CampesterolCAS# 474-62-4 |
Quality Control & MSDS
Number of papers citing our products
Chemical structure
3D structure
| Cas No. | 474-62-4 | SDF | Download SDF |
| PubChem ID | 312822 | Appearance | White powder |
| Formula | C28H48O | M.Wt | 400.7 |
| Type of Compound | Steroids | Storage | Desiccate at -20°C |
| Synonyms | (24R)-5-Ergosten-3β-ol | ||
| Solubility | DMSO : < 1 mg/mL (insoluble or slightly soluble) | ||
| Chemical Name | 17-(5,6-dimethylheptan-2-yl)-10,13-dimethyl-2,3,4,7,8,9,11,12,14,15,16,17-dodecahydro-1H-cyclopenta[a]phenanthren-3-ol | ||
| SMILES | CC(C)C(C)CCC(C)C1CCC2C1(CCC3C2CC=C4C3(CCC(C4)O)C)C | ||
| Standard InChIKey | SGNBVLSWZMBQTH-UHFFFAOYSA-N | ||
| Standard InChI | InChI=1S/C28H48O/c1-18(2)19(3)7-8-20(4)24-11-12-25-23-10-9-21-17-22(29)13-15-27(21,5)26(23)14-16-28(24,25)6/h9,18-20,22-26,29H,7-8,10-17H2,1-6H3 | ||
| 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. | ||
| Description | Campesterol is a plant sterol with cholesterol lowering and anticarcinogenic effects, it and other plant sterols often decrease LDL cholesterol levels overall. Campesterol has anti-inflammatory effect, it inhibits several pro-inflammatory and matrix degradation mediators typically involved in osteoarthritis- induced cartilage degradation, also sometimes used to treat some specific prostate conditions. |
| Targets | LDL | ApoA1 | ABCA1 | CETP |
| In vitro | A comparative calorimetric study of the effects of cholesterol and the plant sterols campesterol and brassicasterol on the thermotropic phase behavior of dipalmitoylphosphatidylcholine bilayer membranes.[Pubmed: 24704414]Biochim Biophys Acta. 2014 Jul;1838(7):1941-9.We present a comparative differential scanning calorimetric study of the effects of the animal sterol cholesterol (Chol) and the plant sterols Campesterol (Camp) and brassicasterol (Bras) on the thermotropic phase behavior of dipalmitoylphosphatidylcholine (DPPC) bilayers. |
| In vivo | Increased flux of the plant sterols campesterol and sitosterol across a disrupted blood brain barrier.Increased flux of the plant sterols campesterol and sitosterol across a disrupted blood brain barrier.[Pubmed: 25683892]Steroids. 2015 Feb 12.The intact blood-brain barrier in mammalians prevents exchange of cholesterol loaden particles between periphery and brain and thus nearly all cholesterol in this organ originates from de novo synthesis. Dietary cholesterol homologues from plants, Campesterol and sitosterol, are known to get enriched to some extent in the mammalian brain. Treatment of low HDL-C subjects with the CETP modulator dalcetrapib increases plasma campesterol only in those without ABCA1 and/or ApoA1 mutations.[Pubmed: 25281277]Lipids. 2014 Dec;49(12):1245-9.
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| Cell Research | Synthesis and assessment of the relative toxicity of the oxidised derivatives of campesterol and dihydrobrassicasterol in U937 and HepG2 cells.[Pubmed: 22561884]Biochimie. 2013 Mar;95(3):496-503.The cytotoxic effects of the oxidised derivatives of the phytosterols, stigmasterol and β-sitosterol, have previously been shown to be similar but less potent than those of the equivalent cholesterol oxides in the U937 cell line. |
Campesterol Dilution Calculator
Campesterol Molarity Calculator
| 1 mg | 5 mg | 10 mg | 20 mg | 25 mg | |
| 1 mM | 2.4956 mL | 12.4782 mL | 24.9563 mL | 49.9127 mL | 62.3908 mL |
| 5 mM | 0.4991 mL | 2.4956 mL | 4.9913 mL | 9.9825 mL | 12.4782 mL |
| 10 mM | 0.2496 mL | 1.2478 mL | 2.4956 mL | 4.9913 mL | 6.2391 mL |
| 50 mM | 0.0499 mL | 0.2496 mL | 0.4991 mL | 0.9983 mL | 1.2478 mL |
| 100 mM | 0.025 mL | 0.1248 mL | 0.2496 mL | 0.4991 mL | 0.6239 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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Campesterol is a plant sterol with cholesterol lowering and anticarcinogenic effects.
