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    Quercitrin
    Information
    CAS No. 522-12-3 Price $40 / 20mg
    Catalog No.CFN98850Purity>=98%
    Molecular Weight448.4 Type of CompoundFlavonoids
    FormulaC21H20O11Physical DescriptionYellow powder
    Download Manual    COA    MSDSSimilar structuralComparison (Web)
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    Our products had been exported to the following research institutions and universities, And still growing.
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    Biological Activity
    Description: Quercitrin is an antibacterial agent and inhibits the oxidation of low-density lipoproteins and prevent an allergic reaction; quercitrin and DNJ in combination as a potent anticariogenic agent against S. mutans.Quercitrin has antioxidant, anti-inflammatory, anti-cancer, and anti-allergic activities. Quercitrin has antiproliferative and apoptotic effects on lung cancer cells and colon cancer cells by modulating the immune response; it promotes osteoblast differentiation in MC3T3-E1 cells and also inhibit osteoclastogenesis in RAW264.7 cells.
    Targets: Caspase | MMP(e.g.TIMP) | NF-kB | JNK | HO-1 | ERK | p38MAPK | PARP
    In vitro:
    Arch Med Res. 2014 Aug;45(6):445-54.
    Molecular mechanisms of quercitrin-induced apoptosis in non-small cell lung cancer.[Pubmed: 25193878]
    Quercitrin (QR; quercetin-3-O-rhamnoside) has been used previously as an antibacterial agent and has been shown to inhibit the oxidation of low-density lipoproteins and prevent an allergic reaction. Furthermore, it was demonstrated that Quercitrin exerts protective effects against H2O2-induced dysfunction in lung fibroblast cells. However, the mechanisms of Quercitrin effects on cancer cell proliferation and apoptosis is not well understood. The aim of this study is to investigate the cytotoxic and apoptotic effects of Quercitrin and the molecular mechanisms of Quercitrin-induced apoptosis in non-small cell lung cancer (NSCLC) cell lines.
    METHODS AND RESULTS:
    Time- and dose-dependent antiproliferative and apoptotic effects of Quercitrin determined by WST-1 cell proliferation assay, lactate dehydrogenase (LDH) cytotoxicity assay, determination of nucleosome enrichment factor, changes in caspase-3 activity, loss of mitochondrial membrane potential (MMP) and also the localization of phosphatidylserine in the plasma membrane. Changes in whole genome gene expression levels were examined by Illumina Human HT-12v4 beadchip microarrays. There were significant increases in caspase-3 activity, loss of MMP, and increases in apoptotic cell population in response to Quercitrin in A549 and NCI-H358 NSCLC cells in a time- and dose-dependent manner.
    CONCLUSIONS:
    Our results demonstrated that genes involved in leukocyte transendothelial migration, cell adhesion and phosphatidylinositol signaling system pathways were the most statistically significant pathways in NCI-H358 and A549 cells. These results revealed that Quercitrin has antiproliferative and apoptotic effects on lung cancer cells by modulating the immune response. After confirming its anticarcinogenic effects in vivo, Quercitrin could be a novel and strong anticancer agent against NSCLC.
    PLoS One. 2014 Mar 12;9(3):e91736.
    Inhibition of major virulence pathways of Streptococcus mutans by quercitrin and deoxynojirimycin: a synergistic approach of infection control.[Pubmed: 24622055]
    To evaluate the synergistic effect of Quercitrin and Deoxynojirimycin (DNJ) together with their individual inhibitory effect against virulence pathways of Streptococcus mutans.
    METHODS AND RESULTS:
    MICs of both the compounds were determined by the microdilution method, followed by their in vitrosynergy using checkerboard and time kill assay. The nature of interaction was classified as synergistic on the basis of fractional inhibitory concentration index (FICI) value of ≤0.5. Furthermore, the activity of Quercitrin and DNJ was evaluated individually and in combination against various cariogenic properties of S. mutans UA159 such as acidogenesis, aciduracity, glucan production, hydrophobicity, biofilm and adherence. Moreover, expression of virulent genes in S. mutans was analysed by quantitative RT- PCR (qRT-PCR) and inhibition of F1F0-ATPase, lactate dehydrogenase and enolase was also evaluated. Finally, scanning electron microscopy (SEM) was used to investigate structural obliteration of biofilm. The in vitro synergism between Quercitrin and DNJ was observed, with a FICI of 0.313. Their MIC values were found to be 64 μg/ml and 16 μg/ml respectively. The synergistic combination consistently showed best activity against all the virulence factors as compared to Quercitrin and DNJ individually. A reduction in glucan synthesis and biofilm formation was observed at different phases of growth. The qRT-PCR revealed significant downregulation of various virulent genes. Electron micrographs depicted the obliteration of biofilm as compared to control and the activity of cariogenic enzymes was also inhibited.
