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More articles cited ChemFaces products.
Phytomedicine.2019, 57:95-104Food Chem Toxicol.2020, 135:110863Journal of Food Composition and A...2021...J Separation Science & Technology...2016...Natural Product Res.&Deve....2022...J Hepatocell Carcinoma....2022...J Sci Food Agric.2017, 97(5):1656-1662Phytochem Anal.2016, 27(5):296-303
Biomed Sci Letters.2020, 26:319-326J Pharm Biomed Anal.2021, 196:113931. J Adv Res.2019, 17:85-94J Mol Recognit.2020, 33(2):e2819Inflammation.2021, doi: 10.1007J Ginseng Res.2022, 46(1):104-114. Int. J. Mol. Sci. 2022, 23(3),1696.Int J Mol Sci.2022, 23(13):7115.
Molecules 2021, 26(4),1092.Nat Prod Commun.2014, 9(5):679-82Korean J Acupunct2020, 37:104-121Evid Based Complement Alternat Me...2020...LWT2021, 138:110397.J Adv Res.2021, 35:245-257. Int J Mol Sci.2017, 19(1)
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J. of The Korean Society of Food Culture2017, 144-149The Journal of Agromedicine and Medical Sciences2018, 4(1)LWT2020, 110397Eur J Pharmacol.2018, 832:96-103J Nat Sc Biol Med2019, 10(2):149-156In Vitro Cellular & Developmental Biology - Plant 2021, 57:874–882.Molecules.2021, 26(18):5665.Molecules.2019, 24(10):E1926Appl. Sci.2020, 10,1304Applied Biological Chemistry 2022, 65,5(2022).
Related Screening Libraries
||Kurarinone exhibits anti-tumor, estrogenic, and anti-inflammatory activities, it also shows strong inhibitory effect on immune responses. Kurarinone may ameliorate chronic inflammatory skin diseases through the suppression of pathogenic CD4(+) T-cell differentiation and the overall immune response. Kurarinone sensitizes TNF-related apoptosis inducing ligand (TRAIL)-induced tumor cell apoptosis via suppression of NF-κB-dependent cFLIP expression; it may be by way of down-regulating Smad3 expression to interfere its induction on intercellular signal transduction and consequently ameliorate renal interstitial fibrosis.|
||JAK | STAT | NF-kB | Bcl-2/Bax | IkB | IKK | TNF-α | CD4(+)|
|J. Nat.Prod., 2004, 67(11):1829-32. |
|Estrogenic and anticarcinogenic properties of kurarinone, a lavandulyl flavanone from the roots of Sophora flavescens.[Pubmed: 15568770 ]|
|Kurarinone, a lavandulyl flavanone, was isolated from a polyphenolic extract of the roots of Sophora flavescens using fractionation guided by estrogenic activity, which was determined by recombinant yeast and Ishikawa Var-I bioassays. |
METHODS AND RESULTS:
Kurarinone showed weak estrogenic activity both in the yeast screen and in the Ishikawa Var-I assay with EC(50) values of 4.6 and 1.66 microM, respectively. Furthermore, Kurarinone was found to have potent cytotoxic activity (IC(50) value = 22.2 microM) against human MCF-7/6 breast cancer cells in the sulforhodamine-B assay.
|Biochem. Pharmacol., 2013, 85(8):1134-44. |
|Kurarinone regulates immune responses through regulation of the JAK/STAT and TCR-mediated signaling pathways.[Pubmed: 23333426 ]|
|Sophora flavescens is a medicinal herb that contains flavonoids and quinolizidine alkaloids and has a wide range of biological activities due to its anti-inflammatory, anti-bacterial and anti-cancer properties. We isolated a series of flavonoids from the roots of Sophora flavescens and examined their ability to inhibit immune responses. |
METHODS AND RESULTS:
Among the flavonoids, Kurarinone exhibited the strongest inhibitory effect on immune responses. Kurarinone suppressed the differentiation of CD4(+) T cells by inhibiting the expression and production of T-cell lineage-specific master regulators and cytokines. Our results also demonstrated that Kurarinone directly suppressed the cytokine-induced Janus kinase/signal transducer and activator of transcription (JAK/STAT) signaling and T-cell receptor (TCR) pathways. In two established animal models of chronic inflammatory skin disease, one in which psoriasis-like skin disease was induced by an interleukin 23 (IL-23) injection into mouse ears and another in which 2,4,6-trinitrochlorobenzene (TNCB) application on the abdomens of mice was used to induce contact dermatitis, Kurarinone repressed disease development by inhibiting the expression of pro-inflammatory mediators, including cytokines, chemokines and enzyme in murine ear skin.
This study provides new evidence that Kurarinone may ameliorate chronic inflammatory skin diseases through the suppression of pathogenic CD4(+) T-cell differentiation and the overall immune response.
|Int Immunopharmacol . 2018 Sep;62:227-236. |
|The flavonoid kurarinone inhibits clinical progression of EAE through inhibiting Th1 and Th17 cell differentiation and proliferation[Pubmed: 30031314]|
Introduction: The flavonoid Kurarinone suppresses CD4+ T-cell-mediated chronic inflammatory dermatitis. However, Kurarinone's effects upon autoimmune central nervous system (CNS) disease remain unknown. We investigated the potential therapeutic effects and molecular mechanism(s) of Kurarinone in an experimental autoimmune encephalomyelitis (EAE) murine model of multiple sclerosis (MS).
