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Ethyl caffeate


  • Brand : BIOFRON

  • Catalogue Number : BD-D0041

  • Specification : HPLC≥98%

  • CAS number : 102-37-4

  • Formula : C11H12O4

  • Molecular Weight : 208.2

  • PUBCHEM ID : 5317238

  • Volume : 20mg

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Catalogue Number


Analysis Method





Molecular Weight




Botanical Source

This product is isolated and purified from the roots of Ferula assafoetida L.

Structure Type





Ethyl (2E)-3-(3,4-dihydroxyphenyl)acrylate/Ethyl caffeate/caffeic acid ethyl ester/(E)-ethyl 3-(3,4-dihydroxyphenyl)acrylate/3,4-Dihydroxycinnamic acid ethyl ester/ethyl (2E)-3-(3,4-dihydroxyphenyl)prop-2-enoate/2-Propenoic acid, 3-(3,4-dihydroxyphenyl)-, ethyl ester/ETHYL TRANS-CAFFEATE/ETHYL 3,4-DIHYDROXYCINNAMATE/2-Propenoic acid, 3-(3,4-dihydroxyphenyl)-, ethyl ester, (2E)-



1.3±0.1 g/cm3


Flash Point

148.4±18.6 °C

Boiling Point

377.0±32.0 °C at 760 mmHg

Melting Point


InChl Key


WGK Germany


HS Code Reference

Personal Projective Equipment

Correct Usage

For Reference Standard and R&D, Not for Human Use Directly.

Meta Tag

provides coniferyl ferulate(CAS#:102-37-4) MSDS, density, melting point, boiling point, structure, formula, molecular weight etc. Articles of coniferyl ferulate are included as well.>> amp version: coniferyl ferulate

No Technical Documents Available For This Product.




To explore the in-vitro and in-vivo antimalarial potential of caffeic acid and derivatives.

Two common phenolic acids (caffeic acid and chlorogenic acid) were evaluated for in-vitro and in-vivo antiplasmodial activity in comparison with some semi-synthetic derivatives that were synthesized. An in-vitro assay based on plasmodial lactate dehydrogenase activity, and the classical in-vivo 5-day suppressive test from Peters on an artemisinin-resistant Plasmodium berghei strain was used. Parasitic stage sensitivity to ethyl caffeate was determined in this work.

Phenolic acid esters derivatives showed better antiplasmodial activity than corresponding phenolic acids. The derivative with the highest in-vitro activity being caffeic acid ethyl ester, exhibiting an IC50 = 21.9 ± 9.4 μm. Ethyl caffeate and methyl caffeate were then evaluated for antimalarial activity in vivo and ethyl caffeate showed a growth inhibition of 55% at 100 mg/kg. Finally, it seems that ethyl caffeate blocks the growth of young parasitic forms.

Our study provides evidence for an antimalarial potential of caffeic acid derivatives which are common in several medicinal plants traditionally used against malaria. It also demonstrates the possibility to use such derivatives in the treatment of malaria.

© 2018 Royal Pharmaceutical Society.


Plasmodium falciparum ; Malaria; caffeic acid; ethyl caffeate


In-vitro and in-vivo antimalarial activity of caffeic acid and some of its derivatives.


Alson SG1,2, Jansen O1, Cieckiewicz E1, Rakotoarimanana H2, Rafatro H2, Degotte G1,3, Francotte P3, Frederich M1.

Publish date

2018 Oct




The present study was designed to assess the antiarthritic potential of ECF in collagen-induced arthritis (CIA) and explore its underlying mechanism. Methods. In vitro, lymphocyte proliferation assay was measured by CCK-8 kit. In vivo, the therapeutic potential of ECF on CIA was investigated; surface marker, Treg cell, and intracellular cytokines (IL-17A and IFN-γ) were detected by flow cytometry. Th1 cell differentiation assay was performed, and mRNA expression in interferon-γ-related signaling was examined by q-PCR analysis. Results. In vitro, ECF markedly inhibited the proliferation of splenocytes in response to ConA and anti-CD3. In vivo, ECF treatment reduced the severity of CIA, inhibited IFN-γ and IL-6 secretion, and decreased the proportion of CD11b+Gr-1+ splenic neutrophil. Meanwhile, ECF treatment significantly inhibited the IFN-γ expression in CD4+T cell without obviously influencing the development of Th17 cells and T regulatory cells. In vitro, ECF suppressed the differentiation of naive CD4+ T cells into Th1. Furthermore, ECF intensely blocked the transcriptional expression in interferon-γ-related signaling, including IFN-γ, T-bet, STAT1, and STAT4. Conclusion. Our results indicated that ECF exerted antiarthritic potential in collagen-induced arthritis by suppressing Th1 immune response and interferon-γ-related signaling.


Ethyl Caffeate Ameliorates Collagen-Induced Arthritis by Suppressing Th1 Immune Response.


Xu S1,2, Zuo A3, Guo Z1, Wan C4.

Publish date





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°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.

Copyright © 2017 Elsevier B.V. All rights reserved.


Caffeic acid; Castor oil; Castor oil-based caffeoyl structured lipids; Lipase; Reaction selectivity; Transesterification


Enzymatic incorporation of caffeoyl into castor oil to prepare the novel castor oil-based caffeoyl structured lipids.


Sun S1, Wang P2, Zhu S3.

Publish date

2017 May 10

Description :

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.