Cafestol

CAS# 469-83-0

Cafestol

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Quality Control of Cafestol

Number of papers citing our products

Chemical structure

Cafestol

3D structure

Chemical Properties of Cafestol

Cas No. 469-83-0 SDF Download SDF
PubChem ID 108052 Appearance White powder
Formula C20H28O3 M.Wt 316.44
Type of Compound Diterpenoids Storage Desiccate at -20°C
Synonyms Cafesterol
Solubility Soluble in chloroform
SMILES CC12CCC3=C(C1CCC45C2CCC(C4)C(C5)(CO)O)C=CO3
Standard InChIKey DNJVYWXIDISQRD-HWUKTEKMSA-N
Standard InChI InChI=1S/C20H28O3/c1-18-7-5-16-14(6-9-23-16)15(18)4-8-19-10-13(2-3-17(18)19)20(22,11-19)12-21/h6,9,13,15,17,21-22H,2-5,7-8,10-12H2,1H3/t13-,15-,17+,18-,19+,20+/m1/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.

Source of Cafestol

From Coffea Bean

Biological Activity of Cafestol

Description1. Cafestol has anticarcinogenic activity. 2. Cafestol acts as an agonist ligand for both FXR and PXR, and this may contribute to its impact on cholesterol homeostasis. 3. Cafestol has an anti-inflammatory property, it inhibits Cyclic-Strain-induced interleukin-8, intercellular adhesion molecule-1, and monocyte chemoattractant protein-1 production in vascular endothelial cells. 4. Cafestol has protective effects against the CCl(4)-induced hepatotoxicity, which possibly involve mechanisms related to its ability to block the CYP2E1-mediated CCl(4) bioactivation and free radical scavenging effects. 5. Cafestol is a novel extracellular signal-regulated kinase inhibitor with AP-1-targeted inhibition of prostaglandin E2 production in lipopolysaccharide-activated macrophages. 6. Cafestol has a peripheral antinociceptive effect and suggest that this effect is mediated by the release of endogenous opioids. 7. Cafestol inhibits angiogenesis by affecting the angiogenic signaling pathway. 8. Cafestol has antidiabetic activity, it increases glucose-stimulated insulin secretion in vitro and increases glucose uptake in human skeletal muscle cells. 9. Cafestol has a weak inhibitory effect on osteoclastogenesis and promotes osteoblast differentiation.
TargetsHO-1 | IL Receptor | p38MAPK | COX | PGE | P450 (e.g. CYP17) | NF-kB | ERK | MEK | AP-1 | FAK | Nrf2 | IkB | IKK

Cafestol Dilution Calculator

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Preparing Stock Solutions of Cafestol

1 mg 5 mg 10 mg 20 mg 25 mg
1 mM 3.1602 mL 15.8008 mL 31.6016 mL 63.2031 mL 79.0039 mL
5 mM 0.632 mL 3.1602 mL 6.3203 mL 12.6406 mL 15.8008 mL
10 mM 0.316 mL 1.5801 mL 3.1602 mL 6.3203 mL 7.9004 mL
50 mM 0.0632 mL 0.316 mL 0.632 mL 1.2641 mL 1.5801 mL
100 mM 0.0316 mL 0.158 mL 0.316 mL 0.632 mL 0.79 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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References on Cafestol

Cafestol, a coffee-specific diterpene, is a novel extracellular signal-regulated kinase inhibitor with AP-1-targeted inhibition of prostaglandin E2 production in lipopolysaccharide-activated macrophages.[Pubmed:20045950]

Biol Pharm Bull. 2010;33(1):128-32.

Coffee is a popular beverage worldwide with various nutritional benefits. Diterpene Cafestol, one of the major components of coffee, contributes to its beneficial effects through various biological activities such as chemopreventive, antitumorigenic, hepatoprotective, antioxidative and antiinflammatory effects. In this study, we examined the precise molecular mechanism of the antiinflammatory activity of Cafestol in terms of prostaglandin E(2) (PGE(2)) production, a critical factor involved in inflammatory responses. Cafestol inhibited both PGE(2) production and the mRNA expression of cyclooxygenase (COX)-2 from lipopolysaccharide (LPS)-treated RAW264.7 cells. Interestingly, this compound strongly decreased the translocation of c-Jun into the nucleus and AP-1 mediated luciferase activity. In kinase assays using purified extracellular signal-regulated kinase 2 (ERK2) or immunoprecipitated ERK prepared from LPS-treated cells in the presence or absence of Cafestol, it was found that this compound can act as an inhibitor of ERK2 but not of ERK1 and mitogen-activated protein kinase kinase 1 (MEK 1). Therefore our data suggest that Cafestol may be a novel ERK inhibitor with AP-1-targeted inhibitory activity against PGE(2) production in LPS-activated RAW264.7 cells.

