Foenumoside BCAS# 877661-00-2 |
Quality Control & MSDS
Package In Stock
Number of papers citing our products
| Cas No. | 877661-00-2 | SDF | Download SDF |
| PubChem ID | N/A | Appearance | Powder |
| Formula | C60H96O25 | M.Wt | 1217.39 |
| Type of Compound | Triterpenoids | Storage | Desiccate at -20°C |
| Solubility | Soluble in Chloroform,Dichloromethane,Ethyl Acetate,DMSO,Acetone,etc. | ||
| General tips | For obtaining a higher solubility , please warm the tube at 37 ℃ and shake it in the ultrasonic bath for a while.Stock solution can be stored below -20℃ for several months. We recommend that you prepare and use the solution on the same day. However, if the test schedule requires, the stock solutions can be prepared in advance, and the stock solution must be sealed and stored below -20℃. In general, the stock solution can be kept for several months. Before use, we recommend that you leave the vial at room temperature for at least an hour before opening it. |
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| About Packaging | 1. The packaging of the product may be reversed during transportation, cause the high purity compounds to adhere to the neck or cap of the vial.Take the vail out of its packaging and shake gently until the compounds fall to the bottom of the vial. 2. For liquid products, please centrifuge at 500xg to gather the liquid to the bottom of the vial. 3. Try to avoid loss or contamination during the experiment. |
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| Shipping Condition | Packaging according to customer requirements(5mg, 10mg, 20mg and more). Ship via FedEx, DHL, UPS, EMS or other couriers with RT, or blue ice upon request. | ||
Foenumoside B Dilution Calculator
Foenumoside B Molarity Calculator
| 1 mg | 5 mg | 10 mg | 20 mg | 25 mg | |
| 1 mM | 0.8214 mL | 4.1071 mL | 8.2143 mL | 16.4286 mL | 20.5357 mL |
| 5 mM | 0.1643 mL | 0.8214 mL | 1.6429 mL | 3.2857 mL | 4.1071 mL |
| 10 mM | 0.0821 mL | 0.4107 mL | 0.8214 mL | 1.6429 mL | 2.0536 mL |
| 50 mM | 0.0164 mL | 0.0821 mL | 0.1643 mL | 0.3286 mL | 0.4107 mL |
| 100 mM | 0.0082 mL | 0.0411 mL | 0.0821 mL | 0.1643 mL | 0.2054 mL |
| * Note: If you are in the process of experiment, it's necessary to make the dilution ratios of the samples. The dilution data above is only for reference. Normally, it's can get a better solubility within lower of Concentrations. | |||||
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Foenumoside B isolated from Lysimachia foenum-graecum extract suppresses LPS-induced inflammatory response via NF-kappaB/AP-1 inactivation in murine macrophages and in endotoxin-induced shock model.[Pubmed:29782861]
Eur J Pharmacol. 2018 Aug 5;832:120-128.
Foenumoside B (FSB), a bioactive component isolated from the Lysimachia foenum-graecum extract (LFE), has been shown to possess anti-inflammatory effects, but the underlying molecular mechanisms involved have not been elucidated. Accordingly, the authors investigated the mechanisms responsible for the anti-inflammatory effects of FSB in murine macrophages activated by LPS. FSB suppressed the LPS-induced expressions of iNOS and COX-2 at protein and mRNA levels and consequently decreased NO and PGE2 production in RAW264.7 and primary macrophages. FSB also reduced the LPS-induced inductions of TNF-alpha, IL-6 and IL-1beta at protein and mRNA levels. Studies of the molecular mechanisms involved in the anti-inflammatory effects of FSB showed that it inhibited the transcriptional activities of NF-kappaB and AP-1, and the nuclear translocation of NF-kappaB via inhibition of the phosphorylations of AKT, p38 and STAT3. In a sepsis model, pretreatment with FSB inhibited the LPS-stimulated mRNA and protein levels of proinflammatory mediators, such as, iNOS, COX-2, TNF-alpha, IL-6 and IL-1beta in plasma and liver. Importantly, FSB increased the survival rate of mice in the LPS-induced sepsis model. Taken together, these results show that the anti-inflammatory effects of FSB against LPS-induced inflammatory conditions are associated with inhibitions of the phosphorylations of AKT, p38 and STAT3 followed by the transcriptional suppressions of NF-kappaB and AP-1, and thus, reduced expressions of pro-inflammatory genes.
