Ethyl caffeate

CAS# 102-37-4

Ethyl caffeate

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Chemical structure

Ethyl caffeate

3D structure

Chemical Properties of Ethyl caffeate

Cas No. 102-37-4 SDF Download SDF
PubChem ID 5317238 Appearance Powder
Formula C11H12O4 M.Wt 208.2
Type of Compound Phenylpropanoids Storage Desiccate at -20°C
Synonyms 66648-50-8;Caffeic Acid Ethyl Ester; Ethyl Trans-Caffeate
Solubility DMSO : 250 mg/mL (1200.71 mM; Need ultrasonic)
Chemical Name ethyl (E)-3-(3,4-dihydroxyphenyl)prop-2-enoate
SMILES CCOC(=O)C=CC1=CC(=C(C=C1)O)O
Standard InChIKey WDKYDMULARNCIS-GQCTYLIASA-N
Standard InChI InChI=1S/C11H12O4/c1-2-15-11(14)6-4-8-3-5-9(12)10(13)7-8/h3-7,12-13H,2H2,1H3/b6-4+
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 Ethyl caffeate

The roots of Ferula assafoetida L.

Biological Activity of Ethyl caffeate

DescriptionEthyl caffeate is a potent chemopreventive compound against skin carcinogenesis caused by solar UV exposure, it strongly inhibits neoplastic transformation of JB6 Cl41 cells without toxicity. PI3K, ERK1/2, and p38 kinase activities were suppressed by direct binding with HOEC in vitro. Ethyl caffeate also has anti-inflammatory, hepatprotective activities.
TargetsPI3K | ERK | p38MAPK | AP-1 | NF-kB | Akt | NOS | COX | PGE
In vitro

A mechanistic study on the anti-cancer activity of ethyl caffeate in human ovarian cancer SKOV-3 cells.[Pubmed: 24892518 ]

Chem Biol Interact. 2014 Aug 5;219:151-8.

In the present study, we investigated the effect and molecular mechanism of Ethyl caffeate (EC), a natural phenolic compound isolated from Ligularia fischeri, on human ovarian cancer cell proliferation and progression.
METHODS AND RESULTS:
EC-mediated inhibition of cell proliferation in SKOV-3 cells was accompanied by reduced expression of cell cycle-related proteins such as cyclin-dependent kinases and cyclins, resulting in pRb hypophosphorylation and G₁ phase cell cycle arrest. Moreover, EC treatment markedly inhibited cell migration and invasion. These regulatory effects of EC on ovarian cancer cell proliferation, migration and invasion were associated with inactivation of mitogenic signaling pathways such as Akt, ERK and p38(MAPK), and down-regulation of cell surface signaling molecules including receptor tyrosine kinases, integrin α3β1 and N-cadherin.
CONCLUSIONS:
Taken together, these findings suggest further evaluation and development of EC for the treatment and prevention of ovarian cancer.

Ethyl caffeate suppresses NF-kappaB activation and its downstream inflammatory mediators, iNOS, COX-2, and PGE2 in vitro or in mouse skin.[Pubmed: 16041399]

Br J Pharmacol. 2005 Oct;146(3):352-63.

Ethyl caffeate, a natural phenolic compound, was isolated from Bidens pilosa, a medicinal plant popularly used for treating certain inflammatory syndromes. The purpose of this study was to investigate the structural activity, and the anti-inflammatory functions and mechanism(s) of Ethyl caffeate.
METHODS AND RESULTS:
Ethyl caffeate was found to markedly suppress the lipopolysaccharide (LPS)-induced nitric oxide (NO) production (IC(50) = 5.5 microg ml(-1)), mRNA and protein expressions of inducible nitric oxide synthase (iNOS), and prostaglandin E(2) (PGE(2)) production in RAW 264.7 macrophages. Transient gene expression assays using human cox-2 promoter construct revealed that Ethyl caffeate exerted an inhibitory effect on cox-2 transcriptional activity in 12-O-tetradecanoylphorbol-13-acetate (TPA)-treated MCF-7 cells. Immunohistochemical studies of mouse skin demonstrated that TPA-induced COX-2 expression was significantly inhibited by Ethyl caffeate with a superior effect to that of celecoxib, a nonsteroidal anti-inflammatory drug. The phosphorylation and degradation of inhibitor kappaB (IkappaB) and the translocation of nuclear transcription factor-kappaB (NF-kappaB) into the nucleus, as well as the activation of mitogen-activated protein kinases (MAPKs) induced by LPS in macrophages, were not affected by Ethyl caffeate. Ethyl caffeate, however, could inhibit NF-kappaB activation by impairing the binding of NF-kappaB to its cis-acting element. These results suggest that Ethyl caffeate suppresses iNOS and COX-2 expressions partly through the inhibition of the NF-kappaB.DNA complex formation. Structure-activity relationship analyses suggested that the catechol moiety and alpha,beta-unsaturated ester group in Ethyl caffeate are important and essential structural features for preventing NF-kappaB.DNA complex formation.
CONCLUSIONS:
This study provides an insight into the probable mechanism(s) underlying the anti-inflammatory and therapeutic properties of Ethyl caffeate.

