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Everything about Caffeic Acid Phenethyl Ester


  1.Caffeic Acid Phenethyl Ester–CAS:104594-70-9
  2.Caffeic Acid Phenethyl Ester: Technical Informations
  3. Caffeic Acid Phenethyl Ester: Physical Characteristics
  4.Attenuating effects of caffeic acid phenethyl ester and betaine on abamectin-induced hepatotoxicity and nephrotoxicity?
  5. Caffeic Acid Phenethyl Ester(CAS:104594-70-9)Synthesis
  6.Caffeic Acid Phenethyl Ester Supplement



Caffeic Acid Phenethyl Ester(CAPE) powder video



I.Caffeic Acid Phenethyl Ester(CAPE) powder basic Characters:


Name: Caffeic Acid Phenethyl Ester(CAPE) powder
CAS: 104594-70-9
Molecular Formula: C17H16O4
Molecular Weight: 284.31
Melt Point: 127-129°C
Storage Temp: -20°C
Color: Off-White powder



1. Caffeic Acid Phenethyl Ester–CAS:104594-70-9aasraw


Caffeic acid phenethyl ester (CAPE) is a bioactive compound of propolis extract. The literature search elaborates that CAPE possesses antimicrobial, antioxidant, anti-inflammatory, and cytotoxic properties. The principal objective of this review article is to sum up and critically assess the existing data about therapeutic effects of CAPE in different disorders. The findings elaborate that CAPE is a versatile therapeutically active polyphenol and an effective adjuvant of chemotherapy for enhancing therapeutic efficacy and diminishing chemotherapy-induced toxicities.
Caffeic acid phenethyl ester (CAPE) is a natural bioactive compound. It occurs in many plants. It is acquired from propolis obtained through extraction from honeybee hives. The chemical name of CAPE is 2-phenylethyl (2E)-3-(3,4-dihydroxyphenyl)acrylate. It is also termed as phenylethyl caffeate or phenethyl caffeate. Its molecular formula is C17H16O4. The chemical structure of CAPE is given in Figure.For the first time, Grunberger et al. identified this hydrophobic polyphenol. This polyphenolic ester can also be synthesized by reacting caffeic acid with phenethyl alcohols. CAPE is a polyphenol with hydroxyl groups within the catechol ring which is responsible for its crucial role in many biological activities. The literature search showed an extensive research on the biological features of CAPE. The available studies narrate it as an effective moiety against various pathologies such as infections, oxidative stress, inflammation, cancer, diabetes, neurodegeneration, and anxiety. These therapeutic characteristics of CAPE have been summarized in this review article.



2. Caffeic Acid Phenethyl Ester: Technical Informationsaasraw


Formal Name (E)-3-(3,4-dihydroxyphenyl)-2-propenoic acid, 2-phenylethyl ester
CAS Number 104594-70-9
  • CAPE
  • 2-Phenylethyl Caffeate
  • β-Phenylethyl Caffeate
Molecular Formula C17H16O4
Formula Weight 284.3
Purity ≥98%
Formulation A crystalline solid
λmax 246, 300, 331 nm
SMILES O=C(OCCc1ccccc1)\C=C/c1ccc(O)c(O)c1
InChI Code 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+



3. Caffeic Acid Phenethyl Ester: Physical Characteristicsaasraw


(1) Activities of CAPE

Large number of studies has been conducted on various features of the biological and pharmacological activities of CAPE and its mode of action. Some of them are summarized below.


(2) Antimicrobial Activity of CAPE

There are many studies which demonstrate the antimicrobial activity of CAPE against Enterococcus faecalis, Listeria monocytogenes, Staphylococcus aureus [9–11], and Haemophilus influenzae showing that RNA, DNA, and cellular proteins are possible targets of CAPE [9, 12]. Thus, dietary intake of CAPE is useful for the treatment of sore throat, common cold, and wound. There is evidence that CAPE possesses promising fungicidal activity on fungi infecting tomato without causing any harm to the fruit [13]. Moreover, poly(lactic-co-glycolic acid) (PLGA) sutures containing CAPE have been proposed to have antibacterial activity against Staphylococcus aureus and Escherichia DH5α bacteria; this activity of CAPE was attributed to the synthesis of reactive oxygen species (ROS) that destroy the outer membrane of bacteria [14]. In recent studies [15–17], CAPE has been proposed as a valuable inhibitor of HIV-1 integrase; therefore, this polyphenol is believed to be a potential anti-HIV therapy. Fesen et al. reported that the integration step is efficiently inhibited by CAPE than the initial cleavage step by HIV-1 integrase [18]. In addition, CAPE and its esters, in a concentration range of 1.0 to 109.6 mM, have also been tested in an HCV replicon cell line of genotype 1b and found effective against replication of hepatitis C virus suggesting it a promising anti-HCV compound.