The cholesterol-raising factor from coffee beans, cafestol, as an agonist ligand for the farnesoid and pregnane X receptors.[Pubmed:17456796]

Mol Endocrinol. 2007 Jul;21(7):1603-16.

Cafestol, a diterpene present in unfiltered coffee brews such as Scandinavian boiled, Turkish, and cafetiere coffee, is the most potent cholesterol-elevating compound known in the human diet. Several genes involved in cholesterol homeostasis have previously been shown to be targets of Cafestol, including cholesterol 7alpha-hydroxylase (CYP7A1), the rate-limiting enzyme in bile acid biosynthesis. We have examined the mechanism by which Cafestol elevates serum lipid levels. Changes in several lipid parameters were observed in Cafestol-treated APOE3Leiden mice, including a significant increase in serum triglyceride levels. Microarray analysis of these mice identified alterations in hepatic expression of genes involved in lipid metabolism and detoxification, many of which are regulated by the nuclear hormone receptors farnesoid X receptor (FXR) and pregnane X receptor (PXR). Further studies demonstrate that Cafestol is an agonist ligand for FXR and PXR, and that Cafestol down-regulates expression of the bile acid homeostatic genes CYP7A1, sterol 12alpha-hydroxylase, and Na(+)-taurocholate cotransporting polypeptide in the liver of wild-type but not FXR null mice. Cafestol did not affect genes known to be up-regulated by FXR in the liver of wild-type mice, but did increase expression of the positive FXR-target genes intestinal bile acid-binding protein and fibroblast growth factor 15 (FGF15) in the intestine. Because FGF15 has recently been shown to function in an enterohepatic regulatory pathway to repress liver expression of bile acid homeostatic genes, its direct induction in the gut may account for indirect effects of Cafestol on liver gene expression. PXR-dependent gene regulation of cytochrome P450 3A11 and other targets by Cafestol was also only seen in the intestine. Using a double FXR/PXR knockout mouse model, we found that both receptors contribute to the Cafestol-dependent induction of intestinal FGF15 gene expression. In conclusion, Cafestol acts as an agonist ligand for both FXR and PXR, and this may contribute to its impact on cholesterol homeostasis.

Antiangiogenic properties of cafestol, a coffee diterpene, in human umbilical vein endothelial cells.[Pubmed:22525673]

Biochem Biophys Res Commun. 2012 May 11;421(3):567-71.

As angiogenesis plays important roles in tumor growth and metastasis, searching for antiangiogenic compounds is a promising tactic for treating cancers. Cafestol, a diterpene found mainly in unfiltered coffee, provides benefit through varied biological activity, including antitumorigenic, antioxidative, and anti-inflammatory effects. This study aimed to investigate the effects of Cafestol on angiogenesis and to uncover the associated mechanism. We show that Cafestol inhibits angiogenesis of human umbilical vascular endothelial cells. This inhibition affects the following specific steps of the angiogenic process: proliferation, migration, and tube formation. The inhibitory effects of Cafestol are accompanied by decreasing phosphorylation of FAK and Akt and by a decrease in nitric oxide production. Overall, Cafestol inhibits angiogenesis by affecting the angiogenic signaling pathway.

Cafestol has a weaker inhibitory effect on osteoclastogenesis than kahweol and promotes osteoblast differentiation.[Pubmed:26154488]

Biofactors. 2015 Jul-Aug;41(4):222-31.

Bone homeostasis is regulated by a balance between osteoclast (OCL)-mediated bone resorption and osteoblast (OBL)-mediated bone formation. Thus, developing a compound that simultaneously inhibits OCL function and promotes OBL function would be useful as a new medical therapy for bone diseases. Here, we examined the effects of Cafestol, a coffee diterpene, on the differentiation of OCLs and OBLs. Cafestol prevented OCL formation in a dose-dependent manner and suppressed the bone-resorbing activity of OCLs. Interestingly, the viability of OCLs treated with 10-50 microM Cafestol was significantly higher than that of untreated cells. At the molecular level, Cafestol markedly decreased RANKL-induced phosphorylation of extracellular signal-regulated kinase (Erk) and inhibitor of nuclear factor kappa B alpha (IkappaBalpha). Compared to kahweol, another coffee-specific diterpene, the inhibitory effects of Cafestol were milder on OCL differentiation, and Cafestol and kahweol showed different characteristics in induction of the phase IotaIota antioxidant enzymes and sensitivities in nuclear factor-erythroid 2-related factor 2 (Nrf2)-deficient BMMs. In addition to inhibiting OCLs, Cafestol enhanced the differentiation of osteoblastic cells by increasing the mRNA levels of differentiation markers. Thus, Cafestol inhibits OCL differentiation and promotes OBL differentiation, suggesting that Cafestol may be a novel agent for bone diseases.

