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    Chlorogenic acid
    CAS No. 327-97-9 Price $30 / 20mg
    Catalog No.CFN99116Purity>=98%
    Molecular Weight354.31Type of CompoundPhenylpropanoids
    FormulaC16H18O9Physical DescriptionPowder
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    Related Screening Libraries
    Size /Price /Stock 10 mM * 100 uL in DMSO / Inquiry / In-stock
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  • Biological Activity
    Description: Chlorogenic acid, a phenolic compound found ubiquitously in plants, is an antioxidant and metal chelator, it has antiviral activity by inhibiting HBV replication, it inhibits the inflammatory reaction in HSE via the suppression of TLR2/TLR9-Myd88 signaling pathways. Some derivatives of chlorogenic acid are hypoglycemic agents and may affect lipid metabolism, chlorogenic acid can improve glucose tolerance, decrease some plasma and liver lipids, and improve mineral pool distribution in vivo.
    Targets: HBV | PEG | NO | NOS | ERK | ROS | COX
    In vitro:
    Anticancer Drugs. 2015 Feb 24.
    Chlorogenic acid enhances the effects of 5-fluorouracil in human hepatocellular carcinoma cells through the inhibition of extracellular signal-regulated kinases.[Pubmed: 25714249]
    There is an urgent need to search for novel chemosensitizers in the field of cancer therapy. Chlorogenic acid (CGA), a type of polyphenol present in the diet, has many biological activities.
    The present study is designed to explore the influence of CGA on the effects of 5-fluorouracil (5-FU) on human hepatocellular carcinoma cells (HepG2 and Hep3B). Treatment with 5-FU induced the inhibition of hepatocellular carcinoma cells' proliferation, and the combined treatment with CGA enhanced this inhibition. 5-FU also increased the production of reactive oxygen species (ROS). The combination of 5-FU and CGA led to a more prominent production of ROS and significantly inactivated ERK1/2, although CGA and 5-FU exerted no significant changes when used alone. A previous report has shown that ROS are upstream mediators that inactivate ERK in hepatocellular carcinoma cells. Combined with our results, this indicates that the combination of 5-FU and CGA leads to the inactivation of ERK through the overproduction of ROS. This mediates the enhancement of 5-FU-induced inhibition of hepatocellular carcinoma cells' proliferation, that is, CGA sensitizes hepatocellular carcinoma cells to 5-FU treatment by the suppression of ERK activation through the overproduction of ROS.
    CGA has shown potential as a chemosensitizer of 5-FU chemotherapy in hepatocellular carcinoma.
    Cell Oncol (Dordr) . 2015 Apr;38(2):111-8.
    Chlorogenic acid inhibits hypoxia-induced angiogenesis via down-regulation of the HIF-1α/AKT pathway[Pubmed: 25561311]
    Background: The hypoxia-inducible factor-1 (HIF-1) is known to play an important role in cellular responses to hypoxia, including the transcriptional activation of a number of genes involved in tumor angiogenesis. Chlorogenic acid (CGA), one of the most abundant polyphenols in the human diet, has been reported to inhibit cancer cell growth. The effect of CGA on tumor angiogenesis and its underlying mechanisms are, as yet, unknown. Methods: The effect of CGA on HIF-1α expression was assessed by Western blot and reverse transcriptase-polymerase chain reaction (RT-PCR) assays in A549 lung cancer cells. The transcriptional activity of the HIF-1 complex was confirmed using a luciferase assay. To assess whether angiogenic factors are increased under hypoxic conditions in these cells, vascular endothelial growth factor (VEGF) expression levels were measured by RT-PCR and Western blotting. The direct effect of CGA on human vascular endothelial cells (HUVEC) under hypoxic conditions was analyzed using in vitro assays, including tube-formation, wound healing and Transwell invasion assays. To investigate the effect of CGA on angiogenesis in vivo, we performed a Matrigel plug assay in a mouse model. Finally, the effect of CGA on AKT and ERK activation (phosphorylation) as a putative mechanism underlying the effect of CGA on VEGF-mediated angiogenesis inhibition was assessed using Western blotting. Results: We found that CGA significantly decreases the hypoxia-induced HIF-1α protein level in A549 cells, without changing its mRNA level. CGA was, however, found to suppress the transcriptional activity of HIF-1α under hypoxic conditions, leading to a decrease in the expression of its downstream target VEGF. We also found that CGA can block hypoxia-stimulated angiogenesis in vitro and VEGF-stimulated angiogenesis in vivo using HUVEC cells. In addition, we found that CGA can inhibit the HIF-1α/AKT signaling pathway, which plays an important role in VEGF activation and angiogenesis. Conclusions: Our data indicate that CGA plays a role in the suppression of angiogenesis via inhibition of the HIF-1α/AKT pathway. CGA may represent a novel therapeutic option for the treatment of (lung) cancer.
    In vivo:
    Int J Pharm. 2011 Jan 17;403(1-2):136-8.