Materials and methods: Myelin oligodendrocyte glycoprotein (MOG35-55) peptide-induced EAE was constructed in wild-type mice. Effects of Kurarinone (100 mg/kg/day) upon clinical scores were assessed based on physical traits and signs. Spinal cord sections were extracted to assess inflammation, demyelination, and mRNA expression of key pro-inflammatory cytokines and chemokines. CNS-infiltrating mononuclear cells (MNCs) and splenocytes were harvested; flow cytometry was then applied to determine CD4+ and CD8+ T-cell percentages as well as Th1/Th2/Th17 subset percentages. Purified naïve CD4+ T-cells underwent in vitro T-cell polarization and proliferation to assess Kurarinone's effects.
Results: Prophylactic and treatment regimens of Kurarinone significantly improved clinical scores in the MOG35-55 peptide-induced EAE model (P < 0.05). Kurarinone significantly lowered CNS inflammation and demyelination (61% and 83% decreases, respectively; P < 0.05), significantly decreased MNC infiltration into CNS tissue (42% decrease; P < 0.05), and significantly inhibited levels of several pro-inflammatory cytokines and chemokines (P < 0.05). Kurarinone significantly lowered CD4+ and CD8+ CNS T-cell counts (51% and 80% decreases, respectively; P < 0.05) and significantly reduced CNS Th1 and Th17 cell percentages (24% and 44% decreases, respectively; P < 0.05). Kurarinone significantly inhibited in vitro Th1, Th2, and Th17 cell differentiation and proliferation (P < 0.05).
Conclusions: Kurarinone significantly inhibits the clinical progression of EAE through the inhibition of Th1 and Th17 cell differentiation and proliferation. Kurarinone may show promise as an immunomodulatory therapeutic agent in treating MS.
Keywords: Encephalomyelitis; Flavonoid; Kurarinone; Multiple sclerosis.|
||The roots of Sophora flavescens Ait.
||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: firstname.lastname@example.org
||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.
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.IF=36.216(2019)PMID: 29328914
Cell Metab. 2020 Mar 3;31(3):534-548.e5. doi: 10.1016/j.cmet.2020.01.002.IF=22.415(2019)PMID: 32004475
Mol Cell. 2017 Nov 16;68(4):673-685.e6. doi: 10.1016/j.molcel.2017.10.022.IF=14.548(2019)PMID: 29149595
ACS Nano. 2018 Apr 24;12(4): 3385-3396. doi: 10.1021/acsnano.7b08969.IF=13.903(2019)PMID: 29553709
Nature Plants. 2016 Dec 22;3: 16206. doi: 10.1038/nplants.2016.205.IF=13.297(2019)PMID: 28005066
Sci Adv. 2018 Oct 24;4(10): eaat6994. doi: 10.1126/sciadv.aat6994.IF=12.804(2019)PMID: 30417089
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* 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.
|Exp. Mol. Med., 2012, 44(11): 653-64. |
|Kurarinone promotes TRAIL-induced apoptosis by inhibiting NF-κB-dependent cFLIP expression in HeLa cells.[Pubmed: 22932446 ]|
|This study was designed to investigate the effects of the prenylated flavonoid Kurarinone on TNF-related apoptosis inducing ligand (TRAIL)-induced apoptosis and its underlying mechanism. |
METHODS AND RESULTS:
A low dose of Kurarinone had no significant effect on apoptosis, but this compound markedly promoted tumor cell death through elevation of Bid cleavage, cytochrome c release release and caspase activation in HeLa cells treated with TRAIL. Caspase inhibitors inhibited Kurarinone-mediated cell death, which indicates that the cytotoxic effect of this compound is mediated by caspase-dependent apoptosis. The cytotoxic effect of Kurarinone was not associated with expression levels of Bcl-2 and IAP family proteins, such as Bcl-2, Bcl-xL, Bid, Bad, Bax, XIAP, cIAP-1 and cIAP-2. In addition, this compound did not regulate the death-inducing receptors DR4 and DR5. On the other hand, Kurarinone significantly inhibited TRAIL-induced IKK activation, IκB degradation and nuclear translocation of NF-κB, as well as effectively suppressed cellular FLICE-inhibitory protein long form (cFLIPL) expression. The synergistic effects of Kurarinone on TRAIL-induced apoptosis were mimicked when Kurarinone was replaced by the NF-κB inhibitor withaferin A or following siRNA-mediated knockdown of cFLIPL. Moreover, cFLIP overexpression effectively antagonized Kurarinone-mediated TRAIL sensitization.
These data suggest that Kurarinone sensitizes TRAIL-induced tumor cell apoptosis via suppression of NF-κB-dependent cFLIP expression, indicating that this compound can be used as an anti-tumor agent in combination with TRAIL.