3,4,5-Tricaffeoylquinic acidCAS# 86632-03-3 |
Quality Control & MSDS
Number of papers citing our products
Chemical structure
3D structure
| Cas No. | 86632-03-3 | SDF | Download SDF |
| PubChem ID | 6440783 | Appearance | Powder |
| Formula | C34H30O15 | M.Wt | 678.59 |
| Type of Compound | Phenylpropanoids | Storage | Desiccate at -20°C |
| Solubility | Soluble in Chloroform,Dichloromethane,Ethyl Acetate,DMSO,Acetone,etc. | ||
| Chemical Name | (3R,5R)-3,4,5-tris[[(E)-3-(3,4-dihydroxyphenyl)prop-2-enoyl]oxy]-1-hydroxycyclohexane-1-carboxylic acid | ||
| SMILES | C1C(C(C(CC1(C(=O)O)O)OC(=O)C=CC2=CC(=C(C=C2)O)O)OC(=O)C=CC3=CC(=C(C=C3)O)O)OC(=O)C=CC4=CC(=C(C=C4)O)O | ||
| Standard InChIKey | OAFXTKGAKYAFSI-JFPZSYFPSA-N | ||
| 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. |
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| 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. |
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| 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. | ||
| Description | 3,4,5-Tricaffeoylquinic acid may attenuate the TNF-α- and LPS-stimulated production of inflammatory mediators in keratinocytes by suppressing the Toll-like receptor 4 expression-mediated activation of the Akt, ERK and NF-ĸB pathways, it may exert an inhibitory effect against the pro-inflammatory mediator-induced skin disease. 3,4,5-Tricaffeoylquinic acid may attenuate the proteasome inhibitor-induced programmed cell death in PC12 cells by suppressing the activation of the mitochondrial pathway and the caspase-8- and Bid-dependent pathways, the effect be attributed to its inhibitory effect on the formation of reactive oxygen species and depletion of GSH. |
| Targets | HIV | TNF-α | Akt | NF-kB | Beta Amyloid | Bcl-2/Bax | p53 | Caspase | p53 | IL Receptor | ERK |
| In vitro | 3,4,5-Tricaffeoylquinic acid inhibits tumor necrosis factor-α-stimulated production of inflammatory mediators in keratinocytes via suppression of Akt- and NF-κB-pathways.[Pubmed: 21704193]Int Immunopharmacol. 2011 Nov;11(11):1715-23.Keratinocytes may play an important role in the pathogenesis of skin disease in atopic dermatitis. Caffeoyl derivatives are demonstrated to have anti-inflammatory and anti-oxidant effects. However, the effect of 3,4,5-Tricaffeoylquinic acid prepared from Aconium koreanum on the pro-inflammatory cytokine-stimulated keratinocyte responses remains uncertain. 3,4,5-tricaffeoylquinic Acid inhibits the lipopolysaccharide-stimulated production of inflammatory mediators in keratinocytes.[Pubmed: 22947851 ]Pharmacology. 2012;90(3-4):183-92.Microbial product lipopolysaccharide (LPS) has been shown to be involved in the pathogenesis of inflammatory skin diseases. Caffeoyl derivatives have demonstrated anti-inflammatory and antioxidant effects. However, the effect of 3,4,5-Tricaffeoylquinic acid (3,4,5-triCQA) on the production of microbial product-induced inflammatory mediators in keratinocytes has not yet been studied. |
| Kinase Assay | 3,4,5-tricaffeoylquinic acid attenuates proteasome inhibition-mediated programmed cell death in differentiated PC12 cells.[Pubmed: 24825618]Neurochem Res. 2014 Aug;39(8):1416-25.The dysfunction of the proteasome system is suggested to be implicated in neuronal degeneration. Caffeoylquinic acid derivatives have demonstrated anti-oxidant and anti-inflammatory effects. However, the effect of 3,4,5-Tricaffeoylquinic acid on the neuronal cell death induced by proteasome inhibition has not been studied. |
3,4,5-Tricaffeoylquinic acid Dilution Calculator
3,4,5-Tricaffeoylquinic acid Molarity Calculator
| 1 mg | 5 mg | 10 mg | 20 mg | 25 mg | |
| 1 mM | 1.4736 mL | 7.3682 mL | 14.7364 mL | 29.4729 mL | 36.8411 mL |
| 5 mM | 0.2947 mL | 1.4736 mL | 2.9473 mL | 5.8946 mL | 7.3682 mL |
| 10 mM | 0.1474 mL | 0.7368 mL | 1.4736 mL | 2.9473 mL | 3.6841 mL |
| 50 mM | 0.0295 mL | 0.1474 mL | 0.2947 mL | 0.5895 mL | 0.7368 mL |
| 100 mM | 0.0147 mL | 0.0737 mL | 0.1474 mL | 0.2947 mL | 0.3684 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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3,4,5-Tricaffeoylquinic acid inhibits tumor necrosis factor-alpha-stimulated production of inflammatory mediators in keratinocytes via suppression of Akt- and NF-kappaB-pathways.[Pubmed:21704193]
Int Immunopharmacol. 2011 Nov;11(11):1715-23.