Suppression of Adipocyte Differentiation by Foenumoside B from Lysimachia foenum-graecum Is Mediated by PPARgamma Antagonism.[Pubmed:27176632]
PLoS One. 2016 May 13;11(5):e0155432.
Lysimachia foenum-graecum extract (LFE) and its active component Foenumoside B (FSB) have been shown to inhibit adipocyte differentiation, but their mechanisms were poorly defined. Here, we investigated the molecular mechanisms responsible for their anti-adipogenic effects. Both LFE and FSB inhibited the differentiation of 3T3-L1 preadipocytes induced by peroxisome proliferator-activated receptor-gamma (PPARgamma) agonists, accompanied by reductions in the expressions of the lipogenic genes aP2, CD36, and FAS. Moreover, LFE and FSB inhibited PPARgamma transactivation activity with IC50s of 22.5 mug/ml and 7.63 mug/ml, respectively, and showed selectivity against PPARalpha and PPARdelta. Rosiglitazone-induced interaction between PPARgamma ligand binding domain (LBD) and coactivator SRC-1 was blocked by LFE or FSB, whereas reduced NCoR-1 binding to PPARgamma by rosiglitazone was reversed in the presence of LFE or FSB. In vivo administration of LFE into either ob/ob mice or KKAy mice reduced body weights, and levels of PPARgamma and C/EBPalpha in fat tissues. Furthermore, insulin resistance was ameliorated by LFE treatment, with reduced adipose tissue inflammation and hepatic steatosis. Thus, LFE and FSB were found to act as PPARgamma antagonists that improve insulin sensitivity and metabolic profiles. We propose that LFE and its active component FSB offer a new therapeutic strategy for metabolic disorders including obesity and insulin resistance.
Foenumoside B from Lysimachia foenum-graecum inhibits adipocyte differentiation and obesity induced by high-fat diet.[Pubmed:22197824]
Biochem Biophys Res Commun. 2012 Jan 13;417(2):800-6.
We have previously reported anti-obesity effects of Lysimachia foenum-graecum in high-fat diet (HFD)-induced obesity model. Here we isolated a triterpene saponin Foenumoside B as an active component of L. foenum-graecum. Foenumoside B blocked the differentiation of 3T3-L1 preadipocytes in a dose-dependent manner with an IC50 of 0.2 mug/ml in adipogenesis assay and suppressed the induction of PPARgamma, the master regulator of adipogenesis. Foenumoside B induced the activation of AMP-activated protein kinase (AMPK), and modulated the expression of genes involved in lipid metabolism towards lipid breakdown in differentiated adipocytes. In mouse model, oral administration of Foenumoside B (10mg/kg/day for 6 weeks) reduced HFD-induced body weight gain significantly without affecting food intake. Treatment of Foenumoside B suppressed lipid accumulation in white adipose tissues and the liver, and lowered blood levels of glucose, triglycerides, ALT, and AST in HFD-induced obese mice. Consistent with the in vitro results, Foenumoside B activated AMPK signaling, suppressed the expression of lipogenic genes, and enhanced the expression of lipolytic genes in vivo. Foenumoside B also blocked HFD-induced proinflammatory cytokine production in adipose tissue, suggesting its protective role against insulin resistance. Taken together, these findings demonstrate that Foenumoside B represents the anti-obesity effects of L. foenum-graecum, and suggest therapeutic potential of Foenumoside B in obesity and obesity-related metabolic diseases.
