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More articles cited ChemFaces products.
J Med Food.2021, 24(2):151-160.LWT2020, 110397Evid Based Complement Alternat Me...2015...J of Food Quality2020, 8851285.Int J Mol Sci.2021, 22(19):10405.Evid Based Complement Alternat Me...2020...Int J Mol Med.2019, 43(6):2516-2522J Ethnopharmacol.2017, 198:87-90
J Ethnopharmacol.2016, 192:370-381Toxicol Mech Methods.2021, 1-12.FASEB J.2019, 33(8):9685-9694University of Stuttgart2021, 11682.Eur J Pharm Sci.2016, 94:33-45J Ethnopharmacol.2020, 260:112988.Biochem Biophys Res Commun....2017...Molecules.2021, 26(2):E255.
J of the Korean Society of Food S...2016...Eur J Pharmacol.2021, 899:174010. Environ Toxicol.2020, doi: 10.1002Sci Rep.2018, 8(1):12970Food Chem. 2020, 320:126530Food Chem.2022, 378:131975.Nat Prod Communications2018, 10.1177
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Int J Food Sci Nutr.2019, 70(7):825-833Phytomedicine.2019, 61:152813Oxid Med Cell Longev.2020, 2020:8887251.Sci Rep.2017, 7(1):3249Molecules.2019, 25(1):E103J of Advanced Scientific R.2020, 11(3), p109-120.Food Quality and Safety2018, 2:213-219J Korean Society of Food Science & Nutrition2021, 50(9): 962-970Int J Mol Sci.2021, 22(16):8604.Evid Based Complement Alternat Med.2021, 2021:8707280.
Related Screening Libraries
||Coumestrol is a novel inducer of mitochondrial biogenesis through the activation of Sirt1, it suppresses the accumulation of HIF-1α via suppression of SPHK1 pathway in hypoxic PC-3 cells. Coumestrol can function by inhibiting oncogenic disease, at least in part, through CKII inhibition-mediated cellular senescence. Coumestrol treatment is effective in preventing neuronal loss in all times of administration as well as able to rescue the Na+, K+ -ATPase activity, suggesting its potential benefits for either prevention or therapeutics use against cerebral ischemia in males.|
||HIF | Akt | GSK-3 | ROS | NADPH-oxidase | NOS | PKA | PI3K | ERK | cAMP | p53 | p21 | NADPH-oxidase | Estrogen receptor | Sodium Channel | ATPase | Potassium Channel | Progestogen receptor|
|J Agric Food Chem. 2014 May 14;62(19):4298-305. |
|Coumestrol induces mitochondrial biogenesis by activating Sirt1 in cultured skeletal muscle cells.[Pubmed: 24712520 ]|
|The mitochondrion is a central organelle in cellular energy homeostasis; thus, reduced mitochondrial activity has been associated with aging and metabolic disorders. This paper provides biological evidence that Coumestrol, which is a natural isoflavone, activates mitochondrial biogenesis.
METHODS AND RESULTS:
In cultured myocytes, Coumestrol activated the silent information regulator two ortholog 1 (Sirt1) through the elevation of the intracellular NAD(+)/NADH ratio. Coumestrol also increased the mitochondrial contents and induced the expression of key proteins in the mitochondrial electron transfer chain in cultured myocytes. A Sirt1 inhibitor and Sirt1-targeting siRNAs abolished the effect of Coumestrol on mitochondrial biogenesis. Similar to an increase in mitochondrial content, Coumestrol improved myocyte function with increased ATP concentration.
Taken together, the data suggest that Coumestrol is a novel inducer of mitochondrial biogenesis through the activation of Sirt1.
|J Endocrinol . 2016 Mar;228(3):149-60. |
|Coumestrol suppresses proliferation of ES2 human epithelial ovarian cancer cells[Pubmed: 26698565]|
Coumestrol, which is predominantly found in soybean products as a phytoestrogen, has cancer preventive activities in estrogen-responsive carcinomas. However, effects and molecular targets of Coumestrol have not been reported for epithelial ovarian cancer (EOC). In the present study, we demonstrated that Coumestrol inhibited viability and invasion and induced apoptosis of ES2 (clear cell-/serous carcinoma origin) cells. In addition, immunoreactive PCNA and ERBB2, markers of proliferation of ovarian carcinoma, were attenuated in their expression in Coumestrol-induced death of ES2 cells. Phosphorylation of AKT, p70S6K, ERK1/2, JNK1/2, and p90RSK was inactivated by Coumestrol treatment in a dose- and time-dependent manner as determined in western blot analyses. Moreover, PI3K inhibitors enhanced effects of Coumestrol to decrease phosphorylation of AKT, p70S6K, S6, and ERK1/2. Furthermore, Coumestrol has strong cancer preventive effects as compared to other conventional chemotherapeutics on proliferation of ES2 cells. In conclusion, Coumestrol exerts chemotherapeutic effects via PI3K and ERK1/2 MAPK pathways and is a potentially novel treatment regimen with enhanced chemoprevention activities against progression of EOC.
