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New Zealand J. Forestry Sci.2014, 44:17Proc Natl Acad Sci USA....2016...J Separation Science & Technology...2016...Food and Bioprocess Technology...2017...JPC-Journal of Planar Chromatogra...2017...Biol Pharm Bull.2018, 41(11):1645-1651Korean J Dent Mater.2018, 45(2):139-146Sci Rep. 2018, 462(8)
BMC Complement Altern Med....2019...Journal of Third Military Medical...2019...Plos One.2019, 15(2):e0220084Biosci Biotechnol Biochem....2020...Agronomy2020, 10(10),1489J of App. Res. on Med&Aromatic Pl...2020...Pharmaceuticals (Basel)....2020...Int J Mol Sci.2020, 21(19):7209.
Molecules.2020, 25(15):3353.Molecules.2020, 25(23):5636.Plant Sci.2020, 301:110656.J Biotechnol.2020, 318:10-19.Biochem Biophys Res Commun....2020...Korean Herb. Med. Inf....2020...Environ Toxicol.2020, doi: 10.1002
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Biochemical Systematics and Ecology2018, 81Front Pharmacol.2020, 11:566490.Agronomy2020, 10(3),388.Food Chem.2019, 275:746-753Pharmacogn Mag.2015, 11:S585-91JABS2020, 14:2(2020)Acta Physiologiae Plantarum2015, 37:1736J Basic Clin Physiol Pharmacol.2016, 27(1):1-8Nat Chem Biol.2018, 14(8):760-763Molecules.2015, 20(11):20014-30
Related Screening Libraries
||Diosmetin has anti-osteoporosis, cytoprotective, antibacterial, anti-pigmentation, anti-inflammatory and antioxidant properties, it induces osteoblastic differentiation through the PKCδ-Rac1-MEK3/6-p38 and PKCδ-Rac1-MEK1/2- ERK1/2-Runx2 pathways.Diosmetin has intracellular antioxidant detoxifying effect, the mechanism is associated with both nonenzymatic and enzymatic defense systems.Diosmetin and luteolin exert synergistic cytostatic effects in human hepatoma HepG2 cells via CYP1A-catalyzed metabolism, activation of JNK and ERK and P53/P21 up-regulation.
||TNF-α | PKC | MEK | p38MAPK | ERK | JNK | P53 | P21 | NF-kB | IL Receptor | NOS | P450 (e.g. CYP17) | Antifection|
|Phytomedicine. 2013 May 15;20(7):611-4. |
|Synergistic effects of diosmetin with erythromycin against ABC transporter over-expressed methicillin-resistant Staphylococcus aureus (MRSA) RN4220/pUL5054 and inhibition of MRSA pyruvate kinas[Pubmed: 23541215]|
|Increasing prevalence of methicillin-resistant Staphylococcus aureus (MRSA) worldwide with limited therapeutic options is a growing public health concern. Natural products have been shown to possess antibacterial actions against MRSA. Flavonoids from natural products have been shown to possess antibacterial actions against MRSA by antagonizing its resistance mechanisms. Diosmin and Diosmetin are natural flavonoids found in a variety of citrus fruits. |
METHODS AND RESULTS:
The aim of this study was to investigate whether diosmin and Diosmetin could inhibit the growth of MRSA and the in vitro enzymatic activity of a newly discovered MRSA drug target, pyruvate kinase (PK). By using a panel of MRSA strains with known resistant mechanisms, neither diosmin nor Diosmetin was shown to possess direct antibacterial activities against all tested MRSA strains. However, in checkerboard assay, we found that Diosmetin together with erythromycin, could synergistically inhibit the growth of ABC-pump overexpressed MRSA-RN4220/pUL5054, and time kill assay also showed that the antibacterial activities of Diosmetin with erythromycin were bactericidal. Diosmetin was further shown to significantly suppress the MRSA PK activities in a dose dependent manner.
