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    Morusin
    Information
    CAS No. 62596-29-6 Price $198 / 20mg
    Catalog No.CFN97083Purity> 98%
    Molecular Weight420.5 Type of CompoundFlavonoids
    FormulaC25H24O6Physical DescriptionYellow powder
    Download Manual    COA    MSDS    SDFSimilar structuralComparison (Web)
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    Morusin Description
    Source: The root bark of Morus alba L.
    Biological Activity or Inhibitors: 1. Morusin possesses antitumor effects of cell lines including HT-29, A549, MCF-7, and MDA-MB-231, through suppressing STAT3 and NFκB attenuation mediated apoptosis induction.
    2. Morusin possesses anti-oxidant and anti-inflammatory effects.
    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.
    Calculate Dilution Ratios(Only for Reference)
    1 mg 5 mg 10 mg 20 mg 25 mg
    1 mM 2.3781 mL 11.8906 mL 23.7812 mL 47.5624 mL 59.453 mL
    5 mM 0.4756 mL 2.3781 mL 4.7562 mL 9.5125 mL 11.8906 mL
    10 mM 0.2378 mL 1.1891 mL 2.3781 mL 4.7562 mL 5.9453 mL
    50 mM 0.0476 mL 0.2378 mL 0.4756 mL 0.9512 mL 1.1891 mL
    100 mM 0.0238 mL 0.1189 mL 0.2378 mL 0.4756 mL 0.5945 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.
    Morusin References Information
    Citation [1]

    Toxicol Lett. 2015 Jan 22;232(2):490-8.

    Antitumor progression potential of morusin suppressing STAT3 and NFκB in human hepatoma SK-Hep1 cells.[Pubmed: 25476160]
    Morusin is a prenylated flavonoid that has been isolated from the root bark of the mulberry tree (Morus species, Moraceae), a Chinese traditional medicine. It has been synthesized by our laboratory from commercially available phloroglucinol, and has demonstrated to possess antitumor effects of cell lines including A549, MCF-7, and MDA-MB-231. In this study, at non-cytotoxic concentrations, Morusin altered invasive morphology and suppressed cell-matrix adhesion, cell motility and cell invasion in SK-Hep1 cells. Morusin also increased the expression of E-cadherin, an epithelial cell junction protein, decreased the expression of vimentin, a mesecnchymal marker, and α2-, α6-, β1- integrin, which regulated cancer attachment and migration. In addition, Morusin reduced the activity of matrix metalloproteinase-2 and 9 (MMP-2 and MMP-9), which were involved in extracellular matrix (ECM) degradation and promoting cancer cell invasion. Furthermore, Morusin suppressed the signal transducer and activator of transcription 3 (STAT3) and nuclear factor-κB (NFκB) signaling pathways, which modulate the protein expression involved in the invasion process. Finally, Morusin decreased the lung colonization of the SK-Hep1 cells in the nude mice. These results indicate Morusin possesses antitumor progression potential through suppressing STAT3 and NFκB.
    Citation [2]

    Am J Cancer Res. 2014 Dec 15;5(1):289-99.

    Morusin induces cell death through inactivating STAT3 signaling in prostate cancer cells.[Pubmed: 25628938]
    STAT3 has been recognized as an efficacious drug target for prostate cancer because of its constitutive activation in this fatal disease. We recently identified the root bark of Morus alba Linn. as a potential STAT3 inhibitor among 33 phytomedicines traditionally used in Korea. Morusin, an active compound isolated from the root bark of Morus alba, has shown anti-oxidant and anti-inflammatory effects. In the present study, we examined whether Morusin has a potential as an anti-cancer agent in prostate cancer. We found that Morusin suppressed viability of prostate cancer cells, but little effect in normal human prostate epithelial cells. Morusin also reduced STAT3 activity by inhibiting its phosphorylation, nuclear accumulation, and DNA binding activity. In addition, Morusin down-regulated expression of STAT3 target genes encoding Bcl-xL, Bcl-2, Survivin, c-Myc and Cyclin D1, which are involved in regulation of apoptosis and cell cycle. Furthermore, Morusin induced apoptosis in human prostate cancer cells by reducing STAT3 activity. Taken together, these results suggest that Morusin could be a potentially therapeutic agent for prostate cancer by reducing STAT3 activity and inducing apoptosis.
    Citation [3]

    Mol Carcinog. 2014 Dec 31.

