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More articles cited ChemFaces products.
Int J Mol Med.2015 Dec 28.PhytomedicineFeb. 11. 2016Oncotarget. 2016 Aug 19Clin Exp Pharmacol Physiol.2015 Aug 1Molecules. 2017 Feb 8;
J. Int. J. of Food Properties 13 Feb 2017Scientific ResearchJune 20, 2017Mol Immunol. 2016 Oct;78:121-132.Journal of Pharmaceutical Analysis2016 May 5; Acta Physiologiae Plantarum.2014 10.
Polytechnic University of Catalonia2016PLoS One. 2017 Mar 9;Hum Exp Toxicol. 2016 Dec 9.J Sep Sci.2018 Jan 23.
Our products had been exported to the following research institutions and universities, And still growing.
University of Toulouse (France)Centralised Purchases Unit (CPU)... (India)Institute of Pathophysiology Med... (Austria)Kyushu University (Japan)
The Ohio State University (USA)Helmholtz Zentrum München (Germany)Melbourne University (Australia)University of Medicine and Pharm... (Romania)
Centrum Menselijke Erfelijkheid (Belgium)University of Melbourne (Australia)Research Unit Molecular Epigenet... (Germany)
||Dihydromethysticin non-competitively inhibits the specific binding of [3H]-batrachotoxinin-A 20-alpha-benzoate to receptor site 2 of voltage-gated Na+ channels.The induction of CYP3A23 by dihydromethysticin and desmethoxyyangonin involves transcription activation, probably through a pregnane X receptor (PXR).-independent or PXR-involved indirect mechanism.
||Sodium Channel | P450 (e.g. CYP17)|
|Drug Metab Dispos. 2004 Nov;32(11):1317-24. |
|Desmethoxyyangonin and dihydromethysticin are two major pharmacological kavalactones with marked activity on the induction of CYP3A23.[Pubmed: 15282211]|
|Kava kava (Piper methysticum), an herbal remedy, is widely used for the treatment of mild to moderate cases of anxiety. The therapeutic activity is presumably achieved through multiple constituents called kavalactones. Recently, kava extracts were shown to induce CYP3A4 and activate human pregnane X receptor (PXR).
METHODS AND RESULTS:
This study was undertaken to test the ability of purified kavalactones to induce CYP3A23 and activate PXR. Rat hepatocytes were treated with desmethoxyyangonin, dihydrokawain, Dihydromethysticin, kawain, methysticin, or yangonin, and the expression of CYP3A23 was monitored. Among the kavalactones, only desmethoxyyangonin and Dihydromethysticin markedly induced the expression of CYP3A23 (approximately 7-fold). A similar magnitude of induction was detected with combined six kavalactones at a noninductive concentration when individually used. The induced expression, however, was markedly reduced or completely abolished if Dihydromethysticin, desmethoxyyangonin, or both were excluded from the mixtures. Interestingly, regardless of whether Dihydromethysticin or desmethoxyyangonin was used alone or together with other kavalactones, similar amounts of total kavalactones were needed to produce comparable induction, suggesting that the inductive activity of Dihydromethysticin and desmethoxyyangonin is additively/synergistically enhanced by other kavalactones. In addition, treatment with Dihydromethysticin, desmethoxyyangonin, or pregnenolone 16alpha-carbonitrile (PCN) markedly increased the levels of CYP3A23 mRNA, and inhibition of mRNA synthesis abolished the induction. In contrast to PCN, Dihydromethysticin and desmethoxyyangonin only slightly activated rat or human PXR.
These findings suggest that the induction of CYP3A23 by Dihydromethysticin and desmethoxyyangonin involves transcription activation, probably through a PXR-independent or PXR-involved indirect mechanism.
||The herbs of Piper methysticum
||Chloroform, Dichloromethane, Ethyl Acetate, DMSO, Acetone, etc.
||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: email@example.com
||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
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.2017.12.030PMID: 29496173
Calculate Dilution Ratios(Only for Reference)
* 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.
|Planta Med. 1998 Jun;64(5):458-9. |
|Kavain, dihydrokavain, and dihydromethysticin non-competitively inhibit the specific binding of [3H]-batrachotoxinin-A 20-alpha-benzoate to receptor site 2 of voltage-gated Na+ channels.[Pubmed: 9690349 ]|
METHODS AND RESULTS:
The mode of action of the kava pyrones, kavain, dihydrokavain and Dihydromethysticin on the specific binding of [3H]-batrachotoxinin-A 20-alpha-benzoate to epitope 2 of voltage-dependent Na+ channels was investigated by performing saturation experiments in the presence and absence of these kava pyrones. The tested compounds significantly decreased the apparent total number of binding sites (Bmax) for [3H]-batrachotoxinin-A 20-alpha-benzoate (control: 0.5 pmol/mg protein, kava pyrones: 0.2-0.27 pmol/mg protein) with little change in the equilibrium constants (KD) for [3H]-batrachotoxin-A 20-alpha-benzoate (control: 28.2 nM, kava pyrones: 24-31 nM).
The results indicate for the kava pyrones a non-competitive inhibition of the specific [3H]-batrachotoxinin-A 20-alpha-benzoate binding to receptor site 2 of voltage-gated Na+ channels.