In vivo

Ethyl caffeate from Verdicchio wine: chromatographic purification and in vivo evaluation of its antifibrotic activity.[Pubmed: 19813225]

J Sep Sci. 2009 Nov;32(21):3585-90.

Ethyl caffeate (CfE, caffeic acid ethyl ester) was extracted from dealcoholized Verdicchio, a white wine from Marche (Italy) with ethyl acetate and then purified with semipreparative reversed-phase high-performance liquid chromatography (RP-HPLC) using an ODS2 column (25 cm x 20 mm id) at an isocratic flow of 5 mL/min (the mobile phase A was formic acid 4.5% in water and the mobile phase B was acetonitrile).
METHODS AND RESULTS:
The CfE extract administered intraperitoneally at 1 mumol/L in rats previously treated with 10 mg/kg dimethylnitrosamine was able to prevent the dimethylnitrosamine-induced loss in body and liver weight, as well as to reduce the degree of liver injury, as determined by alanine aminotransferase values and necroinflammatory score, after a 1-week treatment. This was associated with a reduced hepatic stellate cells activation (from 16.8 to 8.3% of smooth muscle actin positive parenchyma) and proliferation (from 11.3 to 5.5 cells/mm(2)). The collagen synthesis was also reduced: the percentage of Sirius Red positive parenchyma decreased from 21.7 to 7.2%.
CONCLUSIONS:
The CfE levels of Verdicchio wine determined with RP-HPLC-DAD were about 14 times the active levels tested in the in vivo test. CfE can be considered as a promising natural compound for future application in chronic liver disease.

Protocol of Ethyl caffeate

Kinase Assay

(+)-2-(1-Hydroxyl-4-oxocyclohexyl) ethyl caffeate suppresses solar UV-induced skin carcinogenesis by targeting PI3K, ERK1/2, and p38.[Pubmed: 24845061]

Cancer Prev Res (Phila). 2014 Aug;7(8):856-65.

For decades, skin cancer incidence has increased, mainly because of oncogenic signaling pathways activated by solar ultraviolet (UV) irradiation (i.e., sun exposure). Solar UV induces multiple signaling pathways that are critical in the development of skin cancer, and therefore the development of compounds capable of targeting multiple molecules for chemoprevention of skin carcinogenesis is urgently needed.
METHODS AND RESULTS:
Herein, we examined the chemopreventive effects and the molecular mechanism of (+)-2-(1-hydroxyl-4-oxocyclohexyl) Ethyl caffeate (HOEC), isolated from Incarvillea mairei var. grandiflora (Wehrhahn) Grierson. HOEC strongly inhibited neoplastic transformation of JB6 Cl41 cells without toxicity. PI3K, ERK1/2, and p38 kinase activities were suppressed by direct binding with HOEC in vitro. Our in silico docking data showed that HOEC binds at the ATP-binding site of each kinase. The inhibition of solar UV-induced PI3K, ERK1/2, and p38 kinase activities resulted in suppression of their downstream signaling pathways and AP1 and NF-κB transactivation in JB6 cells. Furthermore, topical application of HOEC reduced skin cancer incidence and tumor volume in SKH-1 hairless mice chronically exposed to solar UV.
CONCLUSIONS:
In summary, our results show that HOEC exerts inhibitory effects on multiple kinase targets and their downstream pathways activated by solar UV in vitro and in vivo. These findings suggest that HOEC is a potent chemopreventive compound against skin carcinogenesis caused by solar UV exposure.

Structure Identification
J Med Chem. 2012 Nov 26;55(22):10177-86.

Order and disorder: differential structural impacts of myricetin and ethyl caffeate on human amylase, an antidiabetic target.[Pubmed: 23050660]

The increasing prevalence of diabetes has accelerated the search for new drugs derived from natural sources. To define the functional features of two such families of compounds, the flavonols and the Ethyl caffeates, we have determined the high-resolution structures of representative inhibitors in complex with human pancreatic α-amylase.
METHODS AND RESULTS:
Myricetin binds at the active site and interacts directly with the catalytic residues despite its bulky planar nature. Notably, it reduces the normal conformational flexibility of the adjacent substrate binding cleft. In contrast, bound Ethyl caffeate acts by disordering precisely those polypeptide chain segments that make up the active site binding cleft. It also operates from binding sites far removed from the active site, a property not observed in any other class of human α-amylase inhibitor studied to date.
CONCLUSIONS:
Given the current inadequacy of drugs directed at diabetes, the use of optimized flavonols and Ethyl caffeates may present an alternative therapeutic route.