Cafestol and kahweol, two coffee specific diterpenes with anticarcinogenic activity.[Pubmed:12067578]

Food Chem Toxicol. 2002 Aug;40(8):1155-63.

Epidemiological studies have found an inverse association between coffee consumption and the risk of certain types of cancers such as colorectal cancers. Animal data support such a chemopreventive effect of coffee. Substantial research has been devoted to the identification of coffee components that may be responsible for these beneficial effects. In animal models and cell culture systems, the coffee diterpenes Cafestol and kahweol (C+K) were shown to produce a broad range of biochemical effects resulting in a reduction of the genotoxicity of several carcinogens including 7,12-dimethylbenz[a]anthracene (DMBA), aflatoxin B(1) (AFB(1)), benzo[a]pyrene (B[a]P) and 2-amino-1-methyl-6-phenylimidazo[4,5-b]pyridine (PhIP). Different mechanisms appear to be involved in these chemoprotective effects: an induction of conjugating enzymes (e.g. glutathione S-transferases, glucuronosyl S-transferases), an increased expression of proteins involved in cellular antioxidant defense (e.g. gamma-glutamyl cysteine synthetase and heme oxygenase-1) and an inhibition of the expression and/or activity of cytochromes P450 involved in carcinogen activation (e.g. CYP2C11, CYP3A2). In animal models, the C+K-mediated induction of conjugating and antioxidant enzymes has been observed in hepatic, intestinal and kidney tissues. In the small intestine, these inductions were shown to be mediated by Nrf2-dependent transcriptional activation. In vitro investigations obtained in cell cultures of human origin indicate that the effects and mechanisms observed in animal test systems with C+K are likely to be of relevance for humans. In human liver epithelial cell lines transfected to express AFB(1)-activating P450s, C+K treatment resulted in a reduction of AFB(1)-DNA binding. This protection was correlated with an induction of GST-mu, an enzyme known to be involved in AFB(1) detoxification. In addition, C+K was found to inhibit P450 2B6, one of the human enzymes responsible for AFB(1) activation. Altogether, the data on the biological effects of C+K provide a plausible hypothesis to explain some of the anticarcinogenic effects of coffee observed in human epidemiological studies and in animal experiments.

Hepatoprotective and antioxidant effects of the coffee diterpenes kahweol and cafestol on carbon tetrachloride-induced liver damage in mice.[Pubmed:17590492]

Food Chem Toxicol. 2007 Nov;45(11):2118-25.

The hepatoprotective effects of kahweol and Cafestol, coffee-specific diterpenes, on the carbon tetrachloride (CCl(4))-induced liver damage as well as the possible mechanisms involved in these protections were investigated. Pretreatment with kahweol and Cafestol prior to the administration of CCl(4) significantly prevented the increase in the serum levels of hepatic enzyme markers (alanine aminotransferase and aspartate aminotransferase) and reduced oxidative stress, such as reduced glutathione content and lipid peroxidation, in the liver in a dose-dependent manner. The histopathological evaluation of the livers also revealed that kahweol and Cafestol reduced the incidence of liver lesions induced by CCl(4). Treatment of the mice with kahweol and Cafestol also resulted in a significant decrease in the cytochrome P450 2E1 (CYP2E1), the major isozyme involved in CCl(4) bioactivation, specific enzyme activities, such as p-nitrophenol and aniline hydroxylation. Kahweol and Cafestol exhibited antioxidant effects on FeCl(2)-ascorbate induced lipid peroxidation in a mouse liver homogenate, and on superoxide radical scavenging activity. These results suggest that the protective effects of kahweol and Cafestol against the CCl(4)-induced hepatotoxicity possibly involve mechanisms related to their ability to block the CYP2E1-mediated CCl(4) bioactivation and free radical scavenging effects.

Suppressive effects of the kahweol and cafestol on cyclooxygenase-2 expression in macrophages.[Pubmed:15225655]

FEBS Lett. 2004 Jul 2;569(1-3):321-6.