    Morusin inhibits glioblastoma stem cell growth in vitro and in vivo through stemness attenuation, adipocyte transdifferentiation, and apoptosis induction.[Pubmed: 25557841]
    Glioblastoma multiforme (GBM) cancer stem cells (GSCs) are responsible for the progression and recurrence of GBM after conventional therapy. Morusin possesses anti-cancer activity in vitro. The purpose of this study is to confirm the growth inhibition effect of Morusin on human GSCs growth in vitro and in vivo and to explore the possible mechanism of its activity. Human GSCs were enriched under nonadhesive culture system, and characterized through neurosphere formation, toluidine blue staining, immunofluorescence staining, Western blotting analysis of stemness markers of CD133, nestin, Sox2 and Oct4, and tumorigenecity in vivo; the growth inhibition effect of Morusin on human GSCs in vitro and in vivo were tested by cell cytotoxicity, neurosphere formation inhibition, adipogenic differentiation, apoptosis induction, and tumor growth inhibition in vivo assays. The potential molecular mechanisms underlying the growth inhibition effect of Morusin on GSCs in vitro and in vivo were investigated with Western blotting evaluation of stemness, adipogenic, and apoptotic proteins in Morusin treated GSCs and tumor tissues. GSCs enriched under nonadhesive culture system possess stemness characterstics; Morusin inhibited GSCs growth in vitro and in vivo, it reduced stemness of GSCs, induced them adipocyte-like transdifferention and apoptosis. Morusin has the potential to inhibit human GSCs growth in vitro and in vivo through stemness attenuation, adipocyte transdifferentiation, and apoptosis induction.
    Citation [4]

    Mol Cell Biochem. 2013 Jul;379(1-2):7-18.

    Morusin inhibits human cervical cancer stem cell growth and migration through attenuation of NF-κB activity and apoptosis induction.[Pubmed: 23543150]
    Morusin possesses anti-cancer activity through attenuation of NF-κB activity, which is up-regulated in cancer stem cells. The purpose of this study is to confirm the growth and migration inhibition effect of Morusin on human cervical CSCs, and to clarify its partial mechanism of activity. The growth and migration inhibition effects of Morusin on human cervical CSCs were tested by cell proliferation, tumor sphere formation, and transwell assay; apoptotic death of human cervical CSCs in response to Morusin was measured with DAPI staining, apoptotic DNA fragmentation; NF-κBp65, Bcl-2, Bax, and caspase-3 protein expressions were detected through Western blotting. Under this non-adhesive culture system, typical tumor spheres appeared within 5-7 days, the tumor sphere formation, self-renewal, and cell migration, expressions of putative stem cell markers, EMT markers, and relevant transcription factors of the tumor sphere cells were increased significantly. After Morusin treatment, the proliferation, tumor sphere formation, and migration of human cervical CSCs were decreased significantly, DAPI-stained apoptotic cells increased, apoptotic DNA fragmentations formed evidently; the expression levels of NF-κBp65 and Bcl-2 decreased significantly, Bax, and caspase-3 increased significantly in a dose-dependent manner. Using the non-adhesive culture system, human cervical CSCs were enriched and expanded. Morusin has the potential to target and kill CSCs, and can inhibit human cervical growth and migration through NF-κB attenuation mediated apoptosis induction.
    Citation [5]

    Biochem Biophys Res Commun. 2008 Jul 18;372(1):236-42.

    Morusin induces apoptosis and suppresses NF-kappaB activity in human colorectal cancer HT-29 cells.[Pubmed: 18485277]
    Morusin is a pure compound isolated from root bark of Morusaustralis (Moraceae). In this study, we demonstrated that Morusin significantly inhibited the growth and clonogenicity of human colorectal cancer HT-29 cells. Apoptosis induced by Morusin was characterized by accumulation of cells at the sub-G(1) phase, fragmentation of DNA, and condensation of chromatin. Morusin also inhibited the phosphorylation of IKK-alpha, IKK-beta and IkappaB-alpha, increased expression of IkappaB-alpha, and suppressed nuclear translocation of NF-kappaB and its DNA binding activity. Dephosphorylation of NF-kappaB upstream regulators PI3K, Akt and PDK1 was also displayed. In addition, activation of caspase-8, change of mitochondrial membrane potential, release of cytochrome c and Smac/DIABLO, and activation of caspase-9 and -3 were observed at the early time point. Downregulation in the expression of Ku70 and XIAP was exhibited afterward. Caspase-8 or wide-ranging caspase inhibitor suppressed Morusin-induced apoptosis. Therefore, the antitumor mechanism of Morusin in HT-29 cells may be via activation of caspases and inhibition of NF-kappaB.