CimifuginCAS# 37921-38-3 |
Quality Control & MSDS
3D structure
Package In Stock
Number of papers citing our products
| Cas No. | 37921-38-3 | SDF | Download SDF |
| PubChem ID | 441960 | Appearance | White-beige powder |
| Formula | C16H18O6 | M.Wt | 306.3 |
| Type of Compound | Flavonoids | Storage | Desiccate at -20°C |
| Synonyms | Cimitin | ||
| Solubility | DMSO : ≥ 3.1 mg/mL (10.12 mM) *"≥" means soluble, but saturation unknown. | ||
| Chemical Name | (2S)-7-(hydroxymethyl)-2-(2-hydroxypropan-2-yl)-4-methoxy-2,3-dihydrofuro[3,2-g]chromen-5-one | ||
| SMILES | CC(C)(C1CC2=C(O1)C=C3C(=C2OC)C(=O)C=C(O3)CO)O | ||
| Standard InChIKey | ATDBDSBKYKMRGZ-ZDUSSCGKSA-N | ||
| Standard InChI | InChI=1S/C16H18O6/c1-16(2,19)13-5-9-11(22-13)6-12-14(15(9)20-3)10(18)4-8(7-17)21-12/h4,6,13,17,19H,5,7H2,1-3H3/t13-/m0/s1 | ||
| 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. |
||
| 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. |
||
| 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. | ||
| Description | Cimifugin evidently inhibits FITC-induced type 2 allergic contact dermatitis,and its mechanism might related to regulating the balance of Th1 /Th2 by inhibiting type 2 cytokines. Cimifugin displayed low to moderate inhibition towards AChE and BChE (3.12 and 21.63%, respectively) at 200 ug/mL. |
| Targets | IFN-γ | IL Receptor | AChE | BChE |
| In vivo | Cimifugin inhibits allergic contact dermatitis by regulating type 2 cytokines.[Reference: WebLink]Pharmacol. Clin. Chinese Mat. Med., 2014, 30(2):28-30.This study was carried out to investigate the effective and mechanism of Cimifugin on type 2 allergic contact dermatitis induced by FITC. |
| Kinase Assay | Development of an Efficient Protocol for Cimifugin Isolation from Peucedanum schottii and Evaluation of Enzyme Inhibitory Activity.[Reference: WebLink]Natural Product Communications, 2016, 11(8).
|
| Structure Identification | Biomed Chromatogr. 2012 Oct;26(10):1234-40.Comparative pharmacokinetics of prim-O-glucosylcimifugin and cimifugin by liquid chromatography-mass spectrometry after oral administration of Radix Saposhnikoviae extract, cimifugin monomer solution and prim-O-glucosylcimifugin monomer solution to rats.[Pubmed: 22253022]A sensitive and reliable liquid chromatography-mass spectrometry method has been developed and validated for simultaneous determination of Cimifugin and prim-O-glucosylCimifugin in rat plasma after oral administration of Radix Saposhnikoviae (RS) extract, prim-O-glucosylCimifugin monomer solution and Cimifugin monomer solution.
|
Cimifugin Dilution Calculator
Cimifugin Molarity Calculator
| 1 mg | 5 mg | 10 mg | 20 mg | 25 mg | |
| 1 mM | 3.2648 mL | 16.3239 mL | 32.6477 mL | 65.2955 mL | 81.6193 mL |
| 5 mM | 0.653 mL | 3.2648 mL | 6.5295 mL | 13.0591 mL | 16.3239 mL |
| 10 mM | 0.3265 mL | 1.6324 mL | 3.2648 mL | 6.5295 mL | 8.1619 mL |
| 50 mM | 0.0653 mL | 0.3265 mL | 0.653 mL | 1.3059 mL | 1.6324 mL |
| 100 mM | 0.0326 mL | 0.1632 mL | 0.3265 mL | 0.653 mL | 0.8162 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. | |||||
Calcutta University
University of Minnesota
University of Maryland School of Medicine
University of Illinois at Chicago
The Ohio State University
University of Zurich
Harvard University
Colorado State University
Auburn University
Yale University
Worcester Polytechnic Institute
Washington State University
Stanford University
University of Leipzig
Universidade da Beira Interior
The Institute of Cancer Research
Heidelberg University
University of Amsterdam
University of Auckland
TsingHua University
The University of Michigan
Miami University
DRURY University
Jilin University
Fudan University
Wuhan University
Sun Yat-sen University
Universite de Paris
Deemed University
Auckland University
The University of Tokyo
Korea University
Cimifugin is a major components of Yu-ping-feng-san, a Chinese medical formula that is used clinically for allergic diseases and characterized by reducing allergy relapse.
References:
[1]. Shen D, et al. Screening active components from Yu-ping-feng-san for regulating initiative key factors in allergic sensitization. PLoS One. 2014 Sep 8;9(9):e107279.
