Cimiracemate ACAS# 478294-16-5 |
Quality Control & MSDS
Number of papers citing our products
Chemical structure
Cas No. | 478294-16-5 | SDF | Download SDF |
PubChem ID | N/A | Appearance | Powder |
Formula | C19H18O7 | M.Wt | 358.4 |
Type of Compound | Phenylpropanoids | 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. |
Cimiracemate A Dilution Calculator
Cimiracemate A Molarity Calculator
1 mg | 5 mg | 10 mg | 20 mg | 25 mg | |
1 mM | 2.7902 mL | 13.9509 mL | 27.9018 mL | 55.8036 mL | 69.7545 mL |
5 mM | 0.558 mL | 2.7902 mL | 5.5804 mL | 11.1607 mL | 13.9509 mL |
10 mM | 0.279 mL | 1.3951 mL | 2.7902 mL | 5.5804 mL | 6.9754 mL |
50 mM | 0.0558 mL | 0.279 mL | 0.558 mL | 1.1161 mL | 1.3951 mL |
100 mM | 0.0279 mL | 0.1395 mL | 0.279 mL | 0.558 mL | 0.6975 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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Osteoprotective Effect of Cimiracemate in Glucocorticoid-Induced Osteoporosis by Osteoprotegerin/Receptor Activator of Nuclear Factor kappa B/Receptor Activator of Nuclear Factor Kappa-Beta Ligand Signaling.[Pubmed:30695776]
Pharmacology. 2019;103(3-4):163-172.
OBJECTIVES: Present investigation determines the protective effect of Cimiracemate A against glucocorticoid-induced osteoporosis rat. METHODS: Osteoporosis was induced by injecting methylprednisolone acetate (21 mg/kg) for the period of 6 weeks, and the rats were treated with Cimiracemate A 5 and 10 mg/kg, p.o. 60 min after the administration of methylprednisolone acetate (21 mg/kg) for the duration of 6 weeks. Effect of Cimiracemate A was observed by estimating the microarchitecture of bone and histopathological changes by micro-CT scan and light microscope. Moreover, lipid profile, mediators of inflammation, and parameters that affect bone formation were determined in the serum and western blot assay, and reverse transcription polymerase chain reaction was done for the estimation of protein expression in the bone tissues. Moreover, cytotoxic effect of Cimiracemate A on bone marrow macrophages and bone marrow stromal cells was determined by 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide assay. RESULTS: Result of the investigation suggests that treatment with Cimiracemate A ameliorates the microarchitecture of bone and histopathological changes in the glucocorticoid-induced osteoporosis rat. Level of lipid and mediators of inflammation was significantly reduced in the serum of Cimiracemate A-treated rats than the negative control group. However, the activity of tartrate-resistant acid phosphatase and the level of collagen type I fragments in the serum were found to be reduced, and osteocalcin level was enhanced in Cimiracemate A-treated rats than the negative control group. Moreover, treatment with Cimiracemate A attenuates the expression of receptor activator of nuclear factor kappa-Beta ligand (RANKL), receptor activator of nuclear factor kappa B (RANK), and osteoprotegerin (OPG) protein in glucocorticoid-induced osteoporosis rats. CONCLUSION: In conclusion, our study suggests that Cimiracemate A protects the glucocorticoid-induced osteoporosis by regulating the RANKL/RANK/OPG signaling pathway.
Identification of the bioactive constituent and its mechanisms of action in mediating the anti-inflammatory effects of black cohosh and related Cimicifuga species on human primary blood macrophages.[Pubmed:19835377]
J Med Chem. 2009 Nov 12;52(21):6707-15.
Cimicifuga species have been used as traditional medicinal herbs to treat inflammation and symptoms associated with menopause in Asia, Europe, and North America. However, the underlying mechanism of their anti-inflammatory effects remains to be investigated. With bioactivity guided purification involving the use of partitioning extraction and high performance liquid chromatography, we isolated one of the key bioactive constituents from the rhizome extracts of Cimicifuga racemosa. By NMR spectroscopy, the molecule was identified to be Cimiracemate A (1). This compound (140 muM) suppressed the lipopolysaccharide-induced TNF-alpha production in the blood macrophages by 47 +/- 19% and 58 +/- 30% at LPS concentrations of 1 ng/mL and 10 ng/mL, respectively. The anti-inflammatory activity of compound 1 may be due to its modulation of a signaling mitogen activated protein kinase and transcription factor nuclear factor-kappaB activities. Compound 1 was found in other Cimicifuga species. Our data indicate that compound 1 or its chemical analogues may have the potential to be further developed as a new class of therapeutic agent.
Black cohosh (Cimicifuga racemosa L.) protects against menadione-induced DNA damage through scavenging of reactive oxygen species: bioassay-directed isolation and characterization of active principles.[Pubmed:12428954]
J Agric Food Chem. 2002 Nov 20;50(24):7022-8.
The roots/rhizomes of Cimicifuga racemosa L. (Nutt.) (black cohosh) have traditionally been used to treat menopausal symptoms through an unknown mechanism of action. In an effort to determine if black cohosh had additional health benefits, methanol extracts were investigated for their potential to scavenge reactive oxygen species and to protect against menadione-induced DNA damage. These extracts effectively scavenged 1,1-diphenyl-2-picrylhydrazyl (DPPH) free radicals. In addition, the extracts showed dose-dependent decreases in DNA single-strand breaks and oxidized bases induced by the quinone menadione using the comet (single-cell gel electrophoresis assay) and fragment length associated repair enzyme assays, respectively. Bioassay-directed fractionation of the methanolic extracts using the DPPH assay as a monitor led to the isolation of nine antioxidant active compounds: caffeic acid (1), methyl caffeate (2), ferulic acid (3), isoferulic acid (4), fukinolic acid (5), cimicifugic acid A (6), cimicifugic acid B (7), cimicifugic acid F (8), Cimiracemate A (9), and cimiracemate B (10). Six of these antioxidants were found to reduce menadione-induced DNA damage in cultured S30 breast cancer cells with the following order of potency: methyl caffeate (2) > caffeic acid (1) > ferulic acid (3) > Cimiracemate A (9) > cimiracemate B (10) > fukinolic acid (5). These data suggest that black cohosh can protect against cellular DNA damage caused by reactive oxygen species by acting as antioxidants.