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    Plumbagin
    Plumbagin
    Information
    CAS No. 481-42-5 Price $70 / 100mg
    Catalog No.CFN90444Purity>=98%
    Molecular Weight188.17Type of CompoundQuinones
    FormulaC11H8O3Physical DescriptionPowder
    Download Manual    COA    MSDSSimilar structuralComparison (Web)
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    Plumbagin Description
    Source: The herbs of Plumbago zeylanica L.
    Biological Activity or Inhibitors: 1. Plumbagin exhibits anti-tumor and anti-proliferative activities in various tumor cell lines as well as in animal tumor models.
    2. Plumbagin may be considered as a potential natural FOXM1 inhibitor, which could contribute to the development of new anticancer agent for therapy of gliomas.
    3. Plumbagin offers significant protective role against DEX-induced cellular damage via regulating oxidative stress, apoptosis, and osteogenic markers.
    4. Plumbagin may serve as an anti-fibrotic medication through inactivating the NF-κB/TLR-4 pathway that is associated with inflammatory reactions, thereby mitigating liver fibrosis.
    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 5.3143 mL 26.5717 mL 53.1434 mL 106.2869 mL 132.8586 mL
    5 mM 1.0629 mL 5.3143 mL 10.6287 mL 21.2574 mL 26.5717 mL
    10 mM 0.5314 mL 2.6572 mL 5.3143 mL 10.6287 mL 13.2859 mL
    50 mM 0.1063 mL 0.5314 mL 1.0629 mL 2.1257 mL 2.6572 mL
    100 mM 0.0531 mL 0.2657 mL 0.5314 mL 1.0629 mL 1.3286 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.
    Plumbagin References Information
    Citation [1]

    Cancer Lett. 2015 Feb 1;357(1):265-78.

    Plumbagin induces apoptosis in lymphoma cells via oxidative stress mediated glutathionylation and inhibition of mitogen-activated protein kinase phosphatases (MKP1/2).[Pubmed: 25444924]
    Plumbagin, a vitamin K3 analog and a pro-oxidant, was employed and it induced apoptosis in both mouse and human T-cell lymphoma cell lines via increased oxidative stress, caspase activity and loss of mitochondrial membrane potential. The pro-oxidant and cytotoxic effects of Plumbagin were sensitive to antioxidants indicating a decisive role of cellular redox balance. Plumbagin induced persistent activation of JNK and pharmacological inhibition as well as shRNA-mediated JNK knock-down rescued cells from Plumbagin-induced apoptosis. Further, Plumbagin induced cytochrome c release, FasL expression and Bax levels via activation of JNK pathway. Exposure of lymphoma cells to Plumbagin led to inhibition of total and specific phosphatase activity, increased total protein S-glutathionylation and induced glutathionylation of dual specific phosphatase- 1 and 4 (MKP-1 and MKP-2). The in vivo anti-tumor efficacy of Plumbagin was demonstrated using a mouse model. In conclusion, oxidative stress mediated tumor cytotoxicity operates through sustained JNK activation via a novel redox-mediated regulation of MKP-1 and MKP-2.
    Citation [2]

    Cell Stress Chaperones. 2015 Jul;20(4):621-9.

    Plumbagin protects against glucocorticoid-induced osteoporosis through Nrf-2 pathway.[Pubmed: 25939783]
    We studied the protective role of Plumbagin against GC-induced cell damage in MC3T3-E1 cells. The effect of dexamethasone (DEX) and Plumbagin on cell viability was determined. DEX showed as IC-50 value of 95 μM. Further, 10 μM Plumbagin treatment effectively ameliorated DEX-induced cell death by increasing the cell viability to 92 %. A further effect of Plumbagin on DEX-induced oxidative stress was determined through reactive oxygen species (ROS) level, lipid peroxide content, and antioxidant status. Plumbagin treatment significantly reversed the levels of oxidative stress and apoptotic markers and protected against DEX-induced cell damage. Further, Plumbagin treatment significantly improved the expression of osteogenic markers compared to DEX treatment. In conclusion, the present study shows that Plumbagin offers significant protective role against DEX-induced cellular damage via regulating oxidative stress, apoptosis, and osteogenic markers.
    Citation [3]

    J Neurooncol. 2015 Feb;121(3):469-77.

