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Myricetin
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Product Name Myricetin
Price: $40 / 20mg
CAS No.: 529-44-2
Catalog No.: CFN98877
Molecular Formula: C15H10O8
Molecular Weight: 318.2 g/mol
Purity: >=98%
Type of Compound: Flavonoids
Physical Desc.: Yellow powder
Source: The root barks of Myrica cerifera L.
Solvent: DMSO, Pyridine, Methanol, Ethanol, etc.
Download: COA    MSDS    SDF    Manual
Similar structural: Comparison (Web)  (SDF)
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Related Screening Libraries
Size /Price /Stock 10 mM * 100 uL in DMSO / Inquiry / In-stock
10 mM * 1 mL in DMSO / Inquiry / In-stock
Related Libraries
Biological Activity
Description: Myricetin, a natural flavonoid with anti-amyloidogenic, anti-oxidant, anticancer, antidiabetic and anti-inflammatory properties, is a novel inhibitor of MEK1 activity and inhibits glucose uptake in isolated rat adipocytes . It also inhibits PI3Kγ with Kd of 0.17 μM. Myricetin exerts potent anti-photoaging activity by regulating MMP-9 expression through the suppression of Raf kinase activity. Myricetin can enhance osteogenic differentiation of hBMSCs by activating the Wnt/β-catenin signaling.
Targets: Calcium Channel | Potassium Channel | NF-kB | ATPase | p38MAPK | JNK | ERK | IL Receptor | TNF-α | Wnt/β-catenin | MEK | MMP(e.g.TIMP) | Raf | GLUT | Topoisomerase | PI3Kγ
In vitro:
J Agric Food Chem. 2014 Oct 1;62(39):9442-9.
Myricetin prevents fibrillogenesis of hen egg white lysozyme.[Pubmed: 25196984]
Myricetin is a natural flavonol found in many grapes, berries, fruits, vegetables, and herbs as well as other plants. Recent studies have identified potential antiamyloidogenic activity for this compound. In this study, the kinetics of amyloid fibril formation by hen egg white lysozyme (HEWL) and the antifibril-forming activity of Myricetin were investigated.
METHODS AND RESULTS:
We demonstrate that Myricetin significantly inhibits the fibrillation of HEWL and the inhibitory effect is dose-dependent. Interestingly, the inhibitory effect toward HEWL fibrillation was stronger than that exerted by the previously characterized fibril-forming inhibitor quercetin, which has high structural similarity with Myricetin.
CONCLUSIONS:
Spectrofluorometric and computational studies suggest that the mechanism underlying the inhibitory action of Myricetin at a molecular level is to reduce the population of partially unfolded HEWL intermediates. This action is achieved by the tight binding of Myricetin to the aggregation-prone region of the β-domain of HEWL and linking to the relatively stable α-domain, thus resulting in the inhibition of amyloid fibril formation.
Tumour Biol. 2014 Dec;35(12):12583-92.
Myricetin exerts anti-proliferative, anti-invasive, and pro-apoptotic effects on esophageal carcinoma EC9706 and KYSE30 cells via RSK2.[Pubmed: 25192723]
Myricetin, a common dietary flavonoid, is widely distributed in fruits and vegetables and is used as a health food supplement based on its anti-tumor properties. However, the effect and mechanisms of Myricetin in esophageal carcinoma are not fully understood. Here, we demonstrated the effect of Myricetin on the proliferation, apoptosis, and invasion of the esophageal carcinoma cell lines EC9706 and KYSE30 and explored the underlying mechanism and target protein(s) of Myricetin.
METHODS AND RESULTS:
CCK-8 assay, transwell invasion assay, wound-healing assay, cell cycle analysis, and apoptosis assay were used to evaluate the effects of Myricetin on cell proliferation, invasion, and apoptosis. Nude mouse tumor xenograft model was built to understand the interaction between Myricetin and NTD RSK2. Pull-down assay was used to verify molecular mechanism. Myricetin inhibited proliferation and invasion and induced apoptosis of EC9706 and KYSE30 cells. Moreover, Myricetin was shown to bind RSK2 through the NH2-terminal kinase domain. Finally, Myricetin inhibited EC9706 and KYSE30 cell proliferation through Mad1 and induced cell apoptosis via Bad. Myricetin inhibits the proliferation and invasion and induces apoptosis in EC9706 and KYSE30 cells via RSK2. Myricetin exerts anti-proliferative, anti-invasive, and pro-apoptotic effects on esophageal carcinoma EC9706 and KYSE30 cells via RSK2.