In Vitro:Campesterol shows a weak cytotoxicity in non-proliferating human umbilical vein endothelial cells (HUVECs). Within the non-cytotoxic concentration range, campesterol significantly inhibits the bFGF-induced proliferation and tube formation of HUVECs in a concentration-dependent manner, while it does not affect the motility of HUVECs. 50 μg/mL of campesterol decreases the cell viability up to about 56% of control(IC50 of over 50 μg/mL)[1].
In Vivo:Campesterol effectively disrupts the bFGF-induced neovascularization in chick chorioallantoic membrane (CAM) in vivo[1].
References:
[1]. Choi JM, et al. Identification of campesterol from Chrysanthemum coronarium L. and its antiangiogenic activities. Phytother Res. 2007 Oct;21(10):954-9.
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Synthesis and assessment of the relative toxicity of the oxidised derivatives of campesterol and dihydrobrassicasterol in U937 and HepG2 cells.[Pubmed:22561884]
Biochimie. 2013 Mar;95(3):496-503.
The cytotoxic effects of the oxidised derivatives of the phytosterols, stigmasterol and beta-sitosterol, have previously been shown to be similar but less potent than those of the equivalent cholesterol oxides in the U937 cell line. The objective of the present study was to compare the cytotoxic effects of the oxidised derivatives of synthetic mixtures of Campesterol and dihydrobrassicasterol in both the U937 and HepG2 cell lines. The parent compounds consisted of a Campesterol: dihydrobrassicasterol mix at a ratio of 2:1 (2CMP:1DHB) and a dihydrobrassicasterol:Campesterol mix at a ratio of 3:1 (3DHB:1CMP). The 2CMP:1DBH oxides were more cytotoxic in the U937 cells than the 3DBH:1CMP oxides but the difference in cytotoxicity was less marked in the HepG2 cells. The order of toxicity of the individual oxidation products was found to be similar to that previously observed for cholesterol, beta-sitosterol and stigmasterol oxidation products in the U937 cell line. There was an increase in apoptotic nuclei in U937 cells incubated with the 7-keto and 7beta-OH derivatives of both 2CMP:1DHB and 3DHB:1CMP and also in the presence of 3DHB:1CMP-3beta,5alpha,6beta-triol and 2CMP:1DHB-5beta,6beta-epoxide. An additional oxidation product synthesised from 2CMP:1DHB, 5,6,22,23-diepoxycampestane, was cytotoxic but did not induce apoptosis. These results signify the importance of Campesterol oxides in the overall paradigm of phytosterol oxide cytotoxicity.
Treatment of low HDL-C subjects with the CETP modulator dalcetrapib increases plasma campesterol only in those without ABCA1 and/or ApoA1 mutations.[Pubmed:25281277]
Lipids. 2014 Dec;49(12):1245-9.
We investigated the effect of dalcetrapib treatment on phytosterol levels in patients with familial combined hyperlipidemia (FCH) or familial hypoalphalipoproteinemia (FHA) due to mutations in apolipoprotein A1 (ApoA1) or ATP-binding cassette transporter A1 (ABCA1). Patients (n = 40) with FCH or FHA received dalcetrapib 600 mg or placebo in this 4-week, double-blind, crossover study. Lipids, apolipoproteins, cholesteryl ester transfer protein (CETP) activity and mass, and phytosterols were assessed. Dalcetrapib increased high-density lipoprotein cholesterol (HDL-C) and ApoA1 levels to a similar extent in FHA (+22.8, +13.9%) and FCH (+18.4, +12.1%), both p < 0.001 vs. placebo. Changes in CETP activity and mass were comparable for FHA (-31.5, +120.9%) and FCH (-26.6, +111.9%), both p < 0.0001 vs. placebo. Campesterol and lathosterol were unchanged in FHA (+3.8, +3.0%), but only Campesterol was markedly increased in FCH (+25.0%, p < 0.0001 vs. placebo). Campesterol increased with dalcetrapib treatment in FCH but not in FHA, despite comparable HDL-C and ApoA1 increases, suggesting that ApoA1 and/or ABCA1 is essential for HDL lipidation by enterocytes in humans.