    In vitro and in vivo antioxidant properties of chlorogenic acid and caffeic acid.[Pubmed: 20933071 ]
    Dietary polyphenols are thought to be beneficial for human health as antioxidants. Coffee beans contain a common polyphenol, Chlorogenic acid. Chlorogenic acid is the ester of caffeic acid and quinic acid. Although these polyphenols have received much attention, there is little evidence indicating a relationship between the effect and the rate of absorption.
    In this study, we focused on the beneficial effects of Chlorogenic acid and caffeic acid, a major metabolite of Chlorogenic acid. We carried out in vitro and in vivo experiments. In the in vitro study, caffeic acid had stronger antioxidant activity than that of Chlorogenic acid. The uptake of Chlorogenic acid by Caco-2 cells was much less than that of caffeic acid. The physiological importance of an orally administered compound depends on its availability for intestinal absorption and subsequent interaction with target tissues. We then used an intestinal ischemia-reperfusion model to evaluate antioxidant activities in vivo.
    We found that both Chlorogenic acid and caffeic acid had effects on intestinal ischemia-reperfusion injury. Since caffeic acid has a stronger antioxidant activity than that of Chlorogenic acid and Chlorogenic acid is hydrolyzed into caffeic acid in the intestine, it is possible that caffeic acid plays a major role in the protective effect of Chlorogenic acid against ischemia-reperfusion injury.
    J Nutr Biochem. 2002 Dec;13(12):717-726.
    Chlorogenic acid modifies plasma and liver concentrations of: cholesterol, triacylglycerol, and minerals in (fa/fa) Zucker rats.[Pubmed: 12550056]
    Chlorogenic acid, a phenolic compound found ubiquitously in plants, is an in vitro antioxidant and metal chelator. Some derivatives of Chlorogenic acid are hypoglycemic agents and may affect lipid metabolism. Concentrations of cholesterol and triacylglycerols are of interest due to their association with diseases such as non-insulin-dependent-diabetes- mellitus and obese insulin resistance.
    As little is known about the effects of Chlorogenic acid in vivo, studies using obese, hyperlipidemic, and insulin resistant (fa/fa) Zucker rats were conducted to test the effect of Chlorogenic acid on fasting plasma glucose, plasma and liver triacylglycerols and cholesterol concentrations. Aditionally, the effects of Chlorogenic acid on selected mineral concentrations in plasma, spleen, and liver were determined. Rats were implanted with jugular vein catheters. Chlorogenic acid was infused (5 mg/Kg body weight/day) for 3 weeks via intravenous infusion. Chlorogenic acid did not promote sustained hypoglycemia and significantly lowered the postprandial peak response to a glucose challenge when compared to the same group of rats before Chlorogenic acid treatment. In Chlorogenic acid-treated rats, fasting plasma cholesterol and triacylglycerols concentrations significantly decreased by 44% and 58% respectively, as did in liver triacylglycerols concentrations (24%). We did not find differences (p > 0.05) in adipose triacylglycerols concentration. Significant differences (p < 0.05) in the plasma, liver, and spleen concentration of selected minerals were found in Chlorogenic acid-treated rats.
    In vivo, Chlorogenic acid was found to improve glucose tolerance, decreased some plasma and liver lipids, and improve mineral pool distribution under the conditions of this study.
    Biomol Ther (Seoul) . 2014 Sep;22(5):420-5.
    Protective Effects of Chlorogenic Acid against Experimental Reflux Esophagitis in Rats[Pubmed: 25414772]
    Esophageal reflux of gastric contents causes esophageal mucosal damage and inflammation. Recent studies show that oxygen-derived free radicals mediate mucosal damage in reflux esophagitis (RE). Chlorogenic acid (CGA), an ester of caffeic acid and quinic acid, is one of the most abundant polyphenols in the human diet and possesses anti-inflammatory, antibacterial and anti-oxidant activities. In this context, we investigated the effects of CGA against experimental RE in rats. RE was produced by ligating the transitional region between the forestomach and the glandular portion and covering the duodenum near the pylorus ring with a small piece of catheter. CGA (10, 30 and 100 mg/kg) and omeprazole (positive control, 10 mg/kg) were administered orally 48 h after the RE operation for 12 days. CGA reduced the severity of esophageal lesions, and this beneficial effect was confirmed by histopathological observations. CGA reduced esophageal lipid peroxidation and increased the reduced glutathione/oxidized glutathione ratio. CGA attenuated increases in the serum level of tumor necrosis factor-α, and expressions of inducible nitric oxide synthase and cyclooxygenase-2 protein. CGA alleviates RE-induced mucosal injury, and this protection is associated with reduced oxidative stress and the anti-inflammatory properties of CGA
    Chlorogenic acid Description
    Source: The barks of Eucommia ulmoides Oliv.
    Solvent: DMSO, Pyridine, Methanol, Ethanol, etc.
    Storage: Providing storage is as stated on the product vial and the vial is kept tightly sealed, the product can be stored for up to 24 months(2-8C).