CONCLUSIONS:
Our results provide novel insight into Myricetin as a potential agent for the prevention and treatment of esophageal carcinoma.
Biochem J. 2005 Mar 15;386(Pt 3):471-8.
Myricetin, quercetin and catechin-gallate inhibit glucose uptake in isolated rat adipocytes.[Pubmed: 15469417]
The facilitative glucose transporter, GLUT4, mediates insulin-stimulated glucose uptake in adipocytes and muscles, and the participation of GLUT4 in the pathogenesis of various clinical conditions associated with obesity, visceral fat accumulation and insulin resistance has been proposed. Glucose uptake by some members of the GLUT family, mainly GLUT1, is inhibited by flavonoids, the natural polyphenols present in fruits, vegetables and wine. Therefore it is of interest to establish if these polyphenolic compounds present in the diet, known to be effective antioxidants but also endowed with several other biological activities such as protein-tyrosine kinase inhibition, interfere with GLUT4 function.
METHODS AND RESULTS:
In the present study, we show that three flavonoids, quercetin, Myricetin and catechin-gallate, inhibit the uptake of methylglucose by adipocytes over the concentration range of 10-100 microM. These three flavonoids show a competitive pattern of inhibition, with K(i)=16, 33.5 and 90 microM respectively. In contrast, neither catechin nor gallic acid inhibit methylglucose uptake. To obtain a better understanding of the interaction among GLUT4 and flavonoids, we have derived a GLUT4 three-dimensional molecular comparative model, using structural co-ordinates from a GLUT3 comparative model and a mechanosensitive ion channel [PDB (Protein Data Bank) code 1MSL] solved by X-ray diffraction.
CONCLUSIONS:
On the whole, the experimental evidence and computer simulation data favour a transport inhibition mechanism in which flavonoids and GLUT4 interact directly, rather than by a mechanism related to protein-tyrosine kinase and insulin signalling inhibition. Furthermore, the results suggest that GLUT transporters are involved in flavonoid incorporation into cells.
Mol Med Rep . 2016 Mar;13(3):2094-100.
Myricetin induces apoptosis via endoplasmic reticulum stress and DNA double-strand breaks in human ovarian cancer cells[Pubmed: 26782830]
The mechanisms underlying Myricetin-induced cancer cell apoptosis remain to be elucidated. Certain previous studies have shown that Myricetin induces apoptosis through the mitochondrial pathway. Apoptosis, however, can also be induced by other classical pathways, including endoplasmic reticulum (ER) stress and DNA double‑strand breaks (DSBs). The aim of the present study was to assess whether these two apoptotic pathways are involved in Myricetin‑induced cell death in SKOV3 ovarian cancer cells. The results revealed that treatment with Myricetin inhibited viability of SKOV3 cells in a dose‑dependent manner. Myricetin induced nuclear chromatin condensation and fragmentation, and also upregulated the protein levels of active caspase 3 in a time‑dependent manner. In addition, Myricetin upregulated ER stress‑associated proteins, glucose‑regulated protein‑78 and C/EBP homologous protein in SKOV3 cells. Phosphorylation of H2AX, a marker of DNA DSBs, was revealed to be upregulated in Myricetin-treated cells. The data indicated that Myricetin induces DNA DSBs and ER stress, which leads to apoptosis in SKOV3 cells.
In vivo:
Biochem Pharmacol. 2015 Jan 1;93(1):59-71.
Myricetin prevents titanium particle-induced osteolysis in vivo and inhibits RANKL-induced osteoclastogenesis in vitro.[Pubmed: 25449599]
Titanium (Ti) particle-induced periprosthetic osteolysis and subsequent aseptic loosening are a primary reason for total hip arthroplasty failure. The aim of this study was to assess the effect of Myricetin on Ti particle-induced osteolysis and osteoclastogenesis.