    CONCLUSIONS:
    The whole study reflects a prospective role of Quercitrin and DNJ in combination as a potent anticariogenic agent against S. mutans.
    In vivo:
    Eur J Immunol. 2005 Feb;35(2):584-92.
    In vivo quercitrin anti-inflammatory effect involves release of quercetin, which inhibits inflammation through down-regulation of the NF-kappaB pathway.[Pubmed: 15668926 ]
    Quercetin is a common antioxidant flavonoid found in vegetables, which is usually present in glycosylated forms, such as Quercitrin (3-rhamnosylquercetin). Previous in vitro experiments have shown that quercetin exerts a bigger effect than Quercitrin in the down-regulation of the inflammatory response. However, such results have not been reproduced in in vivo experimental models of intestinal inflammation, in which quercetin did not show beneficial effects while its glycosides, Quercitrin or rutin, have demonstrated their effectiveness.
    METHODS AND RESULTS:
    In this study, we have reported that the in vivo effects of Quercitrin in the experimental model of rat colitis induced by dextran sulfate sodium can be mediated by the release of quercetin generated after glycoside's cleavage by the intestinal microbiota. This is supported by the fact that quercetin, but not Quercitrin, is able to down-regulate the inflammatory response of bone marrow-derived macrophages in vitro. Moreover, we have demonstrated that quercetin inhibits cytokine and inducible nitric oxide synthase expression through inhibition of the NF-kappaB pathway without modification of c-Jun N-terminal kinase activity (both in vitro and in vivo).
    CONCLUSIONS:
    As a conclusion, our report suggests that Quercitrin releases quercetin in order to perform its anti-inflammatory effect which is mediated through the inhibition of the NF-kappaB pathway.
    Quercitrin Description
    Source: The herbs of Apocynum venetum 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 2.2302 mL 11.1508 mL 22.3015 mL 44.603 mL 55.7538 mL
    5 mM 0.446 mL 2.2302 mL 4.4603 mL 8.9206 mL 11.1508 mL
    10 mM 0.223 mL 1.1151 mL 2.2302 mL 4.4603 mL 5.5754 mL
    50 mM 0.0446 mL 0.223 mL 0.446 mL 0.8921 mL 1.1151 mL
    100 mM 0.0223 mL 0.1115 mL 0.223 mL 0.446 mL 0.5575 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:
    Biochem Pharmacol. 2005 Jun 15;69(12):1839-51.
    Quercetin, but not rutin and quercitrin, prevention of H2O2-induced apoptosis via anti-oxidant activity and heme oxygenase 1 gene expression in macrophages.[Pubmed: 15876423]
    In the present study, we examine the protective mechanism of quercetin (QE) on oxidative stress-induced cytotoxic effect in RAW264.7 macrophages.
    METHODS AND RESULTS:
    Results of Western blotting show that QE but not its glycoside rutin (RUT) and quicitrin-induced HO-1 protein expression in a time- and dose-dependent manner, and HO-1 protein induced by QE was blocked by an addition of cycloheximide or actinomycin D. Induction of HO-1 gene expression by QE was accompanied by inducing ERKs, but not JNKs or p38, proteins phosphorylation. Addition of PD98059, but not SB203580 or SP600125, significantly attenuates QE-induced HO-1 protein and mRNA expression associated with blocking the expression of phosphorylated ERKs proteins. H(2)O(2) addition reduces the viability of cells by MTT assay, and appearance of DNA ladders, hypodiploid cells, and an increase in intracellular peroxide level was detected. Addition of QE, but not QI or RUT, significantly reduced the cytotoxic effect induced by H(2)O(2) associated with blocking the production of intracellular peroxide, DNA ladders, and hypodiploid cells. QE protection of cells from H(2)O(2)-induced apoptosis was significantly suppressed by adding HO inhibitor SnPP or ERKs inhibitor PD98059. Additionally, QE protects cells from H(2)O(2)-induced a decrease in the mitochondrial membrane potential and a release of cytochrome c from mitochondria to cytosol by DiOC6 and Western blotting assay, respectively. Activation of apoptotic proteins including the caspase 3, caspase 9, PARP, D4-GDI proteins was identified in H(2)O(2)-treated cells by Western blotting and enzyme activity assay, and that was significantly blocked by an addition of QE, but not RUT and QI. Furthermore, HO-1 catalytic metabolites carbon monoxide (CO), but not Fe(2+), Fe(3+), biliverdin or bilirubin, performed protective effect on cells from H(2)O(2)-induced cell death with an increase in HO-1 protein expression and ERKs protein phosphorylation.