Ethyl caffeate Dilution Calculator

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Ethyl caffeate Molarity Calculator

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Preparing Stock Solutions of Ethyl caffeate

1 mg 5 mg 10 mg 20 mg 25 mg
1 mM 4.8031 mL 24.0154 mL 48.0307 mL 96.0615 mL 120.0768 mL
5 mM 0.9606 mL 4.8031 mL 9.6061 mL 19.2123 mL 24.0154 mL
10 mM 0.4803 mL 2.4015 mL 4.8031 mL 9.6061 mL 12.0077 mL
50 mM 0.0961 mL 0.4803 mL 0.9606 mL 1.9212 mL 2.4015 mL
100 mM 0.048 mL 0.2402 mL 0.4803 mL 0.9606 mL 1.2008 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 Ethyl caffeate

Enzymatic incorporation of caffeoyl into castor oil to prepare the novel castor oil-based caffeoyl structured lipids.[Pubmed:28344155]

J Biotechnol. 2017 May 10;249:66-72.

In this work, a novel castor oil-based caffeoyl structured lipids was successfully prepared by the enzymatic transesterification using castor oil (CO) as caffeoyl acceptor. During the structured lipids preparation, two competitive reactions, the hydrolysis of CO to form hydrophilic caffeoyl glycerols (CG)+dicaffeoyl glycerols (DCG) and the transesterification of CO with Ethyl caffeate (EC) to form lipophilic caffeoyl mono- and di-acylglycerols (CMAG and CDAG), were found. Reaction progress was monitored using HPLC-ESI-MS and HPLC-UV. The effects of by-product ethanol removal and reaction variables on the transesterification and reaction selectivity were evaluated. Results showed that, the activation energies for the transesterification and for the selective formations of CMAG+CDAG and CG+DCG were 57.60kJ/mol, 58.86kJ/mol, and 60.53kJ/mol, respectively. Under the optimal reaction conditions (enzyme load 23%, 90 degrees C, 1:3 molar ratio of EC to CO, and 46.5h), EC conversion and the yield of CMAG+CDAG were 93.68+/-2.52% and 78.11+/-1.35%, respectively.

Ethyl caffeate suppresses NF-kappaB activation and its downstream inflammatory mediators, iNOS, COX-2, and PGE2 in vitro or in mouse skin.[Pubmed:16041399]

Br J Pharmacol. 2005 Oct;146(3):352-63.

Ethyl caffeate, a natural phenolic compound, was isolated from Bidens pilosa, a medicinal plant popularly used for treating certain inflammatory syndromes. The purpose of this study was to investigate the structural activity, and the anti-inflammatory functions and mechanism(s) of Ethyl caffeate. Ethyl caffeate was found to markedly suppress the lipopolysaccharide (LPS)-induced nitric oxide (NO) production (IC(50) = 5.5 microg ml(-1)), mRNA and protein expressions of inducible nitric oxide synthase (iNOS), and prostaglandin E(2) (PGE(2)) production in RAW 264.7 macrophages. Transient gene expression assays using human cox-2 promoter construct revealed that Ethyl caffeate exerted an inhibitory effect on cox-2 transcriptional activity in 12-O-tetradecanoylphorbol-13-acetate (TPA)-treated MCF-7 cells. Immunohistochemical studies of mouse skin demonstrated that TPA-induced COX-2 expression was significantly inhibited by Ethyl caffeate with a superior effect to that of celecoxib, a nonsteroidal anti-inflammatory drug. The phosphorylation and degradation of inhibitor kappaB (IkappaB) and the translocation of nuclear transcription factor-kappaB (NF-kappaB) into the nucleus, as well as the activation of mitogen-activated protein kinases (MAPKs) induced by LPS in macrophages, were not affected by Ethyl caffeate. Ethyl caffeate, however, could inhibit NF-kappaB activation by impairing the binding of NF-kappaB to its cis-acting element. These results suggest that Ethyl caffeate suppresses iNOS and COX-2 expressions partly through the inhibition of the NF-kappaB.DNA complex formation. Structure-activity relationship analyses suggested that the catechol moiety and alpha,beta-unsaturated ester group in Ethyl caffeate are important and essential structural features for preventing NF-kappaB.DNA complex formation. This study provides an insight into the probable mechanism(s) underlying the anti-inflammatory and therapeutic properties of Ethyl caffeate.