(3) Cytotoxicity of CAPE

An extensive literature is available regarding cytotoxicity studies of CAPE as documented in Tables 1 and 2. In the presence of CAPE, human pancreatic and colon cancer cells undergo apoptosis. The in vitro and in vivo studies reveal the growth inhibition of C6 glioma cells by CAPE.
There are many evidences which elaborate the antiproliferation activity of CAPE. For normal cellular proliferation, adequate levels of nuclear factor (NF)-κB activity must be maintained. In some cancers, elevated activation of NF-κB is observed. To obstruct the NF-κB activation phenomenon, CAPE has been proved to be effective chemopreventive agent. Nutritional ingestion of CAPE may thus be valuable for patients whose tumors express steadily elevated levels of activated NF-κB, for instance, squamous head and neck carcinomas. It has been reported that CAPE render antitumor features devoid of causing cytotoxicity to normal cells. Su et al. proposed that cytotoxicity of CAPE is directly related to its apoptotic effect.
The antitumor activity of CAPE has been investigated to reveal its influence on cancer development including angiogenesis, tumor invasion, and metastasis. Liao et al. carried out a cytotoxicity study of CAPE in colon adenocarcinoma cells (CT26) and reported a dose-dependent decline in cell viability. Moreover, there was reduction in both expression of matrix metalloproteinase and production of vascular endothelial growth factor from CAPE-treated CT26 cells resulting in the reduced angiogenesis and metastasis. These observations provide insight into the promising antimetastatic feature of CAPE. In addition, Song et al. reported that antiangiogenic property of CAPE was also accounted for its anti-inflammatory effect because angiogenesis and chronic inflammation depend on each other. An anti-inflammatory response is obtained by blockage of angiogenesis. As far as mode of anticancer activity of CAPE is concerned, CAPE is capable of (i) inhibiting the xanthine oxidase which can metabolize both purine and pyrimidine bases and obstruct the nucleotide production pathway; (ii) suppressing 5-lipoxygenase; (iii) inhibiting the tumor promoter-mediated oxidative responses in the culture of HeLa cells; (iv) inhibiting the azoxymethane-provoked colonic preneoplastic lesions and enzymatic processes related to colon carcinogenesis; (v) inducing apoptosis; and (vi) modulating the redox state of the cells. Attenuating effects of caffeic acid phenethyl ester and betaine on abamectin-induced hepatotoxicity and nephrotoxicity


4. Attenuating effects of caffeic acid phenethyl ester and betaine on abamectin-induced hepatotoxicity and nephrotoxicityaasraw

Abamectin (ABM) is a widely utilized potent anthelmintic and insecticidal agent. In this study, we investigated the protective effects of caffeic acid phenethyl ester (CAPE) and betaine (BET) against ABM-induced hepatotoxicity and nephrotoxicity in rats. Forty rats were divided into five groups, receiving either oral saline solution (normal control), oral ABM at a dose of 2 mg/kg BW (1/5 LD50), CAPE (10 μmol/kg BW intraperitoneally) followed by ABM, or BET supplementation at a dose of 250 mg/kg BW followed by ABM administration, while group V rats received a combination of i.p. CAPE and oral BET in the same doses before receiving ABM. Biochemical analysis showed that ABM administration significantly (p < 0.05) increased serum levels of aminotransferases, alkaline phosphatase, lactate dehydrogenase, and cholesterol, as well as serum creatinine and urea. Compared to the control group, ABM-intoxicated rats had significantly (p < 0.05) higher tissue concentrations of nitric oxide and malondialdehyde, as well as lower tissue glutathione concentration, total antioxidant capacity, and antioxidant enzymatic activity (glutathione peroxidase, superoxide dismutase, and catalase). Histopathological examination of hepatic and renal tissues of ABM-intoxicated rats showed acute inflammatory and necrotic changes. Pretreatment with CAPE and/or BET reversed the biochemical and histopathological alterations of ABM on the liver and kidneys. Therefore, CAPE and BET (alone or in combination) could be promising protective agents against ABM-induced hepatotoxicity and nephrotoxicity. Future studies should confirm our findings and evaluate the other molecular effects are involved in the combination chemoprotection of CAPE and BET.



