CAS NO: | 491-80-5 |
规格: | ≥98% |
包装 | 价格(元) |
500mg | 电议 |
1g | 电议 |
2g | 电议 |
5g | 电议 |
10g | 电议 |
25g | 电议 |
Molecular Weight (MW) | 284.26 |
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Formula | C16H12O5 |
CAS No. | 491-80-5 |
Storage | -20℃ for 3 years in powder form |
-80℃ for 2 years in solvent | |
Solubility (In vitro) | DMSO: 57 mg/mL (200.5 mM) |
Water: <1 mg/mL | |
Ethanol: 9 mg/mL (31.7 mM) | |
Other info | Chemical Name: 5,7-dihydroxy-3-(4-methoxyphenyl)-4H-chromen-4-one InChi Key: WUADCCWRTIWANL-UHFFFAOYSA-N InChi Code: InChI=1S/C16H12O5/c1-20-11-4-2-9(3-5-11)12-8-21-14-7-10(17)6-13(18)15(14)16(12)19/h2-8,17-18H,1H3 SMILES Code: O=C1C(C2=CC=C(OC)C=C2)=COC3=CC(O)=CC(O)=C13 |
Synonyms | Biochanin; NSC 123538; NSC-123538; Pratensol; NSC123538; olmelin; 4-methyl Genistein; 4-methylGenistein; 5,7-dihydroxy-4'-Methoxyisoflavone; |
In Vitro | In vitro activity: Biochanin A has been reported to inhibit protein tyrosine kinase (PTK) of epidermal growth factor receptor with IC50 values of 91.5 μM. Biochanin A inhibits the hydrolysis of 0.5 μM anandamide by mouse, rat and human fatty acid amide hydrolase (FAAH) with IC50 values of 1.8, 1.4 and 2.4 μM respectively. Biochanin A inhibits 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 has no significant effect of the EGF receptor tyrosine autophosphorylation. Kinase Assay: For experiments with FAAH, rat liver homogenates, mouse brain homogenates and membranes from COS7 cells transfected with the human enzyme are used. Frozen (–80°C) livers from adult C57BL/6 mice and frozen brains (minus cerebella) from adult Wistar or Sprague-Dawley rats are thawed and homogenized in 20 mM HEPES, 1 mM MgCl2, pH 7. The homogenates are centrifuged at ~35000×g for 20 min at 4°C. After resuspension in buffer followed by recentrifugation and a second resuspension in buffer, the pellets are incubated at 37°C for 15 min. This incubation is undertaken in order to hydrolyse all endogenous FAAH substrates. The homogenates are then centrifuged as above, recentrifuged and resuspended in 50 mM Tris-HCl buffer, pH 7.4, containing 1 mM EDTA and 3 mM MgCl2. The homogenates are then frozen at –80°C in aliquots until used for assay. FAAH is assayed in the homogenates and in the COS7 cell membranes using 0.5 μM (unless otherwise stated) [3H]AEA labelled in the ethanolamine part of the molecule. Blank values are obtained by the use of buffer rather than homogenate. In the experiments comparing effects of Biochanin A upon FAAH and FAAH-2, the same assay is used but with 16 nM [3H]oleoylethanolamide ([3H]OEA) as substrate and with an incubation phase at room temperature. The choice of OEA rather than AEA for FAAH-2 is motivated by the relative rates of hydrolysis: OEA is metabolized four times faster than AEA by FAAH-2, whereas for FAAH the rate of hydrolysis of OEA is about a third of that for AEA. When 0.5 μM [3H]AEA is used as substrate, assay conditions for rat brain and mouse liver are chosen so that<10% of added substrate is metabolized. For the human FAAH samples, <5% of the [3H]AEA is metabolized in all cases. For 16 nM [3H]OEA, a limited supply of an expensive ligand meant that optimization is not possible, and the amount of substrate utilized is higher (34±1 and 0.5±0.1% for FAAH and its corresponding mock-transfected, respectively; 40±2 and 21±0.4 for FAAH-2 and its corresponding mock-transfected respectively) |
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In Vivo | In anaesthetized mice, both URB597 and biochanin A inhibited the spinal phosphorylation of extracellular signal-regulated kinase caused by the intraplantar injection of formalin. The effects of both URB597 and biochanin A were found to be significantly reduced by the CB1 receptor antagonist/inverse agonist AM251. In addition, in the tetrad test, biochanin A did not increase brain AEA concentrations, but produced a modest potentiation of the effects of 10 mg·kg-1 i.v. AEA. |
Animal model | Mice |
Formulation & Dosage | 10 mg·kg-1 i.v. AEA. |
References | J Biol Chem. 1987 Apr 25;262(12):5592-5; Br J Pharmacol. 2010 Jun;160(3):549-60. |