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    Kobophenol A
    Kobophenol A
    Information
    CAS No. 124027-58-3 Price $318 / 10mg
    Catalog No.CFN92530Purity>=98%
    Molecular Weight925.0Type of CompoundPhenols
    FormulaC56H44O13Physical DescriptionPowder
    Download Manual    COA    MSDSSimilar structuralComparison (Web)
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    Biological Activity
    Description: Kobophenol A has antimicrobial, and anti-inflammatory activities, it might be a candidate for treatment of inflammatory bone diseases relevant to osteoblast cell death. Kobophenol A inhibits AChE activity in a dose-dependent manner, and the IC50 value is 115.8mM. Kobophenol A has protective effect against nitrosative/oxidative or mitochondrial damages resulted in the inhibition of the ROS, intracellular calcium ion level, and mitochondrial transmembrane potential changes on SH-SY5Y cells.
    Targets: p38MAPK | CDK | ROS | Bcl-2/Bax | JNK | AP-1 | NO | NF-kB | MMP(e.g.TIMP)
    In vitro:
    Int Immunopharmacol. 2013 Nov;17(3):704-13.
    Kobophenol A enhances proliferation of human osteoblast-like cells with activation of the p38 pathway.[Pubmed: 24021754]
    Bone cell proliferation, bone formation, and bone resorption are the main factors involved in the homeostasis of the bone mass. Osteoblast death is a problem experienced by postmenopause women. Herbal medicines have attracted considerable attention for use as a drug or a drug substitute in the treatment of bone-related diseases, such as osteoporosis.
    METHODS AND RESULTS:
    This study investigated the effects of Kobophenol A on the proliferation in human osteoblast cells. Kobophenol A stimulated the proliferation of osteoblast cells by the increases in DNA synthesis and the enhancement of cell cycle progression. Kobophenol A stimulation induced the expression of the cyclin B1 and cyclin-dependent kinase 1 (CDK1). Treatment of osteoblast cells with p38 MAPK inhibitor SB203580 significantly inhibited Kobophenol A-enhanced proliferation. In addition, Kobophenol A induced phosphorylation of p38 MAPK. Treatment of osteoblast cells with Kobophenol A resulted in improvement of ROS scavenging activity. Moreover, Kobophenol A treatment up-regulated the Bcl-2 level, but down-regulated the level of Bax expression. We also demonstrate that Kobophenol A increased alkaline phosphatase (ALP) activity after 2 days.
    CONCLUSIONS:
    Taken together, the results of this study reveal that Kobophenol A has proliferative effects and enhances ALP activity in osteoblast cells and these findings provide insights into the development of a therapeutic approach of Kobophenol A in the prevention of osteoporosis and other bone disorders.
    Chem Pharm Bull (Tokyo). 2014;62(7):713-8. Epub 2014 Apr 24.
    Kobophenol A inhibits sodium nitroprusside-induced cardiac H9c2 cell death through suppressing activation of JNK and preserving mitochondrial anti-apoptotic Bcl-2 and Mcl-1.[Pubmed: 24759620]
    Sodium nitroprusside (SNP) releases nitric oxide (NO), a powerful vasodilator, and thus widely used in intensive care unit for treating hypertension emergency. However, cardiac toxicity after SNP administration is a clinical problem.
    METHODS AND RESULTS:
    For finding a natural compound that suppressing SNP-induced cardiac toxicity, we tested the protective potential of Kobophenol A (Kob A), purified from the root of Caragana sinica, against the toxic effects of SNP. The severe cardiac H9c2 cell death was induced by SNP (2 mM) treatment. Kob A ameliorated SNP-induced cardiac H9c2 cell death, and this protective effect of Kob A may be related to the inhibition of c-Jun NH2-terminal kinase (JNK) and p38 mitogen-activated protein (MAP) kinase activation following SNP administration. In addition, the downregulation of cellular Bcl-2 and Mcl-1 levels by SNP exposure was strongly abrogated in the presence of Kob A.
    CONCLUSIONS:
    These biological properties of Kob A might provide insights into developing new cardioprotectant against SNP-induced cardiac cell death.
    Kobophenol A Description
    Source: The herbs of Carex humilis Leyss.
    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 1.0811 mL 5.4054 mL 10.8108 mL 21.6216 mL 27.027 mL
    5 mM 0.2162 mL 1.0811 mL 2.1622 mL 4.3243 mL 5.4054 mL
    10 mM 0.1081 mL 0.5405 mL 1.0811 mL 2.1622 mL 2.7027 mL
    50 mM 0.0216 mL 0.1081 mL 0.2162 mL 0.4324 mL 0.5405 mL
    100 mM 0.0108 mL 0.0541 mL 0.1081 mL 0.2162 mL 0.2703 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:
    Bioorg Med Chem Lett. 2007 Apr 1;17(7):1879-82. Epub 2007 Jan 27.
    Neuroprotective effects of kobophenol A against the withdrawal of tropic support, nitrosative stress, and mitochondrial damage in SH-SY5Y neuroblastoma cells.[Pubmed: 17300930]
    This study examined the neuroprotective effects of Kobophenol A (kob A), oligomeric stillbene, and a resveratrol tetramer. Neuronal death induced by the withdrawal of tropic support was ameliorated by Kobophenol A. The protective effect of Kobophenol A against nitrosative/oxidative or mitochondrial damages resulted in the inhibition of the ROS, intracellular calcium ion level, and mitochondrial transmembrane potential changes on SH-SY5Y cells.
    Cell Research:
    Int Immunopharmacol. 2011 Sep;11(9):1251-9.
    Protective effect of kobophenol A on nitric oxide-induced cell apoptosis in human osteoblast-like MG-63 cells: involvement of JNK, NF-κB and AP-1 pathways.[Pubmed: 21511059]
    Nitric oxide (NO) is a multifunctional signaling molecule and the cytotoxic species responsible for a variety of pathologic disorders including bone destruction. High NO levels induce the apoptosis of osteoblasts and decrease the bone mineral density.
    METHODS AND RESULTS:
    We investigated the influence of Kobophenol A (kob A) on apoptosis in cultured human osteoblast-like MG-63 cells. Direct NO donor sodium nitroprusside (SNP) that has been recognized as an inducer of apoptosis in various cell lines significantly induced cell death and NO production in MG-63 cells. Coincubation of kob A in SNP-treated MG-63 cells resulted in a significant protection against NO-induced cell death. This is associated with increase in intracellular reactive oxygen species (ROS) scavenging activity and the inhibition of decrease in mitochondrial membrane potential (MMP) by kob A. We also found that kob A inhibited the down-regulation of Bcl-2 and Bcl-X(L), whereas the level of Bax expression was decreased by kob A treatment in SNP-treated MG-63 cells. Furthermore, kob A inhibited SNP-induced phosphorylation of JNK and c-Jun, and SNP-induced reduction in NF-κΒ and AP-1 activities, implicating that protective effect of kob A may occur through the regulation of JNK, NF-κΒ and AP-1 signaling pathways.
    CONCLUSIONS:
    Together, these findings suggest that kob A has a protective effect against NO-mediated osteoblast apoptosis and might be a plausible candidate for treatment of inflammatory bone diseases relevant to osteoblast cell death.