    Wherever possible, you should prepare and use solutions on the same day. However, if you need to make up stock solutions in advance, we recommend that you store the solution as aliquots in tightly sealed vials at -20C. Generally, these will be useable for up to two weeks. Before use, and prior to opening the vial we recommend that you allow your product to equilibrate to room temperature for at least 1 hour.

    Need more advice on solubility, usage and handling? Please email to:

    After receiving: The packaging of the product may have turned upside down during transportation, resulting in the natural compounds adhering to the neck or cap of the vial. take the vial out of its packaging and gently shake to let the compounds fall to the bottom of the vial. for liquid products, centrifuge at 200-500 RPM to gather the liquid at the bottom of the vial. try to avoid loss or contamination during handling.
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    Calculate Dilution Ratios(Only for Reference)
    1 mg 5 mg 10 mg 20 mg 25 mg
    1 mM 2.8224 mL 14.1119 mL 28.2239 mL 56.4477 mL 70.5597 mL
    5 mM 0.5645 mL 2.8224 mL 5.6448 mL 11.2895 mL 14.1119 mL
    10 mM 0.2822 mL 1.4112 mL 2.8224 mL 5.6448 mL 7.056 mL
    50 mM 0.0564 mL 0.2822 mL 0.5645 mL 1.129 mL 1.4112 mL
    100 mM 0.0282 mL 0.1411 mL 0.2822 mL 0.5645 mL 0.7056 mL
    * Note: If you are in the process of experiment, it's need to make the dilution ratios of the samples. The dilution data of the sheet for your reference. Normally, it's can get a better solubility within lower of Concentrations.
    Kinase Assay:
    Int J Clin Exp Pathol. 2014 Dec 1;7(12):8797-801.
    Chlorogenic acid suppresses interleukin-1β-induced inflammatory mediators in human chondrocytes.[Pubmed: 25674248]
    We investigated the anti-inflammatory properties of Chlorogenic acid (CGA) in interleukin-1β-induced chondrocytes. The nitric oxide (NO) and prostaglandin E2 (PGE2) were detected by Griess and Enzyme-linked immunosorbent assay (ELISA) respectively. Quantitative real-time PCR and western blot were performed to measure the expression of inducible NO synthase (iNOS) and cyclooxygenase (COX)-2. Our results indicate that Chlorogenic acid inhibited the production of NO and PGE2 as well as the expression of iNOS and COX-2 in chondrocytes. Our data suggest that Chlorogenic acid possess potential value in the treatment of OA.
    Cell Research:
    Life Sci. 2015 Mar 2. pii: S0024-3205(15)00105-8.
    Involvement of TLR2 and TLR9 in the anti-inflammatory effects of chlorogenic acid in HSV-1-infected microglia.[Pubmed: 25744394]
    There is no effective medication to date for herpes simplex virus encephalitis (HSE). In this study, we investigated the anti-inflammatory effect of Chlorogenic acid (CGA) on herpes simplex virus (HSV)-1-induced responses in BV2 microglia.
    The cellular model was established with BV2 cells stimulated by HSV-1 and then treated with CGA at different concentrations. Cell viability was assayed by the MTT assay. The mRNA expression of Toll-like receptor (TLR)-2, TLR9 and myeloid differentiation factor88 (Myd88) was assayed by real-time quantitative PCR, and the protein expression was assayed by flow cytometry or Western blotting. Tumor necrosis factor-α (TNF-α) and interleukin (IL)-6 were measured by ELISA as well as real-time quantitative PCR. Nuclear NF-κB p65 protein was assayed by Western blotting. The cell survival rate was significantly improved after CGA treatment, and CGA prevented increases in TLR2, TLR9 and Myd88 following HSV-1 challenge in BV2 cells both at the mRNA and protein levels. Moreover, CGA could attenuate HSV-induced TNF-α and IL-6 release into the supernatant. The mRNA levels of TNF-α and IL-6 were also significantly inhibited by CGA. The expression of NF-κB p65 increased significantly in the nucleus in HSV-1-stimulated microglia but could be reduced by CGA.
    CGA inhibits the inflammatory reaction in HSE via the suppression of TLR2/TLR9-Myd88 signaling pathways. CGA may serve as an anti-inflammatory agent and provide a new strategy for treating HSE.
    Animal Research:
    Antiviral Res. 2009 Aug;83(2):186-90.
    Anti-hepatitis B virus activity of chlorogenic acid, quinic acid and caffeic acid in vivo and in vitro.[Pubmed: 19463857 ]
    Chlorogenic acid and its related compounds are abundant plant polyphenols that have a diverse antiviral activity.
    In this study, HepG2.2.15 cells and duck hepatitis B virus infection model were used as in vitro and in vivo models to evaluate their anti-HBV activity. In the cell model, all the three compounds inhibited HBV-DNA replication as well as HBsAg production. Chlorogenic acid and caffeic acid also reduced serum DHBV level in DHBV-infected duckling model. Moreover, the anti-HBV activity of crude extracts of coffee beans, which have a high content of Chlorogenic acid, was studied.
    Both the extracts of regular coffee and that of decaffeinated coffee showed inhibitory effect on HBV replication.