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    CAS No. 104012-37-5 Price $148 / 20mg
    Catalog No.CFN90629Purity>=98%
    Molecular Weight390.51Type of CompoundSesquiterpenoids
    FormulaC23H34O5Physical DescriptionPowder
    Download Manual    COA    MSDSSimilar structuralComparison (Web)
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    Biological Activity
    Description: Tussilagone has anti-cancer, anti-oxidant and anti-inflammatory activities. Tussilagone inhibits dendritic cell function through the induction of heme oxygenase-1; it has potential treatment of neuro-inflammatory diseases through the inhibition of overproduction of nitric oxide and prostaglandin E(2).
    Targets: NF-kB | HO-1 | TLR | IkB | Wnt/β-catenin | c-Myc | NO | NOS | COX | TNF-α | MAPK | p65 | IKK
    In vitro:
    Biochem Biophys Res Commun. 2014 Jan 3;443(1):132-7.
    Tussilagone suppresses colon cancer cell proliferation by promoting the degradation of β-catenin.[Pubmed: 24269588]
    Abnormal activation of the Wnt/β-catenin signaling pathway frequently induces colon cancer progression.
    In the present study, we identified Tussilagone (TSL), a compound isolated from the flower buds of Tussilago farfara, as an inhibitor on β-catenin dependent Wnt pathway. TSL suppressed β-catenin/T-cell factor transcriptional activity and down-regulated β-catenin level both in cytoplasm and nuclei of HEK293 reporter cells when they were stimulated by Wnt3a or activated by an inhibitor of glycogen synthase kinase-3β. Since the mRNA level was not changed by TSL, proteasomal degradation might be responsible for the decreased level of β-catenin. In SW480 and HCT116 colon cancer cell lines, TSL suppressed the β-catenin activity and also decreased the expression of cyclin D1 and c-myc, representative target genes of the Wnt/β-catenin signaling pathway, and consequently inhibited the proliferation of colon cancer cells.
    Taken together, TSL might be a potential chemotherapeutic agent for the prevention and treatment of human colon cancer.
    Arch Pharm Res. 2008 May;31(5):645-52.
    Suppression of inducible nitric oxide synthase and cyclooxygenase-2 expression by tussilagone from Farfarae flos in BV-2 microglial cells.[Pubmed: 18481023]
    Activated microglia produce diverse neurotoxic factors such as nitric oxide (NO) and prostaglandin E(2) (PGE(2)) that may cause neurodegenerative diseases, including Alzheimer's disease and Parkinson's disease.
    From the EtOAc soluble fraction of Farfarae flos (Tussilago farfara), we purified Tussilagone as a bioactive compound by monitoring the inhibitory potential of NO production in activated microglia through the purification procedures. Tussilagone showed dose-dependent inhibition of NO and PGE(2) production in LPS-activated microglia with IC(50) values of 8.67 microM and 14.1 microM, respectively. It suppressed the expression of protein and mRNA of inducible nitric oxide synthase and cyclooxygenase-2 through the inhibition of 1-kappaBalpha degradation and nuclear translocation of p65 subunit of NF-kappaB.
    Therefore Tussilagone from Farfarae flos may have therapeutic potential in the treatment of neuro-inflammatory diseases through the inhibition of overproduction of NO and PGE(2).
    Tussilagone Description
    Source: The flowers of Tussilago farfara.
    Solvent: Chloroform, Dichloromethane, Ethyl Acetate, DMSO, Acetone, 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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    Recently, ChemFaces products have been cited in many studies from excellent and top scientific journals

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    Calculate Dilution Ratios(Only for Reference)
    1 mg 5 mg 10 mg 20 mg 25 mg
    1 mM 2.5608 mL 12.8038 mL 25.6075 mL 51.2151 mL 64.0188 mL
    5 mM 0.5122 mL 2.5608 mL 5.1215 mL 10.243 mL 12.8038 mL
    10 mM 0.2561 mL 1.2804 mL 2.5608 mL 5.1215 mL 6.4019 mL
    50 mM 0.0512 mL 0.2561 mL 0.5122 mL 1.0243 mL 1.2804 mL
    100 mM 0.0256 mL 0.128 mL 0.2561 mL 0.5122 mL 0.6402 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 Immunopharmacol. 2014 Oct;22(2):400-8.
    Tussilagone inhibits dendritic cell functions via induction of heme oxygenase-1.[Pubmed: 25091622]
    Sesquiterpenoid Tussilagone (TUS) has a variety of pharmacological activities, such as anti-oxidant, anti-cancer, and anti-inflammatory activities.
    In this study, we investigated the effects of TUS on dendritic cell (DC) functions and the underlying mechanisms. TUS inhibited lipopolysaccharide (LPS)-induced activation of DCs, as shown by decrease in surface molecule expression, cytokine production, cell migration, and allo-T cell activation. In addition, TUS inhibited LPS-induced activation of NF-κB, MAPKs, and IRF-3 signalings in DCs, although it did not directly affect kinase activities of IRAK1/4, TAK1, and IKK, which suggests that TUS might indirectly inhibit TLR signaling in DCs. As a critical mechanism, we showed that TUS activated heme oxygenase-1 (HO-1), which degrades heme to immunosuppressive products, such as carbon monoxide and bilirubin. HO-1 inhibitor reversed the inhibitory activity of TUS in DCs.
    In conclusion, this study suggests that TUS inhibits DC function through the induction of HO-1.
    Int Immunopharmacol. 2009 Dec;9(13-14):1578-84.
    The anti-inflammatory effect of tussilagone, from Tussilago farfara, is mediated by the induction of heme oxygenase-1 in murine macrophages.[Pubmed: 19800419]
    Tussilagone (TSL), isolated from the flower of buds of Tussilago farfara (Compositae), is a sesquiterpenoid that is known to exert a variety of pharmacological activities. In the present study, we demonstrated that Tussilagone exerts anti-inflammatory activities in murine macrophages by inducing heme oxygenase-1 (HO-1) expression. Treatment of RAW264.7 cells with Tussilagone-induced HO-1 protein expression in a dose- and time-dependent manner without the induction of HO-1 mRNA expression. Tussilagone-mediated HO-1 protein induction was not inhibited by treatment with actinomycin D, a transcriptional inhibitor, but by cycloheximide, a translational inhibitor. Moreover, mitogen-activated protein kinases (MAPKs) inhibitors such as SB203580, SP600125, and U0126 did not block Tussilagone-mediated HO-1 protein expression, suggesting that the Tussilagone-mediated HO induction may be regulated at the translational level. Consistent with the notion that HO-1 has anti-inflammatory properties, Tussilagone inhibited the production of nitric oxide (NO), tumor necrosis factor (TNF)-alpha, and prostaglandin E2 (PGE2) as well as inducible nitric oxide synthase (iNOS) and cyclooxygenase-2 (COX-2) expression in lipopolysaccharide (LPS)-stimulated RAW264.7 cells and murine peritoneal macrophages. Inhibition of HO-1 activity by treatment with zinc protoporphyrin IX (ZnPP), a specific HO-1 inhibitor, abrogated the inhibitory effects of Tussilagone on the production of NO and PGE2 in LPS-stimulated RAW264.7 cells. Taken together, Tussilagone may be an effective HO-1 inducer that has anti-inflammatory effects, and a valuable compound for modulating inflammatory conditions.