METHODS AND RESULTS:
We demonstrated that Myricetin, a natural plant extract, exerts potent inhibitory effects on Ti particle-induced osteolysis in a mouse calvarial model. Further histological analysis indicated that the inhibition of osteoclast formation and function, and the secretion of inflammatory factors, are key targets for therapeutic agents in the treatment of wear particle-induced osteolysis. In vitro, we found that Myricetin suppressed receptor activator of nuclear factor-κB ligand (RANKL)-mediated osteoclast differentiation, bone resorption, and F-actin ring formation in a dose-dependent manner. Moreover, Myricetin significantly reduced the expression of osteoclast-specific markers in mouse bone marrow-derived macrophages, including tartrate-resistant acid phosphatase (TRAP), cathepsin K, the calcitonin receptor, V-ATPase d2, c-fos, and nuclear factor of activated T cells (NFAT) c1. Further investigation revealed that Myricetin inhibited osteoclastogenesis through the suppression of the nuclear factor-κB (NF-κB) signaling pathway and mitogen-activated protein kinase (MAPK) pathways involving extracellular signal-regulated kinase 1/2 (ERK1/2), p38, and c-Jun N-terminal kinase 1/2 (JNK1/2). While, the inhibition of TNF-α and IL-1β secretion was another reason for the suppressive effect of Myricetin on Ti particle-induced osteolysis.
CONCLUSIONS:
Collectively, these findings suggest that Myricetin is a potential natural agent for the treatment of periprosthetic osteolysis and other osteoclast-related osteolytic diseases.
Myricetin Description
Source: The root barks of Myrica cerifera L.
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: service@chemfaces.com

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 3.1427 mL 15.7134 mL 31.4268 mL 62.8536 mL 78.5669 mL
5 mM 0.6285 mL 3.1427 mL 6.2854 mL 12.5707 mL 15.7134 mL
10 mM 0.3143 mL 1.5713 mL 3.1427 mL 6.2854 mL 7.8567 mL
50 mM 0.0629 mL 0.3143 mL 0.6285 mL 1.2571 mL 1.5713 mL
100 mM 0.0314 mL 0.1571 mL 0.3143 mL 0.6285 mL 0.7857 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.
Protocol
Kinase Assay:
J Med Food. 2015 May;18(5):516-23.
Myricetin inhibits the release of glutamate in rat cerebrocortical nerve terminals.[Pubmed: 25340625]
The excessive release of glutamate is a critical element in the neuropathology of acute and chronic brain disorders. The purpose of the present study was to investigate the effect and possible mechanism of Myricetin, a naturally occurring flavonoid with a neuroprotective profile, on endogenous glutamate release in the nerve terminals (synaptosomes) of the rat cerebral cortex.
METHODS AND RESULTS:
The release of glutamate was evoked by the K(+) channel blocker 4-aminopyridine (4-AP) and measured by one-line enzyme-coupled fluorometric assay. We also used a membrane potential-sensitive dye to assay the synaptosomal plasma membrane potential, and a Ca(2+) indicator Fura-2 to monitor cytosolic Ca(2+) concentrations ([Ca(2+)]C). Results show that Myricetin inhibited 4-AP-evoked glutamate release, and this effect was prevented by chelating extracellular Ca(2+) ions and the vesicular transporter inhibitor bafilomycin A1. However, the glutamate transporter inhibitor dl-threo-beta-benzyl-oxyaspartate had no effect on Myricetin action. Myricetin did not alter the synaptosomal membrane potential, but decreased 4-AP-induced increases in the cytosolic free Ca(2+) concentration. Furthermore, the Myricetin effect on 4-AP-evoked glutamate release was prevented by blocking the Cav2.2 (N-type) and Cav2.1 (P/Q-type) channels, but not by blocking intracellular Ca(2+) release.
CONCLUSIONS:
These results suggest that Myricetin inhibits glutamate release from cerebrocortical synaptosomes by attenuating voltage-dependent Ca(2+) entry. This implies that the inhibition of glutamate release is an important pharmacological activity of Myricetin that may play a critical role in the apparent clinical efficacy of this compound.
Food Chem. 2013 Aug 15;139(1-4):910-8.