[2]. Wang X, et al. Pharmacokinetics of cimifugin in rat plasma after oral administration of the extract of Saposhnikovia divaricatae root. Determination of cimifugin by high performance liquid chromatography coupled with solid phase extraction. Arzneimittelfo
- Jolkinolide B
Catalog No.:BCN2391
CAS No.:37905-08-1
- Jolkinolide A
Catalog No.:BCN3771
CAS No.:37905-07-0
- Scarlet 808
Catalog No.:BCC9139
CAS No.:3789-75-1
- Ro 08-2750
Catalog No.:BCC7307
CAS No.:37854-59-4
- Nepodin
Catalog No.:BCN6894
CAS No.:3785-24-8
- Germacrene D
Catalog No.:BCN3851
CAS No.:37839-63-7
- Phaseollidin
Catalog No.:BCN5432
CAS No.:37831-70-2
- ACDPP hydrochloride
Catalog No.:BCC7302
CAS No.:37804-11-8
- Betamethasone
Catalog No.:BCC4765
CAS No.:378-44-9
- Cimigenol
Catalog No.:BCC8149
CAS No.:3779-59-7
- Boc-D-Pro-OH
Catalog No.:BCC3437
CAS No.:37784-17-1
- Ifosfamide
Catalog No.:BCC1164
CAS No.:3778-73-2
- Saracatinib (AZD0530)
Catalog No.:BCC1166
CAS No.:379231-04-6
- Tenofovir alafenamide
Catalog No.:BCC8066
CAS No.:379270-37-8
- Tenofovir Alafenamide Fumarate
Catalog No.:BCC8067
CAS No.:379270-38-9
- tenofovir diphosphate
Catalog No.:BCC6447
CAS No.:166403-66-3
- Geranylacetone
Catalog No.:BCN7567
CAS No.:3796-70-1
- LM 22A4
Catalog No.:BCC6239
CAS No.:37988-18-4
- 2-Amino-4'-fluorobenzophenone
Catalog No.:BCC8530
CAS No.:3800-06-4
- Sulfamonomethoxine sodium
Catalog No.:BCC9157
CAS No.:38006-08-5
- Tenovin-1
Catalog No.:BCC2239
CAS No.:380315-80-0
- (+)-columbianetin
Catalog No.:BCN2331
CAS No.:3804-70-4
- NBMPR
Catalog No.:BCC7516
CAS No.:38048-32-7
- alpha-Epoxydihydroartemisinic acid
Catalog No.:BCN5434
CAS No.:380487-65-0
Cimifugin Inhibits Inflammatory Responses of RAW264.7 Cells Induced by Lipopolysaccharide.[Pubmed:30638197]
Med Sci Monit. 2019 Jan 14;25:409-417.
BACKGROUND RAW264.7 cells are induced by lipopolysaccharide (LPS) as a rheumatoid arthritis (RA) model. The present study investigated the effect of Cimifugin on the proliferation, migration, chemotaxis, and release of inflammation-related factors and inflammation-related signaling pathways of LPS-induced RAW264.7 cells. MATERIAL AND METHODS MTS assay was used to determine the proliferation of RAW264.7 cells. Transwell assay was employed to examine the migration and chemotaxis of the cells. ELISA was performed to measure the contents of chemotactic factors and inflammatory factors in cell culture supernatants. Western blotting was carried out to detect the expression of factors related with MAPKs and NF-kappaB signaling pathways. RESULTS Cimifugin (0-100 mg/L) had no cytotoxicity for RAW264.7 cells. LPS stimulation induced morphological differentiation of RAW264.7 cells, but intervention by Cimifugin inhibited the activation effect by LPS by about 50%. Cimifugin (100 mg/L) decreased the migration and chemotaxis of RAW264.7 cells to 1/3 of that in control cells by decreasing the release of migration- and chemotaxis-associated factors by at least 30%. Cimifugin (100 mg/L) suppressed the release of inflammatory factors from RAW264.7 cells to less than 60% of that in the LPS group. In addition, Cimifugin (100 mg/L) inhibited the activities of MAPKs and NF-kappaB signaling pathways. CONCLUSIONS The present study demonstrates that Cimifugin reduces the migration and chemotaxis of RAW264.7 cells and inhibits the release of inflammatory factors and activation of related signaling pathways induced by LPS. Cimifugin may have potential pharmacological effects against RA.
Cimifugin suppresses allergic inflammation by reducing epithelial derived initiative key factors via regulating tight junctions.[Pubmed:28597545]
J Cell Mol Med. 2017 Nov;21(11):2926-2936.
Cimifugin is a bioactive component of Saposhnikovia divaricata, a Chinese herb for treating allergy. Our previous studies demonstrated that Cimifugin inhibited allergic inflammation efficiently. This study aims to determine the mechanism of Cimifugin on epithelial cells in allergic inflammation. Mice were sensitized and challenged with FITC to establish type 2 atopic dermatitis (AD) model. The initial stage of AD model, in which mice were just sensitized with FITC, was established in vivo and immortalized human epidermal (HaCaT) cells were utilized in vitro. Initiative key cytokines, TSLP and IL-33, were measured by ELISA, the junctions in ECs were observed by electron microscopy and TJs (CLDN-1, occludin and CLDND1) were assessed by Western blot, immunohistochemistry and immunofluorescence. The results showed that TSLP and IL-33 were inhibited significantly by Cimifugin in the initial stage of AD model. Simultaneously, Cimifugin reduced the separated gap among the epithelial cells and increased the expression of TJs. Similar effects on TSLP/IL-33 and TJs were obtained in vitro. The effect of Cimifugin on TSLP decreased significantly when expression of CLDN1 was interfered with siRNA and this implied Cimifugin inhibits initiative cytokines through restoring TJs. Furthermore, Cimifugin administered only in the initial stage obviously attenuated the ultimate allergic inflammation, which indicate that impacts of Cimifugin in the initial stage on TSLP/IL-33 and TJs are sufficient for suppressing allergic inflammation. This study not only revealed the mechanisms of Cimifugin, but also indicated the possibility of initiative key cytokines and TJs as therapeutic targets.
