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    Triptoquinone A
    CAS No. 142950-86-5 Price
    Catalog No.CFN96475Purity>=98%
    Molecular Weight328.40Type of CompoundQuinones
    FormulaC20H24O4Physical DescriptionOrange powder
    Download     COA    MSDSSimilar structuralComparison (Web)
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    Triptoquinone A Description
    Source: The roots of Tripterygium wilfordii Hook.f.
    Biological Activity or Inhibitors: 1. Triptoquinone A has anti-inflammatory activity, it can significantly suppress smooth muscle relaxation and increase in cyclic GMP levels by nitric oxide (NO) in an L-arginine-induced relaxation experiment.
    2. Triptoquinone A may be a useful candidate for the development of a drug as a potent inhibitor of iNOS gene over-expression.
    3. Triptoquinone A prevents ndotoxin-or interleukin-1 beta-promoted induction of nitric oxide synthase in vascular smooth muscle, thus inhibiting development of L-arginine-induced vasorelaxation.
    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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    Cell. 2018 Jan 11;172(1-2):249-261.e12.
    doi: 10.1016/j.cell.2017.12.019.

    PMID: 29328914

    Mol Cell. 2017 Nov 16;68(4):673-685.e6.
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    Calculate Dilution Ratios(Only for Reference)
    1 mg 5 mg 10 mg 20 mg 25 mg
    1 mM 3.0451 mL 15.2253 mL 30.4507 mL 60.9013 mL 76.1267 mL
    5 mM 0.609 mL 3.0451 mL 6.0901 mL 12.1803 mL 15.2253 mL
    10 mM 0.3045 mL 1.5225 mL 3.0451 mL 6.0901 mL 7.6127 mL
    50 mM 0.0609 mL 0.3045 mL 0.609 mL 1.218 mL 1.5225 mL
    100 mM 0.0305 mL 0.1523 mL 0.3045 mL 0.609 mL 0.7613 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.
    Triptoquinone A References Information
    Citation [1]

    Biochem Biophys Res Commun. 1996 Jul 16;224(2):579-85.

    Suppression of inducible nitric oxide synthase mRNA expression by tryptoquinone A.[Pubmed: 8702429 ]
    Triptoquinone A (TQA), which is an anti-inflammatory constituent in plants, was studied for its suppressive effect on nitric oxide production by LPS. TQA significantly suppressed smooth muscle relaxation and increase in cyclic GMP levels by nitric oxide (NO) in an L-arginine-induced relaxation experiment. The mechanistic studies showed that TQA did not directly inhibit NO radicals and inducible nitric oxide synthase (iNOS) enzyme but suppressed IL-1 beta and iNOS mRNA expression by LPS. The suppression level of iNOS gene expression by TQA was comparable to that by dexamethasone. TQA may be a useful candidate for the development of a drug as a potent inhibitor of iNOS gene over-expression.
    Citation [2]

    Life Sci. 1996;59(3):PL49-54.

    Inhibition by triptoquinone-A of LPS- and IL-1 beta-primed induction of NO synthase in rat thoracic aorta.[Pubmed: 8699928]
    We investigated the effect of Triptoquinone A (TQA), an active principal of Triptergium wilfordii, on the induction of nitric oxide synthase (NOS) promoted by endotoxin (LPS) and interleukin-1 beta (IL-1 beta). Prophylactic application of TQA selectively prevented LPS-primed initiation of L-arginine (Arg)-induced relaxation, and cGMP formation of rat thoracic aorta, and LPS-stimulated nitrite production by cultured aortic smooth muscle cells, which appear to be mediated by NOS expressed by LPS in vascular smooth muscle. TQA also prevented IL-1 beta-triggered initiation of Arg-induced relaxation and nitrite accumulation. These results suggest that TQA prevents LPS-or IL-1 beta-promoted induction of NOS in vascular smooth muscle, thus inhibiting development of Arg-induced vasorelaxation.