In conclusion, the inhibition of MRSA PK by Diosmetin could lead to a deficiency of ATP and affect the bacterial efflux pump which might contribute to the antibacterial actions of Diosmetin against MRSA.
|J Agric Food Chem. 2014 Aug 27;62(34):8648-54. |
|Intracellular antioxidant detoxifying effects of diosmetin on 2,2-azobis(2-amidinopropane) dihydrochloride (AAPH)-induced oxidative stress through inhibition of reactive oxygen species generation.[Pubmed: 25075433]|
METHODS AND RESULTS:
The intracellular antioxidant activities of Diosmetin were evaluated by cellular antioxidant activity (CAA) assay, 2,2-azobis(2-amidinopropane) dihydrochloride (AAPH)-induced erythrocyte hemolysis assay and cupric chloride (CuCl2)-induced plasma oxidation assay. The results showed that Diosmetin exhibits strong cellular antioxidant activity (EC50 = 7.98 μmol, CAA value = 58 μmol QE/100 μmol). It was also found that Diosmetin treatment could effectively attenuate AAPH-induced erythrocyte hemolysis (91.0% inhibition at 100 μg/mL) and CuCl2-induced plasma oxidation through inhibition of intracellular reactive oxygen species (ROS) generation. Diosmetin could significantly restore AAPH-induced increase of intracelluar antioxidant enzyme (SOD, GPx, and CAT) activities to normal levels, as well as inhibit intracellular malondialdehyde (MDA) formation.
Thus, the intracellular antioxidant detoxifying mechanism of Diosmetin is associated with both nonenzymatic and enzymatic defense systems.
|J Bone Miner Res. 2008 Jun;23(6):949-60. |
|Diosmetin induces human osteoblastic differentiation through the protein kinase C/p38 and extracellular signal-regulated kinase 1/2 pathway.[Pubmed: 18269307 ]|
|The survival of osteoblasts is one of the determinants of the development of osteoporosis. This study is the first to investigate the osteoblastic differentiation induced by Diosmetin, a flavonoid derivative, in osteoblastic cell lines MG-63, hFOB, and MC3T3-E1 and bone marrow stroma cell line M2-10B4.
METHODS AND RESULTS:
Osteoblastic differentiation was determined by assaying alkaline phosphatase (ALP) activity and mineralization degree and measuring various osteoblast-related markers using ELISA. Expression and phosphorylation of Runt-related transcription factor 2 (Runx2), protein kinase Cdelta (PKCdelta), extracellular signal-regulated kinase (ERK), p38, and c-jun-N-terminal kinase (JNK) was assessed by immunoblot. Rac1 activity was determined by immunoprecipitation, and Runx2 activity was assessed by EMSA. Genetic inhibition was performed by small hairpin RNA plasmids or small interfering RNA (siRNA) transfection.
Diosmetin exhibited an effect on osteoblastic maturation and differentiation by means of ALP activity, osteocalcin, osteopontin, and type I collagen production, as well as Runx2 upregulation. Induction of differentiation by Diosmetin was associated with increased PKCdelta phosphorylation and the activations of Rac1 and p38 and ERK1/2 kinases. Blocking PKCdelta by siRNA inhibition significantly decreased osteoblastic differentiation by inhibiting Rac1 activation and subsequently attenuating the phosphorylation of p38 and ERK1/2. In addition, blocking p38 and ERK1/2 by siRNA transfection also suppressed Diosmetin-induced cell differentiation.
In this study, we show that Diosmetin induced osteoblastic differentiation through the PKCdelta-Rac1-MEK3/6-p38 and PKCdelta-Rac1-MEK1/2- ERK1/2-Runx2 pathways and that it is a promising agent for treating osteoporosis.
|Biochem Pharmacol. 1993 Jan 7;45(1):13-9. |
|Antioxidant and iron-chelating activities of the flavonoids catechin, quercetin and diosmetin on iron-loaded rat hepatocyte cultures.[Pubmed: 8424806]|
|The cytoprotective effect of three flavonoids, catechin, quercetin and Diosmetin, was investigated on iron-loaded hepatocyte cultures, considering two parameters: the prevention of iron-increased lipid peroxidation and the inhibition of intracellular enzyme release. |
METHODS AND RESULTS:
These two criteria of cytoprotection allowed the calculation of mean inhibitory concentrations (IC50) which revealed that the effectiveness of these flavonoids could be classified as follows: catechin > quercetin > Diosmetin. These IC50 values have been related to structural characteristics of the flavonoids tested. Moreover, the investigation of the capacity of these flavonoids to remove iron from iron-loaded hepatocytes revealed a good relationship between this iron-chelating ability and the cytoprotective effect. The cytoprotective activity of catechin, quercetin and Diosmetin could thus be ascribed to their widely known antiradical property but also to their iron-chelating effectiveness.