Keywords: clear cell carcinoma; Coumestrol; ovary; reproduction; reproductive tract.|
|Food Chem Toxicol . 2017 Jan;99:149-161. |
|Cytotoxic activity of soy phytoestrogen coumestrol against human breast cancer MCF-7 cells: Insights into the molecular mechanism[Pubmed: 27913286]|
Coumestrol is a phytoestrogen present in soybean products and recognized as potential cancer therapeutic agent against breast cancer. However, the clear molecular mechanism of anticancer-activity of Coumestrol in breast carcinoma has not been reported. It is well established that copper levels are elevated in different malignancies. Therefore, the objective of this study was to investigate the copper-dependent cytotoxic action of Coumestrol in human breast cancer MCF-7 cells. Results showed that Coumestrol inhibited proliferation and induced apoptosis in MCF-7 cells, which was prevented by copper chelator neocuproine and ROS scavengers. Coumestrol treatment induced ROS generation coupled to DNA fragmentation, up-regulation of p53/p21, cell cycle arrest at G1/S phase, mitochondrial membrane depolarization and caspases 9/3 activation. All these effects were suppressed by ROS scavengers and neocuproine. These results suggest that Coumestrol targets elevated copper for redox cycling to generate ROS leading to DNA fragmentation. DNA damage leads to p53 up-regulation which directs the cell cycle arrest at G1/S phase and promotes caspase-dependent apoptosis of MCF-7 cells. In conclusion, copper targeted ROS-mediated p53-dependent mechanism better explains the cytotoxic action of Coumestrol in MCF-7 cells. Thus, targeting elevated copper levels might be a potential therapeutic strategy for selective cytotoxic action against malignant cells.
Keywords: Apoptosis; Breast cancer; Copper; Coumestrol; DNA damage; ROS.|
|Biochem Pharmacol. 2015 Jan 1;93(1):42-8. |
|Coumestrol inhibits carotid sinus baroreceptor activity by cAMP/PKA dependent nitric oxide release in anesthetized male rats.[Pubmed: 25449602]|
|Phytoestrogens could offer multiple beneficial effects on the cardiovascular system. Here, we have examined the effects of Coumestrol (CMT) on carotid baroreceptors activity (CBA) and the possible mechanisms in male rats. The functional parameters of carotid baroreceptors were measured by recording sinus nerve afferent discharge in anesthetized male rats with perfused isolated carotid sinus.
METHODS AND RESULTS:
The levels of protein expression were determined by using ELISA and Western blotting. CMT (1 to 100μmolL(-1)) inhibited CBA, which shifted the functional curve of the carotid baroreceptor to the right and downward, with a marked decrease in the peak slope and the peak integral value of carotid sinus nerve discharge in a concentration dependent manner. These effects were not blocked by a specific estrogen receptor antagonist ICI 182,780, but were completely abolished by nitric oxide (NO) synthase inhibitor l-NAME (N(G)-nitro-l-arginine methyl ester). Furthermore, a NO donor, SIN-1(3-morpholion-sydnon-imine), could potentiate these inhibitory effects of CMT. CMT stimulated the phosphorylation of Ser(1176)-eNOS (endothelial nitric oxide synthase) in a dose-dependent manner in carotid bifurcation tissue over a perfusion period of 15min.
The rapid activation of eNOS by CMT was blocked by a highly selective PKA (protein kinase A) inhibitor H89. In addition, inhibition of PI3K (phosphatidylinositol-3-kinase) and ERK (extracellular signal-regulated kinase) pathways had no effect on eNOS activation by CMT. CMT inhibited CBA via eNOS activation and NO synthesis. These effects were mediated by the cAMP/PKA pathway and were unrelated to the estrogenic effect.
||The herbs of Erythrina arborescens
||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.
