models
Human hepatocellular carcinoma xenografts HepG2
Dosages
2 mg/kg
Administration
intraperitoneal injection, 5 doses per week for 3 consecutive weeks

References

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Selleck's Butein has been cited by 2 publications

ERα is a target for butein-induced growth suppression in breast cancer [ Am J Cancer Res, 2020, 10(11):3721-3736]	PubMed: 33294263
A STAT3-NFkB/DDIT3/CEBPβ axis modulates ALDH1A3 expression in chemoresistant cell subpopulations [ Oncotarget, 2015, 6(14):12637-53]	PubMed: 25868979

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SHIPPING AND STORAGE
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