Home Protein Tyrosine Kinase EGFR inhibitor Butein

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Butein EGFR inhibitor

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

Butein EGFR inhibitor Chemical Structure

Chemical Structure

Molecular Weight: 272.25

Purity & Quality Control

Batch: S803601 DMSO]55 mg/mL]false]Ethanol]55 mg/mL]false]Water]Insoluble]false Purity: 99.98%
99.98

Related Products

Signaling Pathway

EGFR Signaling Pathways

EGFR Signaling Pathway

Mechanism of Action

Targets
EGFR [1]

In vitro
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 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, this compound non-significantly inhibits the activities of serine- and threonine-specific protein kinases such as PKC or PKA. [1] This chemical inhibits Nuclear Factor(NF)-κB and NF-κB-regulated gene expression through direct inhibition of IκBα Kinase β on Cysteine 179 Residue. [2] It (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. This compound (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] It (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. This chemical (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] It 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. This compound (50 μM) also could completely inhibit IL-6-induced STAT3 phosphorylation in SNU-387 cells. It downregulates the expression of cyclin D1, Bcl-2, Bcl-xL, survivin, and VEGF, markers of STAT3 activation. This chemical (50 μM) significantly enhance the apoptotic effects of doxorubicin from 18% to 55% and of paclitaxel from 15% to 42%. [5] It is as a powerful antioxidant against lipid and LDL peroxidation. This compound inhibits iron-induced lipid peroxidation in rat brain homogenate with an IC50 of 3.3 μM. It is as potent α-tocopherol in reducing the stable free radical diphenyl-2-picrylhydrazyl (DPPH) with IC0.2 of 9.2 μM. This chemical also inhibits the activity of xanthine oxidase with an IC50 of 5.9 μM. It scavenges the peroxyl radical derived from 2,2-azobis(2-amidinopropane) dihydrochloride (AAPH) in aqueous phase. Furthermore, this compound inhibits copper-catalyzed oxidation of human low-density lipoprotein (LDL) in a concentration-dependent manner. It is a chelator of ferrous and copper ions. [6]
Cell Research 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.

In Vivo
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 this compound-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] This compound shows antifibrogenic activity. It (25 mg/kg/day) reduces serum AST and ALT activation to 35% and 69%, respectively, of control CCl4-induced rat levels. This chemical (25 mg/kg/day) reduces liver hydroxyproline contents and TBAR4 concentration to 54% and 54%, respectively. α1(I) collagen and TIMP-1 expression in this compound-treated rats is 28% and 20.3% compared with the values for the respective CCl4-treated control. [7]
Animal Research Animal Models Human hepatocellular carcinoma xenografts HepG2
Dosages 2 mg/kg
Administration intraperitoneal injection, 5 doses per week for 3 consecutive weeks

References
  • https://pubmed.ncbi.nlm.nih.gov/9571170/
  • https://pubmed.ncbi.nlm.nih.gov/17439942/
  • https://pubmed.ncbi.nlm.nih.gov/15351711/
  • https://pubmed.ncbi.nlm.nih.gov/18472007/
  • https://pubmed.ncbi.nlm.nih.gov/21131551/
  • https://pubmed.ncbi.nlm.nih.gov/9630680/
  • https://pubmed.ncbi.nlm.nih.gov/14735434/

Chemical Information

Molecular Weight 272.25 Formula

C15H12O5
CAS No. 487-52-5 SDF Download SDF
Synonyms N/A
Smiles C1=CC(=C(C=C1C=CC(=O)C2=C(C=C(C=C2)O)O)O)O

Storage and Stability

Storage (From the date of receipt)

In vitro
Batch:

DMSO : 55 mg/mL ( (202.02 mM) Moisture-absorbing DMSO reduces solubility. Please use fresh DMSO.)

Ethanol : 55 mg/mL

Water : Insoluble


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In vivo
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Tech Support

Answers to questions you may have can be found in the inhibitor handling instructions. Topics include how to prepare stock solutions, how to store inhibitors, and issues that need special attention for cell-based assays and animal experiments.

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