Inhibitory effects of myricetin on mammalian DNA polymerase, topoisomerase and human cancer cell proliferation.[Pubmed: 23561189 ]
In this study, the inhibitory activities against mammalian DNA polymerases (pols) of 16 major bioflavonoids were investigated.
METHODS AND RESULTS:
Myricetin (3,3',4',5,5',7-hexahydroxyflavone) was the most potent inhibitor of pols amongst the compounds tested, with IC50 values of 21.3-40.9 μM. This compound did not affect the activities of plant (cauliflower) pol α or prokaryotic pols. Myricetin also inhibited human DNA topoisomerase II (topo II) activity with an IC50 value of 27.5 μM, but did not inhibit the activities of other DNA metabolic enzymes tested. Myricetin also did not influence the direct binding to double stranded DNA as determined by thermal transition analysis. It was found to prevent the proliferation of human colon HCT116 carcinoma cells with an LD50 of 28.2 μM, halt the cell cycle in G2/M phase, and induce apoptosis.
CONCLUSIONS:
These results suggest that the decrease of proliferation may be a result of the inhibition of cellular topoisomerase (topo) II rather than pols.
Cell Research:
Eur J Pharmacol. 2014 Sep 5;738:22-30.
Myricetin enhances osteogenic differentiation through the activation of canonical Wnt/β-catenin signaling in human bone marrow stromal cells.[Pubmed: 24876056]
Myricetina flavonoid compound, has been reported to possess antioxidative, antiproliferative and anti-inflammatory effects. However, no study has yet investigated the effect of Myricetin on osteogenic differentiation of human bone marrow stem cells (hBMSCs). This study was designed to investigate the effects of Myricetin on osteogenic differentiation of hBMSCs in vitro.
METHODS AND RESULTS:
Cell viability was analyzed by MTT and osteogenic differentiation was evaluated by alkaline phosphatase (ALP) activity assay, Alizarin red S dye, real time-polymerase chain reaction (RT-PCR) and Western blot analysis. We found that the ALP activity and the mineralization of hBMSCs were enhanced by treatment with Myricetin. Myricetin increased the mRNA expressions of Osteocalcin (OCN), Collagen type I (COL-I), ALP and Runt-related transcription factor 2 (RUNX2). Additionally, we found that Myricetin activated the Wnt/β-catenin pathway and increased the expression of several downstream genes including T-cell factor-1(TCF-1) and lymphoid enhancer factor-1 (LEF-1). Depletion of β-catenin almost completely blocked the positive role of Myricetin on osteogenic differentiation.
CONCLUSIONS:
Taken together, our findings suggest that Myricetin enhanced osteogenic differentiation of hBMSCs by activating the Wnt/β-catenin signaling. The study may aid in the development of a therapeutic approach utilizing Myricetin for the enhancement of bone health and prevention of osteoporosis.
Animal Research:
Biochem Pharmacol. 2010 May 15; 79(10): 1455–1461.
Myricetin suppresses UVB-induced wrinkle formation and MMP-9 expression by inhibiting Raf.[Pubmed: 20093107]
Chronic exposure to solar ultraviolet (UV) light causes skin photoaging. Many studies have shown that naturally occurring phytochemicals have anti-photoaging effects, but their direct target molecule(s) and mechanism(s) remain unclear.
METHODS AND RESULTS:
We found that Myricetin, a major flavonoid in berries and red wine, inhibited wrinkle formation in mouse skin induced by chronic UVB irradiation (0.18J/cm(2), 3 days/week for 15 weeks). Myricetin treatment reduced UVB-induced epidermal thickening of mouse skin and also suppressed UVB-induced matrix metalloproteinase-9 (MMP-9) protein expression and enzyme activity. Myricetin appeared to exert its anti-aging effects by suppressing UVB-induced Raf kinase activity and subsequent attenuation of UVB-induced phosphorylation of MEK and ERK in mouse skin. In vitro and in vivo pull-down assays revealed that Myricetin bound with Raf in an ATP-noncompetitive manner.
CONCLUSIONS:
Overall, these results indicate that Myricetin exerts potent anti-photoaging activity by regulating MMP-9 expression through the suppression of Raf kinase activity.
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