Increased flux of the plant sterols campesterol and sitosterol across a disrupted blood brain barrier.[Pubmed:25683892]
Steroids. 2015 Jul;99(Pt B):183-8.
The intact blood-brain barrier in mammalians prevents exchange of cholesterol loaden particles between periphery and brain and thus nearly all cholesterol in this organ originates from de novo synthesis. Dietary cholesterol homologues from plants, Campesterol and sitosterol, are known to get enriched to some extent in the mammalian brain. We recently showed that Pdgfb(ret)(/)(ret) mice, with a pericyte deficiency and a leaking blood-brain barrier phenotype, have significantly higher levels of plant sterols in the brain compared to their heterozygous Pdgfb(ret)(/)(+) controls keeping the integrity of the blood-brain barrier (BBB). In order to further study the protective functionality of the BBB we synthesized a mixture of [(2)H6]Campesterol/sitosterol and fed it for 10-40days to genetically different types of animals. There was a significant enrichment of both deuterium stable isotope labeled plant sterols in the brain of both strains of mice, however, with a lower enrichment in the controls. As expected, the percentage and absolute enrichment was higher for [(2)H6]Campesterol than for the more lipophilic [(2)H6]sitosterol. The results confirm that a leaking BBB causes increased flux of plant sterols into the brain. The significant flux of the labeled plant sterols into the brain of the control mice illustrates that the presence of an alkyl group in the 24-position of the steroid side chain markedly increases the ability of cholesterol to pass an intact BBB. We discuss the possibility that there is a specific transport mechanism involved in the flux of alkylated cholesterol species across the BBB.
A comparative calorimetric study of the effects of cholesterol and the plant sterols campesterol and brassicasterol on the thermotropic phase behavior of dipalmitoylphosphatidylcholine bilayer membranes.[Pubmed:24704414]
Biochim Biophys Acta. 2014 Jul;1838(7):1941-9.
We present a comparative differential scanning calorimetric study of the effects of the animal sterol cholesterol (Chol) and the plant sterols Campesterol (Camp) and brassicasterol (Bras) on the thermotropic phase behavior of dipalmitoylphosphatidylcholine (DPPC) bilayers. Camp and Bras differ from Chol in having a C24 methyl group and, additionally for Bras, a C22 trans-double bond. Camp and especially Bras decrease the temperature, cooperativity and enthalpy of the DPPC pretransition more than Chol, although these effects are attenuated at higher sterol levels. This indicates that they destabilize gel-state DPPC bilayers to a greater extent, but are less soluble, than Chol. Not surprisingly, all three sterols have similar effects on the sterol-poor sharp component of the DPPC main phase transition. However, Camp and especially Bras less effectively increase the temperature and decrease the cooperativity and enthalpy of the broad component of the main transition than Chol. This indicates that at higher sterol concentrations, Camp and Bras are less miscible and less effective than Chol at ordering the hydrocarbon chains of the sterol-enriched fluid DPPC bilayers. Overall, these alkyl side chain modifications generally reduce the ability of Chol to produce its characteristic effects on DPPC bilayer physical properties. These differences are likely due to the less extended and more bent conformations of the alkyl side chains of Camp and Bras, producing sterols with a greater effective cross-sectional area and reduced length than Chol. Hence, the structure of Chol is likely optimized for maximum solubility in, as opposed to maximum ordering of, phospholipid bilayers.