    CONCLUSIONS:
    These data suggest that induction of HO-1 protein may participate in the protective mechanism of QE on oxidative stress (H(2)O(2))-induced apoptosis, and reduction of intracellular ROS production and mitochondria dysfunction with blocking apoptotic events were involved. Differential anti-apoptotic effect between QE and its glycosides RUT and QI via distinct HO-1 protein induction was also delineated.
    Cell Research:
    Pathol Oncol Res. 2015 Apr;21(2):333-8.
    Apoptotic Effects of Quercitrin on DLD-1 Colon Cancer Cell Line.[Pubmed: 25096395]
    Quercetin, which is the most abundant bioflavonoid compound, is mainly present in the glycoside form of Quercitrin. Although different studies indicated that Quercitrin is a potent antioxidant, the action of this compound is not well understood. In this study, we investigated whether Quercitrin has apoptotic and antiproliferative effects in DLD-1 colon cancer cell lines.
    METHODS AND RESULTS:
    Time and dose dependent antiproliferative and apoptotic effects of Quercitrin were subsequently determined by WST-1 cell proliferation assay, lactate dehydrogenase (LDH) cytotoxicity assay, detection of nucleosome enrichment factor, changes in caspase-3 activity, loss of mitochondrial membrane potential (MMP) and also the localization of phosphatidylserine (PS) in the plasma membrane. There were significant increases in caspase-3 activity, loss of MMP, and increases in the apoptotic cell population in response to Quercitrin in DLD-1 colon cancer cells in a time- and dose-dependent manner.
    CONCLUSIONS:
    These results revealed that Quercitrin has antiproliferative and apoptotic effects on colon cancer cells. Quercitrin activity supported with in vivo analyses could be a biomarker candicate for early colorectal carcinoma.
    Biochem Pharmacol. 2013 Nov 15;86(10):1476-86.
    Quercitrin and taxifolin stimulate osteoblast differentiation in MC3T3-E1 cells and inhibit osteoclastogenesis in RAW 264.7 cells.[Pubmed: 24060614]
    Flavonoids are natural antioxidants that positively influence bone metabolism. The present study screened among different flavonoids to identify biomolecules for potential use in bone regeneration. For this purpose, we used MC3T3-E1 and RAW264.7 cells to evaluate their effect on cell viability and cell differentiation.
    METHODS AND RESULTS:
    First, different doses of chrysin, diosmetin, galangin, Quercitrin and taxifolin were analyzed to determine the optimum concentration to induce osteoblast differentiation. After 48h of treatment, doses ≥100μM of diosmetin and galangin and also 500μM taxifolin revealed a toxic effect on cells. The same effect was observed in cells treated with doses ≥100μM of chrysin after 14 days of treatment. However, the safe doses of Quercitrin (200 and 500μM) and taxifolin (100 and 200μM) induced bone sialoprotein and osteocalcin mRNA expression. Also higher osteocalcin secreted levels were determined in 100μM taxifolin osteoblast treated samples when compared with the control ones. On the other hand, Quercitrin and taxifolin decreased Rankl gene expression in osteoblasts, suggesting an inhibition of osteoclast formation. Indeed, osteoclastogenesis suppression by Quercitrin and taxifolin treatment was observed in RAW264.7 cells.
    CONCLUSIONS:
    Based on these findings, the present study demonstrates that Quercitrin and taxifolin promote osteoblast differentiation in MC3T3-E1 cells and also inhibit osteoclastogenesis in RAW264.7 cells, showing a positive effect of these flavonoids on bone metabolism.