5. Caffeic Acid Phenethyl Ester(CAS:104594-70-9)Synthesis aasraw


Due to the lethal side effects of synthetic chemical-based drugs, enthusiastic efforts are currently being applied to explore natural therapeutic agents with minimum toxicity. In this context, plant or herbal origin compounds are being studied to investigate the bioactivities of their natural active compounds. Polyphenols represent one of the most inten- sively studied groups of natural compounds.Caffeic acid has been proposed to act as a multipurpose active polyphenol and its derivatives have also been subjected to considerable study. One of the derivatives of caffeic acid is caffeic acid phenethyl ester (CAPE), which possesses prom- ising therapeutic potential against various pathologies such as inflammation, cancer, infection, and neurodegeneration. This naturally bioactive, hydrophobic polyphenolic ester occurs in numerous plants and propolis and can also be prepared by reacting caffeic acid with phenethyl alcohols. The molecular formula of CAPE is C17H16O4 and is chemically recognized as 2-phenylethyl (2E)-3-(3,4- dihydroxyphenyl)acrylate (commonly termed as phenylethyl caffeate or phenethyl caffeate).
To achieve biological effects, CAPE should be adminis- tered at a therapeutic concentration so that prolonged maintenance of blood CAPE-concentration at a particular level could be achieved. Thus pharmacokinetic and bioavailability study of CAPE is crucial for determining its route of administration. Fig. 1 depicts the chemical struc- ture of CAPE consisting of a catechol ring and two hydroxyl groups; the former is considered to be responsible for its therapeutic features. It has been proposed that meta- bolism of CAPE is a saturable process because an increase in the area under the plasma concentrationetime curve for  CAPE was observed in a proportion higher than the increase in its dose. Moreover, volume of distribution and total body clearance values for CAPE were found to be in the ranges of 1555e5209 mL/kg and 42e172 mL/minute/kg, respectively, proposing that these values are in an inverse relationship with the dose of CAPE. Additionally, no relationship was observed between the values of elimination half-life (21.24e26.71 minutes) of CAPE and its dose. Pharmacoki- netic study of CAPE showed its high values of volume of distribution and short elimination half-life, revealing its extensive distribution and swift elimination from the body after intravenous administration. Another pharmaco- kinetic study of CAPE showed comparable results. Furthermore, pharmacokinetic analysis of CAPE and its metabolites should also be carried out after its oral administration. Another study has revealed that CAPE can efficiently cross the bloodebrain barrier in rats. Besides, although CAPE is stable for 6 hours in rat plasma, after which it hydrolyzes to caffeic acid, CAPE hydrolysis does not occur in human plasma showing its stability, possibly owing to the absence of carboxylesterase in this biofluid.

Effects of caffeic acid phenethyl ester and caffeic acid phenethyl ester cancer

After an extensive search, no data were found about toxicity study of CAPE. Rather, slight toxicity of propolis was seen in a range of 2000e7300 g of propolis/kg in mice that is an origin of CAPE. At a dose of approximately 80 mM, CAPE generally inhibits the activated nuclear factor-kB (NF-kB) and other transcription factors via suppressing their binding with DNA.
The objective in writing this review article was to sum- marize various published studies on the therapeutics of CAPE in inflammation and cancer, especially focusing on their molecular targets that are responsible for therapeutic effect of CAPE.