Feeble Antipyretic, Analgesic, and Anti-inflammatory Activities were Found with Regular Dose 4'-O-beta-D-Glucosyl-5-O-Methylvisamminol, One of the Conventional Marker Compounds for Quality Evaluation of Radix Saposhnikoviae.[Pubmed:28216902]
Pharmacogn Mag. 2017 Jan-Mar;13(49):168-174.
INTRODUCTION: 4'-O-beta-D-glucosyl-5-O-methylvisamminol (GML) is a conventional marker compound for quality control of Radix Saposhnikoviae. Despite that, neither pharmacodynamic or pharmacokinetic information is available with regard to GML. As such, the aim of thisstudy was to assess the conventional evaluation indices for the quality of Radix Saposhnikoviae. MATERIALS AND METHODS: Pyretic animal model, hot plate test, and ear edema model were established to evaluate and compare the antipyretic, analgesic, and anti-inflammatory effect of the chromone derivativesCimifugin, prime-O-glucosylCimifugin (PGCN), and GML in Radix Saposhnikoviae. High performance liquid chromatography separation and analysis was used to obtain pharmacokinetic parameters. Simulated gastric fluid and simulated intestinal fluid was used to investigate the metabolite profiles of PGCN and GML in gastrointestinal tract. RESULTS: Cimifugin exerted a marked dose-dependent antipyretic, analgesic, and anti-inflammatory effect, whereas the effects of PGCN were relatively lower. GML had feeble pharmacodynamic effects. Pharmacokinetic study showed that only Cimifugin was detected in the plasma sample of Cimifugin and PGCN-treated animals, with drug concentration in the former much higher than the latter. No components were traced in the plasma samples from GML-treated rats. Stability study showed that PGCN and GML was predominantly biotransformed into Cimifugin and 5-O-methyvisammiol, respectively. The latter was proven to be extremely unstable in liver tissue homogenate and plasma. CONCLUSIONS: A feeble antipyretic, analgesic, and anti-inflammatory activities was observed when GML was orally delivered. Given that Radix Saposhnikoviae extract is generally administered orally, we speculate that this compound might be a nonpharmacolagically active agent in real usage. Thus, it might be unscientific to evaluate the quality of Radix Saposhnikoviae based on the content of GML. SUMMARY: GML-derived Cimifugin, which represents the potential pharma codynamic component of Radix Saposhnikoviae chromones, in plasma was almost nil in contrast to Cimifugin and PGCN. And thus, feeble antipyretic, analgesic, and anti-inflammatory activities were found with GML. Abbreviations used: AUC:area under concentration-time curve, DNP:2,4-Dinitrophenol, HPLC:high performance liquid chromatography, HPLC-MS:high performance liquid chromatography- mass spectrography, GML:4'-O-beta-D-glucosyl-5-O-methylvisamminol, MVL:5-O-methyvisammiol, PGCN:prime-O-glucosylCimifugin, SGF:alkaline phosphatase. SIF:simulated intestinal fluid.
Development of an Efficient Protocol for Cimifugin Isolation from Peucedanum schottii and Evaluation of Enzyme Inhibitory Activity.[Pubmed:30725569]
Nat Prod Commun. 2016 Aug;11(8):1107-1110.
The dichloromethane (DCM) extract of the fruits of Peucedanwn schottii Besser. ex DC. (Apiaceae) was subjected to high-performance counter-current chromatography (HPCCC) for the efficient and fast separation (30 min) and isolation of Cimifugin using an ethyl acetate: water (1:1 v/v, K= 1.01) system. The analytical scale-optimized separation was easily scaled to semi-preparative conditions. Cimifugin (11.25% yield, 96.5% purity) was isolated for the first time from P. schottii and characterized by NMR spectroscopy. Cimifugin and the crude DCM extract were evaluated using ELISA microtiter assays for their inhibitory potential against the cholinesterases (acetylcholinesterase - AChE and butyrylcholinesterase - BChE), and tyrosinase (TYR), which are key enzymes for the treatment of some neurodegenerative diseases, i.e. Alzheimer's and Parkinson's. The crude extract exhibited a weak inhibitory activity against-AChE, BChE, and TYR (4.2, 35.5, and 0% at 100 mug mL-1 and 10.3, 40.0, and 12.2% at 200 mug mL-1, respectively), while Cimifugin displayed low to moderate inhibition towards AChE and BChE (3.1 and 21.6%, respectively) at 200 mug mL'.