Inducible cyclooxygenase-2 (COX-2) has been suggested to play a role in the processes of inflammation and carcinogenesis. Recent studies have shown the chemoprotective effects of kahweol and Cafestol, which are coffee-specific diterpenes. This study investigated the effects of kahweol and Cafestol on the expression of COX-2 in lipopolysaccharide (LPS)-activated RAW 264.7 macrophages. Kahweol and Cafestol significantly suppressed the LPS-induced production of prostaglandin E(2), COX-2 protein and mRNA expression, and COX-2 promoter activity in a dose-dependent manner. Furthermore, kahweol blocked the LPS-induced activation of NF-kappaB by preventing IkappaB degradation and inhibiting IkappaB kinase activity. These results will provide new insights into the anti-inflammatory and anti-carcinogenic properties of kahweol and Cafestol.

Cafestol, a Bioactive Substance in Coffee, Has Antidiabetic Properties in KKAy Mice.[Pubmed:28763212]

J Nat Prod. 2017 Aug 25;80(8):2353-2359.

Daily coffee consumption is inversely associated with risk of type-2 diabetes (T2D). Cafestol, a bioactive substance in coffee, increases glucose-stimulated insulin secretion in vitro and increases glucose uptake in human skeletal muscle cells. We hypothesized that Cafestol can postpone development of T2D in KKAy mice. Forty-seven male KKAy mice were randomized to consume chow supplemented daily with either 1.1 (high), 0.4 (low), or 0 (control) mg of Cafestol for 10 weeks. We collected blood samples for fasting glucose, glucagon, and insulin as well as liver, muscle, and fat tissues for gene expression analysis. We isolated islets of Langerhans and measured insulin secretory capacity. After 10 weeks of intervention, fasting plasma glucose was 28-30% lower in Cafestol groups compared with the control group (p < 0.01). Fasting glucagon was 20% lower and insulin sensitivity improved by 42% in the high-Cafestol group (p < 0.05). Cafestol increased insulin secretion from isolated islets by 75-87% compared to the control group (p < 0.001). Our results show that Cafestol possesses antidiabetic properties in KKAy mice. Consequently, Cafestol may contribute to the reduced risk of developing T2D in coffee consumers and has a potential role as an antidiabetic drug.

Cafestol Inhibits Cyclic-Strain-Induced Interleukin-8, Intercellular Adhesion Molecule-1, and Monocyte Chemoattractant Protein-1 Production in Vascular Endothelial Cells.[Pubmed:29854096]

Oxid Med Cell Longev. 2018 Apr 30;2018:7861518.

Moderate coffee consumption is inversely associated with cardiovascular disease mortality; however, mechanisms underlying this causal effect remain unclear. Cafestol, a diterpene found in coffee, has various properties, including an anti-inflammatory property. This study investigated the effect of Cafestol on cyclic-strain-induced inflammatory molecule secretion in vascular endothelial cells. Cells were cultured under static or cyclic strain conditions, and the secretion of inflammatory molecules was determined using enzyme-linked immunosorbent assay. The effects of Cafestol on mitogen-activated protein kinases (MAPK), heme oxygenase-1 (HO-1), and sirtuin 1 (Sirt1) signaling pathways were examined using Western blotting and specific inhibitors. Cafestol attenuated cyclic-strain-stimulated intercellular adhesion molecule-1 (ICAM-1), monocyte chemoattractant protein- (MCP-) 1, and interleukin- (IL-) 8 secretion. Cafestol inhibited the cyclic-strain-induced phosphorylation of extracellular signal-regulated kinase and p38 MAPK. By contrast, Cafestol upregulated cyclic-strain-induced HO-1 and Sirt1 expression. The addition of zinc protoporphyrin IX, sirtinol, or Sirt1 silencing (transfected with Sirt1 siRNA) significantly attenuated Cafestol-mediated modulatory effects on cyclic-strain-stimulated ICAM-1, MCP-1, and IL-8 secretion. This is the first study to report that Cafestol inhibited cyclic-strain-induced inflammatory molecule secretion, possibly through the activation of HO-1 and Sirt1 in endothelial cells. The results provide valuable insights into molecular pathways that may contribute to the effects of Cafestol.

Description

Cafestol, one of the major components of coffee, is a coffee-specific diterpene from. Cafestol is a ERK inhibitor for AP-1-targeted activity against PGE2 production and the mRNA expression of cyclooxygenase (COX)-2 in LPS-activated RAW264.7 cells. Cafestol has strong inhibitory activity on PGE2 production by suppressing the NF-kB activation pathway. Cafestol contributes to its beneficial effects through various biological activities such as chemopreventive, antitumorigenic, hepatoprotective, antioxidative and antiinflammatory effects.

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