    Plumbagin induces growth inhibition of human glioma cells by downregulating the expression and activity of FOXM1.[Pubmed: 25528634]
    Plumbagin, a natural quinonoid constituent isolated from the root of medicinal plant Plumbago zeylanica L, has exhibited anti-tumor and anti-proliferative activities in various tumor cell lines as well as in animal tumor models.We reported that Plumbagin could effectively inhibit cell proliferation, migration and invasion and induce apoptosis of glioma cells. Cell cycle assay showed that Plumbagin induced G2/M arrest. Interestingly, we found that Plumbagin decreased the expression of FOXM1 both at mRNA level and protein level. Plumbagin also inhibited the transactivation ability of FOXM1, resulting in down-regulating the expression of FOXM1 downstream target genes, such as cyclin D1, Cdc25B, survivin, and increasing the expression of p21(CIP1) and p27(KIP1). Most importantly, down-regulation of FOXM1 by siFOXM1 transfection enhanced Plumbagin-induced change in viability. On the contrary, over-expression of FOXM1 by cDNA transfection reduced Plumbagin-induced glioma cell growth inhibition. These results suggest that Plumbagin exhibits its anticancer activity partially by inactivation of FOXM1 signaling pathway in glioma cells. Our findings indicate that Plumbagin may be considered as a potential natural FOXM1 inhibitor, which could contribute to the development of new anticancer agent for therapy of gliomas.
    Citation [4]

    Cell Physiol Biochem. 2015;35(4):1599-608.

    Anti-fibrotic effect of plumbagin on CCl₄-lesioned rats.[Pubmed: 25824458]
    BACKGROUND/AIMS: Our previous studies have shown that Plumbagin effectively inhibits hepatic stellate cell (HSC) proliferation. Thus, Plumbagin-mediated anti-fibrotic effects in vivo merit further investigation. METHODS: We used rat models to assess the potential benefits of Plumbagin against CCl₄-induced liver fibrosis. RESULTS: The results showed that Plumbagin lowered the serum concentrations of liver functional enzymes (ALT, AST, ALB, TBIL) in CCl₄-fibrotic rats while reducing inflammatory cytokine levels (IL-6, TNF-α). As reflected in pathological examinations, rats that were administered Plumbagin showed decreased collagen markers (HA, LN, PCIII and CIV) in liver tissues and improved hepatocellular impairments. In addition, Plumbagin contributed to down-regulating NF-κB and TLR-4 mRNA in CCl₄-lesioned livers. As revealed in the immunohistochemical assay, Plumbagin-administered rats showed reduced levels of α-SMA and TNF-α immunoreactive cells in liver tissue. CONCLUSION: Collectively, these findings offer appealing evidence that Plumbagin may serve as an anti-fibrotic medication through inactivating the NF-κB/TLR-4 pathway that is associated with inflammatory reactions, thereby mitigating liver fibrosis.
    Citation [5]

    Curr Drug Deliv. 2015 Mar 16.

    Plumbagin Nanoparticles Induce Dose and pH Dependent Toxicity on Prostate Cancer Cells.[Pubmed: 25772029]
    Stable nano-formulation of Plumbagin nanoparticles from Plumbago zeylanica root extract was explored as a potential natural drug against prostate cancer. Size and morphology analysis by DLS, SEM and AFM revealed the average size of nanoparticles prepared was 100±50nm. In vitro cytotoxicity showed concentration and time dependent toxicity on prostate cancer cells. However, Plumbagin crude extract found to be highly toxic to normal cells when compared to Plumbagin nanoformulation, thus confirming nano Plumbagin shows cytocompatibility with normal cells and dose dependent toxicity to prostate cells. In vitro haemolysis assay confirmed the blood biocompatibility of the Plumbagin nanoparticles. In wound healing assay, Plumbagin nanoparticles provided clues which might play an important role in the anti-migration of prostate cancer cells. DNA fragmentation revealed that partial apoptosis induction by Plumbagin nanoparticles could be expected as a potent anti-cancer agent against prostate cancer.