A novel method for the synthesis of glyceryl monocaffeate by the enzymatic transesterification and kinetic analysis.[Pubmed:27507465]

Food Chem. 2017 Jan 1;214:192-198.

A novel enzymatic method for glyceryl monocaffeate (GMC) preparation by the transesterification of Ethyl caffeate (EC) was investigated. The effects of reaction variables (reaction pressure, temperature, reaction time, enzyme load, and substrate ratio) on the enzymatic transesterification were studied and optimized using response surface methodology. HPLC-ESI-MS and HPLC-UV were used to monitor the transesterification. Thermodynamics, kinetic analyses and reaction mechanism were also evaluated. Results showed that, GMC can be successfully prepared by the enzymatic transesterification of EC with glycerol. Under the optimal conditions (enzyme load 22.54%, EC:glycerol=1:12.75 (mol/mol), 72.5 degrees C, and 10.5h), EC conversion and GMC yield were 97.9+/-0.7% and 95.8+/-1.0%, respectively. The activation energies (Ea) for EC conversion and GMC formation were 44.23 and 46.51kJ/mol, respectively. The kinetic values for Vmax, Km(') and KIA were 2.18x10(-3)mol/(Lmin), 0.086mol/L, and 0.52mol/L, respectively. The transesterification mechanism with EC inhibition was also proposed.

Ethyl caffeate from Verdicchio wine: chromatographic purification and in vivo evaluation of its antifibrotic activity.[Pubmed:19813225]

J Sep Sci. 2009 Nov;32(21):3585-90.

Ethyl caffeate (CfE, caffeic acid ethyl ester) was extracted from dealcoholized Verdicchio, a white wine from Marche (Italy) with ethyl acetate and then purified with semipreparative reversed-phase high-performance liquid chromatography (RP-HPLC) using an ODS2 column (25 cm x 20 mm id) at an isocratic flow of 5 mL/min (the mobile phase A was formic acid 4.5% in water and the mobile phase B was acetonitrile). The CfE extract administered intraperitoneally at 1 mumol/L in rats previously treated with 10 mg/kg dimethylnitrosamine was able to prevent the dimethylnitrosamine-induced loss in body and liver weight, as well as to reduce the degree of liver injury, as determined by alanine aminotransferase values and necroinflammatory score, after a 1-week treatment. This was associated with a reduced hepatic stellate cells activation (from 16.8 to 8.3% of smooth muscle actin positive parenchyma) and proliferation (from 11.3 to 5.5 cells/mm(2)). The collagen synthesis was also reduced: the percentage of Sirius Red positive parenchyma decreased from 21.7 to 7.2%. The CfE levels of Verdicchio wine determined with RP-HPLC-DAD were about 14 times the active levels tested in the in vivo test. CfE can be considered as a promising natural compound for future application in chronic liver disease.

Order and disorder: differential structural impacts of myricetin and ethyl caffeate on human amylase, an antidiabetic target.[Pubmed:23050660]

J Med Chem. 2012 Nov 26;55(22):10177-86.

The increasing prevalence of diabetes has accelerated the search for new drugs derived from natural sources. To define the functional features of two such families of compounds, the flavonols and the Ethyl caffeates, we have determined the high-resolution structures of representative inhibitors in complex with human pancreatic alpha-amylase. Myricetin binds at the active site and interacts directly with the catalytic residues despite its bulky planar nature. Notably, it reduces the normal conformational flexibility of the adjacent substrate binding cleft. In contrast, bound Ethyl caffeate acts by disordering precisely those polypeptide chain segments that make up the active site binding cleft. It also operates from binding sites far removed from the active site, a property not observed in any other class of human alpha-amylase inhibitor studied to date. Given the current inadequacy of drugs directed at diabetes, the use of optimized flavonols and Ethyl caffeates may present an alternative therapeutic route.

Discovery of Potential Inhibitors of Aldosterone Synthase from Chinese Herbs Using Pharmacophore Modeling, Molecular Docking, and Molecular Dynamics Simulation Studies.[Pubmed:27781210]

Biomed Res Int. 2016;2016:4182595.