These findings increase further the prospects for the development and clinical application of these potent antioxidants.
||The peels of Citrus limon (L.) Burm.
||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
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.
|Arch Pharm Res. 2014 Feb;37(2):175-85. |
|Inhibition of c-Kit signaling by diosmetin isolated from Chrysanthemum morifolium.[Pubmed: 23709168]|
|The interaction of stem cell factor (SCF) with its cognate receptor c-Kit is closely associated with the survival and maturation of melanocytes. |
METHODS AND RESULTS:
To investigate novel depigmentation agents, we screened 2,000 plant extracts for c-Kit inhibitors to identify active small molecules by using time-resolved fluorescence enzyme assays. For the active extracts identified as inhibitors of c-Kit enzyme, we evaluated the effects of the active extracts and isolated flavonoids on c-Kit phosphorylation in MO7e/melanocytes. Anti-melanogenic activity was also examined in melanocytes and melanoderm model. The flavonoids such as Diosmetin, apigenin, acacetin and luteolin isolated from Chrysanthemum morifolium were found to be active in inhibiting c-Kit both at enzyme and cellular levels. In addition, these flavonoids attenuated SCF-induced proliferation of human primary melanocytes without toxicity and suppressed ultraviolet (UV) B irradiation-mediated melanin synthesis significantly. Among the active flavonoids, Diosmetin was found to inhibit SCF-induced melanogenesis in a human melanoderm model.
These results strongly suggest that C. morifolium extract and Diosmetin have potential to suppress SCF-/UVB-induced melanogenesis, and could be developed as anti-pigmentation agents.
|J Nutr Biochem. 2013 Feb;24(2):496-504. |
|The flavonoids diosmetin and luteolin exert synergistic cytostatic effects in human hepatoma HepG2 cells via CYP1A-catalyzed metabolism, activation of JNK and ERK and P53/P21 up-regulation.[Pubmed: 22749133 ]|
|Various types of tumors are known to overexpress enzymes belonging to the CYP1 family of cytochromes P450.|
METHODS AND RESULTS:
The present study aimed to characterize the metabolism and further antiproliferative activity of the natural flavonoid Diosmetin in the CYP1-expressing human hepatoma cell line HepG2. Diosmetin was converted to luteolin in HepG2 cells after 12 and 30 h of incubation. In the presence of the CYP1A inhibitor α-naphthoflavone, the conversion of Diosmetin to luteolin was attenuated. 3-(4,5-Dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide assays revealed luteolin to be more cytotoxic than Diosmetin. The antiproliferative effect of Diosmetin in HepG2 cells was attributed to blockage at the G2/M phase as determined by flow cytometry. Induction of G2/M arrest was accompanied by up-regulation of phospho-extracellular-signal-regulated kinase (p-ERK), phospho-c-jun N-terminal kinase, p53 and p21 proteins. More importantly, induction of G2/M arrest and p53 and p-ERK up-regulation were reversed by the application of the CYP1 inhibitor α-naphthoflavone.
Taken together, the data provide new evidence on the tumor-suppressing role of cytochrome P450 CYP1A enzymes and extend the hypothesis that the anticancer activity of dietary flavonoids is enhanced by P450-activation.
|Int J Clin Exp Pathol. 2014 Apr 15;7(5):2133-42. |
|Diosmetin ameliorates the severity of cerulein-induced acute pancreatitis in mice by inhibiting the activation of the nuclear factor-κB.[Pubmed: 24966921]|
|Diosmetin (3', 5, 7-trihydroxy-4'-methoxyflavone), the aglycone part of the flavonoid glycosides diosmin occurs naturally in citrus fruit, was considered to exhibit anti-inflammatory and antioxidant properties. Our study aimed to investigate the effect of Diosmetin in a murine model of cerulein-induced acute pancreatitis (AP). |
METHODS AND RESULTS:
Experimental AP was induced in mice by seven intraperitoneal injection of cerulein (50 ug/kg) at hourly intervals. Diosmetin (100 mg/kg) or vehicle was pretreated 2 h before the first cerulein injection. After 6 h, 9 h, 12 h of the first cerulein injection, the severity of acute pancreatitis was evaluated biochemically and morphologically. Pretreatment with Diosmetin significantly reduced serum levels of amylase and lipase; the histological injury; the secretion of tumor necrosis factor (TNF)-α, interleukin (IL)-1β, and IL-6; myeloperoxidase (MPO) activity, trypsinogen activation peptide (TAP) level, the expression of inducible nitric oxide synthase (iNOS); and the nuclear factor (NF)-κB activation in cerulein-induced AP.
This study showed that administration of Diosmetin demonstrated a beneficial effect on the course of cerulein-induced AP in mice. Therefore, Diosmetin may become a new therapeutic agent in future clinical trials for treatment of AP.