Keratinocytes may play an important role in the pathogenesis of skin disease in atopic dermatitis. Caffeoyl derivatives are demonstrated to have anti-inflammatory and anti-oxidant effects. However, the effect of 3,4,5-Tricaffeoylquinic acid prepared from Aconium koreanum on the pro-inflammatory cytokine-stimulated keratinocyte responses remains uncertain. In human keratinocytes, we investigated the effect of 3,4,5-Tricaffeoylquinic acid on the tumor necrosis factor (TNF)-alpha-stimulated production of inflammatory mediators in relation to the nuclear factor (NF)-kappaB and cell signaling Akt, which regulates the transcription genes involved in immune and inflammatory responses. 3,4,5-Tricaffeoylquinic acid inhibited the TNF-alpha-stimulated production of cytokines (IL-1beta and IL-8) and chemokine (CCL17 and CCL27) in keratinocytes. Bay 11-7085 (an inhibitor of NF-kappaB activation) and Akt inhibitor attenuated the TNF-alpha-induced formation of inflammatory mediators. 3,4,5-Tricaffeoylquinic acid, Bay 11-7085, Akt inhibitor and N-acetylcysteine inhibited the TNF-alpha-induced activation of NF-kappaB, activation of Akt, and formation of reactive oxygen and nitrogen species. The results show that 3,4,5-Tricaffeoylquinic acid seems to attenuate the TNF-alpha-stimulated inflammatory mediator production in keratinocytes by suppressing the activation of Akt and NF-kappaB pathways which may be mediated by reactive oxygen species. The findings suggest that 3,4,5-Tricaffeoylquinic acid may exert an inhibitory effect against the pro-inflammatory mediator-induced skin disease.
3,4,5-tricaffeoylquinic Acid inhibits the lipopolysaccharide-stimulated production of inflammatory mediators in keratinocytes.[Pubmed:22947851]
Pharmacology. 2012;90(3-4):183-92.
BACKGROUND AND PURPOSE: Microbial product lipopolysaccharide (LPS) has been shown to be involved in the pathogenesis of inflammatory skin diseases. Caffeoyl derivatives have demonstrated anti-inflammatory and antioxidant effects. However, the effect of 3,4,5-Tricaffeoylquinic acid (3,4,5-triCQA) on the production of microbial product-induced inflammatory mediators in keratinocytes has not yet been studied. EXPERIMENTAL APPROACH: Using human keratinocytes, we investigated the effect of 3,4,5-triCQA on the LPS-stimulated production of inflammatory mediators in relation to the nuclear factor (NF)-kB, Akt and ERK pathways. RESULTS: 3,4,5-triCQA inhibited the LPS-induced expression of Toll-like receptor 4, and the production of cytokines and chemokines in keratinocytes. 3,4,5-triCQA, Bay 11-7085, Akt inhibitor and ERK inhibitor each attenuated the LPS-induced production of inflammatory mediators by inhibiting the NF-kB, Akt and ERK pathways. CONCLUSIONS AND IMPLICATIONS: 3,4,5-triCQA may attenuate the LPS-stimulated production of inflammatory mediators in keratinocytes by suppressing the Toll-like receptor 4 expression-mediated activation of the Akt, ERK and NF-kB pathways. 3,4,5-triCQA may exert a preventive effect against microbial product-induced inflammatory skin diseases.
3,4,5-tricaffeoylquinic acid attenuates proteasome inhibition-mediated programmed cell death in differentiated PC12 cells.[Pubmed:24825618]
Neurochem Res. 2014 Aug;39(8):1416-25.
The dysfunction of the proteasome system is suggested to be implicated in neuronal degeneration. Caffeoylquinic acid derivatives have demonstrated anti-oxidant and anti-inflammatory effects. However, the effect of 3,4,5-Tricaffeoylquinic acid on the neuronal cell death induced by proteasome inhibition has not been studied. Therefore, in the respect of cell death process, we assessed the effect of 3,4,5-Tricaffeoylquinic acid on the proteasome inhibition-induced programmed cell death using differentiated PC12 cells. The proteasome inhibitors MG132 and MG115 induced a decrease in Bid, Bcl-2, and survivin protein levels, an increase in Bax, loss of the mitochondrial transmembrane potential, cytochrome c release, activation of caspases (-8, -9 and -3), and an increase in the tumor suppressor p53 levels. Treatment with 3,4,5-Tricaffeoylquinic acid attenuated the proteasome inhibitor-induced changes in the programmed cell death-related protein levels, formation of reactive oxygen species, GSH depletion and cell death. The results show that 3,4,5-Tricaffeoylquinic acid may attenuate the proteasome inhibitor-induced programmed cell death in PC12 cells by suppressing the activation of the mitochondrial pathway and the caspase-8- and Bid-dependent pathways. The preventive effect of 3,4,5-Tricaffeoylquinic acid appears to be attributed to its inhibitory effect on the formation of reactive oxygen species and depletion of GSH.