Aldosterone synthase (CYP11B2) is a key enzyme for the biosynthesis of aldosterone, which plays a significant role for the regulation of blood pressure. Excess aldosterone can cause the dysregulation of the renin-angiotensin-aldosterone system (RAAS) and lead to hypertension. Therefore, research and development of CYP11B2 inhibitor are regarded as a novel approach for the treatment of hypertension. In this study, the pharmacophore models of CYP11B2 inhibitors were generated and the optimal model was used to identify potential CYP11B2 inhibitors from the Traditional Chinese Medicine Database (TCMD, Version 2009). The hits were further refined by molecular docking and the interactions between compounds and CYP11B2 were analyzed. Compounds with high Fitvalue, high docking score, and expected interactions with key residues were selected as potential CYP11B2 inhibitors. Two most promising compounds, Ethyl caffeate and labiatenic acid, with high Fitvalue and docking score were reserved for molecular dynamics (MD) study. All of them have stability of ligand binding which suggested that they might perform the inhibitory effect on CYP11B2. This study provided candidates for novel drug-like CYP11B2 inhibitors by molecular simulation methods for the hypertension treatment.

(+)-2-(1-Hydroxyl-4-oxocyclohexyl) ethyl caffeate suppresses solar UV-induced skin carcinogenesis by targeting PI3K, ERK1/2, and p38.[Pubmed:24845061]

Cancer Prev Res (Phila). 2014 Aug;7(8):856-65.

For decades, skin cancer incidence has increased, mainly because of oncogenic signaling pathways activated by solar ultraviolet (UV) irradiation (i.e., sun exposure). Solar UV induces multiple signaling pathways that are critical in the development of skin cancer, and therefore the development of compounds capable of targeting multiple molecules for chemoprevention of skin carcinogenesis is urgently needed. Herein, we examined the chemopreventive effects and the molecular mechanism of (+)-2-(1-hydroxyl-4-oxocyclohexyl) Ethyl caffeate (HOEC), isolated from Incarvillea mairei var. grandiflora (Wehrhahn) Grierson. HOEC strongly inhibited neoplastic transformation of JB6 Cl41 cells without toxicity. PI3K, ERK1/2, and p38 kinase activities were suppressed by direct binding with HOEC in vitro. Our in silico docking data showed that HOEC binds at the ATP-binding site of each kinase. The inhibition of solar UV-induced PI3K, ERK1/2, and p38 kinase activities resulted in suppression of their downstream signaling pathways and AP1 and NF-kappaB transactivation in JB6 cells. Furthermore, topical application of HOEC reduced skin cancer incidence and tumor volume in SKH-1 hairless mice chronically exposed to solar UV. In summary, our results show that HOEC exerts inhibitory effects on multiple kinase targets and their downstream pathways activated by solar UV in vitro and in vivo. These findings suggest that HOEC is a potent chemopreventive compound against skin carcinogenesis caused by solar UV exposure.

[Chemical constituents from Murraya euchrestifolia].[Pubmed:29090551]

Zhongguo Zhong Yao Za Zhi. 2017 May;42(10):1916-1921.

The open silica gel, ODS, and Sephadex LH-20 column chromatography, along with the semi-preparative HPLC was used to isolate and purify the chemical constituents from Murraya euchrestifolia. The structures of the isolates were elucidated by their physiochemical properties, NMR, and MS spectroscopic data, as well as comparison with literature data. Eighteen compounds were isolated from the CH2Cl2 fraction of the 95% aqueous EtOH extract of M. euchrestifolia, and their structures were identified as sakuranetin (1), eriodictyol-7,4'-dimethyl ether (2), isosakuranetin (3), 5-hydroxy-7,4'-dimethoxyflavanone (4), eriodictyol-7-methyl ether (5), lichexanthon (6), 5,6,7-trimethoxycoumarin (7), 5-hydroxy-6,8-dimethoxycoumarin (8), 8-hydroxy-6-methoxy-3-n-pentylisocoumarin (9), Ethyl caffeate (10), 4-hydroxy-3,5- dimethoxycinnamic acid ethyl ester (11), methyl 3-(5'-hydroxyprenyl)-coumarate (12), (E)-coniferol (13), beta-hydroxypropiovanillone (14), 3-hydroxy-7,8-didehydro-beta-ionone (15), 3beta-hydroxy-5alpha, 6alpha-epoxy-7-megastigmen-9-one (16), grasshopper ketone (17), and 4-hydroxy-3,5-dimethoxybenzaldehyde (18). Compounds 1-15 and 18 were first obtained from the plants of Murraya genus, and compounds 16 and 17 were isolated from M. euchrestifolia for the first time.

Description

Ethyl Caffeate is a natural phenolic compound isolated from Bidens pilosa. Ethyl caffeate suppresses NF-κB activation and its downstream inflammatory mediators, inducible nitric oxide synthase (iNOS), cyclooxygenase-2 (COX-2), and prostaglandin E2 (PGE2) in vitro or in mouse skin.

Keywords:

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