Caffeic Acid Phenethyl Ester - CAS 104594-70-9
Catalog number: 104594-70-9
Category: Inhibitor
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Molecular Formula:
C17H16O4
Molecular Weight:
284.31
COA:
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Targets:
NF-κB
Description:
Caffeic acid phenethyl ester is a potent and specific inhibitor of NF-κB activation, and also displays antioxidant, immunomodulatory and antiinflammatory activities.
Purity:
>98%
Synonyms:
CAPE; Caffeic Acid Phenethyl Ester; BAF-IN-C09; 2-Phenylethyl Caffeate; β-Phenylethyl Caffeate;
MSDS:
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InChIKey:
SWUARLUWKZWEBQ-VQHVLOKHSA-N
InChI:
InChI=1S/C17H16O4/c18-15-8-6-14(12-16(15)19)7-9-17(20)21-11-10-13-4-2-1-3-5-13/h1-9,12,18-19H,10-11H2/b9-7+
Canonical SMILES:
C1=CC=C(C=C1)CCOC(=O)C=CC2=CC(=C(C=C2)O)O
1.Effect of Caffeic Acid Phenethyl Ester on Vascular Damage Caused by Consumption of High Fructose Corn Syrup in Rats.
Gun A1, Ozer MK2, Bilgic S3, Kocaman N4, Ozan G5. Oxid Med Cell Longev. 2016;2016:3419479. doi: 10.1155/2016/3419479. Epub 2016 Mar 2.
Fructose corn syrup is cheap sweetener and prolongs the shelf life of products, but fructose intake causes hyperinsulinemia, hypertriglyceridemia, and hypertension. All of them are referred to as metabolic syndrome and they are risk factors for cardiovascular diseases. Hence, the harmful effects of increased fructose intake on health and their prevention should take greater consideration. Caffeic Acid Phenethyl Ester (CAPE) has beneficial effects on metabolic syndrome and vascular function which is important in the prevention of cardiovascular disease. However, there are no known studies about the effect of CAPE on fructose-induced vascular dysfunction. In this study, we examined the effect of CAPE on vascular dysfunction due to high fructose corn syrup (HFCS). HFCS (6 weeks, 30% fed with drinking water) caused vascular dysfunction, but treatment with CAPE (50 micromol/kg i.p. for the last two weeks) effectively restored this problem. Additionally, hypertension in HFCS-fed rats was also decreased in CAPE supplemented rats.
2.Protective effects of p-nitro caffeic acid phenethyl ester on acute myocardial ischemia-reperfusion injury in rats.
DU Q1, Hao C1, Gou J1, Li X1, Zou K1, He X1, Li Z1. Exp Ther Med. 2016 Apr;11(4):1433-1440. Epub 2016 Feb 10.
Myocardial ischemia-reperfusion (IR) causes widespread cardiomyocyte dysfunction, including apoptosis and necrosis. The present study aimed to investigate the possible cardioprotective effects of p-nitro caffeic acid phenethyl ester (CAPE-NO2) on myocardial IR-induced injury in vivo. To generate a rat model of myocardial IR, the left anterior descending coronary artery was occluded for 30 min, followed by reperfusion for 2 h. The rats were administered either the sham treatment (the sham and IR control groups) or the therapeutic agents [the caffeic acid phenethyl ester (CAPE) and CAPE-NO2 groups] 10 min prior to the occlusion. Myocardial IR-induced injury is characterized by: A significant increase in the levels of myocardial enzymes, including creatine kinase, lactate dehydrogenase and aspartate transaminase; a marked increase in intercellular adhesion molecule 1 expression levels, lipid peroxidation products and inflammatory mediators; and a significant decrease in myocardial antioxidants, including catalase, total superoxide dismutase and glutathione peroxidase.
3.Could Caffeic Acid Phenethyl Ester Expand the Antitumor Effect of Tamoxifen in Breast Carcinoma?
Motawi TK1, Abdelazim SA1, Darwish HA1, Elbaz EM1, Shouman SA2. Nutr Cancer. 2016 Mar 23:1-11. [Epub ahead of print]
Despite tamoxifen (TAM) is beneficial in treating a significant proportion of patients with breast cancer, many women still relapse after long-term therapy. Caffeic acid phenethyl ester (CAPE) is a component of honeybee propolis, with a plethora of important biological actions including anticancer activity. This study aimed to explore the cytotoxicity, the type of drugs interaction as well as the apoptotic and autophagic pathways of the combined treatment of TAM and CAPE in MCF-7 cells. Their antitumor activity and effect on survival of mice bearing Ehrlich tumor were also analyzed. The results showed synergistic cytotoxic effects, manifested by significant activation of apoptotic machinery, along with downregulation of protein levels of Bcl-2 and beclin-1, upon using the combination regimen. However, the ratio between microtubule-associated protein light chain 3-II and -I was not altered. Moreover, a decrease in vascular endothelial growth factor level was detected.
4.microRNA-34a-Mediated Down-Regulation of the Microglial-Enriched Triggering Receptor and Phagocytosis-Sensor TREM2 in Age-Related Macular Degeneration.
Bhattacharjee S1, Zhao Y1,2, Dua P3, Rogaev EI4,5,6, Lukiw WJ1,5,7,8. PLoS One. 2016 Mar 7;11(3):e0150211. doi: 10.1371/journal.pone.0150211. eCollection 2016.
The aggregation of Aβ42-peptides and the formation of drusen in age-related macular degeneration (AMD) are due in part to the inability of homeostatic phagocytic mechanisms to clear self-aggregating Aβ42-peptides from the extracellular space. The triggering receptor expressed in myeloid/microglial cells-2 (TREM2), a trans-membrane-spanning, sensor-receptor of the immune-globulin/lectin-like gene superfamily is a critical component of Aβ42-peptide clearance. Here we report a significant deficit in TREM2 in AMD retina and in cytokine- or oxidatively-stressed microglial (MG) cells. RT-PCR, miRNA-array, LED-Northern and Western blot studies indicated up-regulation of a microglial-enriched NF-кB-sensitive miRNA-34a coupled to a down-regulation of TREM2 in the same samples. Bioinformatics/transfection-luciferase reporter assays indicated that miRNA-34a targets the 299 nucleotide TREM2-mRNA-3'UTR, resulting in TREM2 down-regulation. C8B4-microglial cells challenged with Aβ42 were able to phagocytose these peptides, while miRNA-34a down-regulated both TREM2 and the ability of microglial-cells to phagocytose.
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CAS 104594-70-9 Caffeic Acid Phenethyl Ester

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