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||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.
|Food Chem. 2013 Nov 1;141(1):381-8. |
|Coumestrol induces senescence through protein kinase CKII inhibition-mediated reactive oxygen species production in human breast cancer and colon cancer cells.[Pubmed: 23768371]|
METHODS AND RESULTS:
An inhibitor of the protein kinase CKII (CKII) was purified from leaves of Glycine max (L.) Merrill and was identified as Coumestrol by structural analysis. Coumestrol inhibited the phosphotransferase activity of CKII toward β-casein, with an IC50 of about 5 μM. It acted as a competitive inhibitor with respect to ATP as a substrate, with an apparent Ki value of 7.67 μM. Coumestrol at 50μM resulted in 50% and 30% growth inhibition of human breast cancer MCF-7 and colorectal cancer HCT116 cells, respectively. Coumestrol promoted senescence through the p53-p21(Cip1/WAF1) pathway by inducing reactive oxygen species (ROS) production in MCF-7 and HCT116 cells. The ROS scavenger N-acetyl-l-cysteine (NAC), NADPH oxidase inhibitor apocynin and p22(phox) siRNA almost completely abolished this event. Overexpression of CKIIα antagonised cellular senescence mediated by Coumestrol, indicating that this compound induced senescence via a CKII-dependent pathway.
Since senescence is an important tumour suppression process in vivo, these results suggest that Coumestrol can function by inhibiting oncogenic disease, at least in part, through CKII inhibition-mediated cellular senescence.
|Bioorg Med Chem Lett. 2014 Jun 1;24(11):2560-4. |
|Coumestrol suppresses hypoxia inducible factor 1α by inhibiting ROS mediated sphingosine kinase 1 in hypoxic PC-3 prostate cancer cells.[Pubmed: 24768446]|
|Among many signals to regulate hypoxia inducible factor 1α (HIF-1α), sphingosine kinase 1 (SPHK1) is also involved in various biological activities such as cell growth, survival, invasion, angiogenesis, and carcinogenesis. Thus, in the present study, molecular mechanisms of Coumestrol were investigated on the SPHK1 and HIF-1α signaling pathway in hypoxic PC-3 prostate cancer cells. |
METHODS AND RESULTS:
Coumestrol significantly suppressed SPHK1 activity and accumulation of HIF-1α in a time- and concentration-dependent manner in hypoxic PC-3 cells. In addition, Coumestrol inhibited the phosphorylation status of AKT and glycogen synthase kinase-3β (GSK 3β) signaling involved in cancer metabolism. Furthermore, SPHK1 siRNA transfection, sphigosine kinase inhibitor (SKI), reactive oxygen species (ROS) enhanced the inhibitory effect of Coumestrol on the accumulation of HIF-1α and the expression of pAKT and pGSK 3β in hypoxic PC-3 cells by combination index.
Overall, our findings suggest that Coumestrol suppresses the accumulation of HIF-1α via suppression of SPHK1 pathway in hypoxic PC-3 cells.
|Neurol Res. 2014 Mar;36(3):198-206. |
|Coumestrol treatment prevents Na+, K+ -ATPase inhibition and affords histological neuroprotection to male rats receiving cerebral global ischemia.[Pubmed: 24512013 ]|
| In this study, we investigated the possible mechanisms underlying the neuroprotective effects of Coumestrol, a potent isoflavonoid with antioxidant activities and binding affinities for both estrogen receptors (ER) ER-alpha and ER-beta that are comparable to those of 17beta-estradiol, in a model of global ischemia in male subjects. |
METHODS AND RESULTS:
Wistar rats underwent global ischemia (10 minutes) or sham surgery and received a single intracerebroventricular (icv) infusion of 20 μg of Coumestrol or vehicle 1 hour before ischemia or 0, 3, 6, or 24 hours after reperfusion. The data analysis revealed an extensive neuronal death in the CA1 hippocampal subfield at 7 days, and a significant decrease in the Na+, K+ -ATPase activity at 1 and 24 hours after ischemia, and both injuries were attenuated by Coumestrol administration.
Coumestrol treatment was effective in preventing neuronal loss in all times of administration as well as able to rescue the Na+, K+ -ATPase activity, suggesting its potential benefits for either prevention or therapeutics use against cerebral ischemia in males.