(1)Results and Discussion-Caffeic Acid Phenethyl Ester

There are many studies in the literature that elaborate the anti-inflammatory activity of CAPE. Moreover, CAPE- induced inhibition of normal cell transformation to the neoplastic cell has also been reported. Table elaborates the dose (mM) or concentration causing 50% growth inhibition (mM) of CAPE effective in different cancer cell-lines. In addition, CAPE selectively destroys the cancerous cells leaving noncancer cells unaffected as observed in human immortal lung fibroblast WI-38 cells. These studies hypothesize that CAPE inhibits the release of arachidonic acid from the cell membrane, and moreover, suppresses the gene responsible for cyclooxygenase-2 (COX-2) expression. Moreover, CAPE suppresses NF-kB activity by limiting the formation of NF-kB DNA and nuclear factor of activated T cells (NFAT)-DNA complexes and thus retarding NF-kB-dependent transcription in Jurkat cells. In 2005, Abdel-Latif et al presented anticancer and anti-inflammatory activities of CAPE in a gastric epithelial cell line, claiming that CAPE inhibits the production of tissue necrosis factor-a (TNF-a) and interleukin (IL)-8; it eventually retards the expression of NF-kB, AP-1, and COX-2. It is noteworthy to mention here that CAPE does not influence other tissues of body, and thus the usage of this natural anticancer agent is free of side effects with effective chemopreventive feature. This outcome elaborates the nutritional importance of CAPE, particularly for patients whose tumors express gradually elevated levels of above given activated transcription factors.
Lipopolysaccharide-mediated inflammation in human neutrophils has also been combated using CAPE which sup- presses the synthesis of TNF-a and IL-6. The same authors also found that CAPE attenuates the phosphorylation of extracellular signal-regulated kinase 1/2 and c-JunN-terminal kinase. Raso et al found that CAPE has potential for reducing inflammation through inhibiting IL-2 gene in acti- vated T-cells that are normally the source of inflammation.

caffeic acid phenethyl ester synthesis and chemotherapy inflammation molecular targets

Biological studies have also revealed the activity of CAPE against angiogenesis, tumor invasion, metastasis, prolifera- tion, and apoptosis in different cancers such as human pancreatic and colon cancer. The improve- ment in the viability of colon adenocarcinoma cells (CT26) has been noted in a dose-dependent manner when these cells are treated with CAPE. This cytotoxic effect of CAPE has been attributed to the reduced expression of matrix metal- loproteinase and synthesis of vascular endothelial growth factor under the effect of CAPE. In this way, this chemical activity obstructs the angiogenesis and metastasis.
CAPE can suppress apoptosis via inhibiting the activated NF-kB, Bak, Bcl-2-associated X protein (Bax), p53, extracellular signal-regulated ki- nase, c-Jun and p21ap, c-JunN-terminal kinase and Fas ligand, p38 mitogen-activated protein kinase (p38 MAPK), and caspase activity. Moreover, upregulation of Bel-2, the cellular inhibitor of apoptosis proteins 1 and 2, and X-linked inhibitor of apoptosis protein, release of cytochrome C, loss of mitochondrial transmembrane potential, and decrease in Mcl-1 by CAPE are also responsible for its antiapoptotic effect.
In many cancer cells, CAPE-mediated-cell cycle arrest has been reported through the suppression of various factors including cyclin B1. CAPE-induced necrosis has also been described . In addition, suppression of Akt.phosphorylation is also induced by CAPE, resulting in the in- hibition of cancer cell invasiveness.
The literature also contains many animal studies that reveal the inhibitory role of CAPE on tumor growth and metastasis. For example, at a dietary level of 0.15% CAPE, C57BL/6J-Min/þmice having a germ-line mutation exhibit 63% suppression in tumor growth through increased apoptosis and cell proliferation. At a dose of 50 mg/kg, CAPE-treated rats showed the emergence of colonerectal carcinoma pro- voked by azoxymethane. In addition, mice with C6 glioma xenografts have exhibited dose-dependent inhibition in tumor metastasis at 1e10 mg intraperitoneal dose of CAPE/kg/ day. As far as mechanisms of anticancer activity of CAPE are concerned, CAPE is capable of affecting various processes as summarized in Fig.
Through numerous experimental studies, the therapeutic potentials of CAPE against various cancers have been explored. The findings of those studies are summarized below and the possible target sites of CAPE action are also described.


(2)Conclusion–Caffeic Acid Phenethyl Ester

This literature mining study revealed anti-inflammatory and anticancer activities of CAPE. The possible molecular targets for the action of CAPE in inflammation and cancer include various transcription factors such as NF-kB. Based on the valuable data about the above presented bioactivities, clinical studies of CAPE should be conducted to explore its toxicities, if any.

Caffeic Acid Phenethyl Ester(CAS:104594-70-9)Supplement Online



6. Caffeic Acid Phenethyl Ester Supplementaasraw


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