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    Mesaconitine
    Information
    CAS No. 2752-64-9 Price $148 / 20mg
    Catalog No.CFN99199Purity>=98%
    Molecular Weight631.71Type of CompoundAlkaloids
    FormulaC33H45NO11Physical DescriptionWhite powder
    Download Manual    COA    MSDS    SDFSimilar structuralComparison (Web)
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    Mesaconitine Description
    Source: The root of Aconitum carmichaeli Debx.
    Biological Activity or Inhibitors: 1. Mesaconitine increases the [Ca2+]i level in endothelial cells by influx of Ca2+ from extracellular spaces, suggests that mesaconitine-induced Ca2+ influx and activation of nitric-oxide synthase in endothelial cells and, thus, induced vasorelaxation in rat aorta.
    2. Mesaconitine has antinociceptive activity, has inhibition of stimulus-triggered and spontaneous epileptiform activity in rat hippocampal slices.
    3. Mesaconitine has antiinflammatory activity, can inhibit carrageenin-induced hind-paw edema in sham-operated mice as well as adrenalectomized mice, it do not affect the biosynthesis of the prostaglandins.
    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 1.583 mL 7.915 mL 15.83 mL 31.6601 mL 39.5751 mL
    5 mM 0.3166 mL 1.583 mL 3.166 mL 6.332 mL 7.915 mL
    10 mM 0.1583 mL 0.7915 mL 1.583 mL 3.166 mL 3.9575 mL
    50 mM 0.0317 mL 0.1583 mL 0.3166 mL 0.6332 mL 0.7915 mL
    100 mM 0.0158 mL 0.0792 mL 0.1583 mL 0.3166 mL 0.3958 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.
    Mesaconitine References Information
    Citation [1]

    Eur J Pharmacol. 2002 Feb 2;436(3):217-25.

    Mesaconitine-induced relaxation in rat aorta: involvement of Ca2+ influx and nitric-oxide synthase in the endothelium.[Pubmed: 11858801]
    The effect of Mesaconitine was dependent on external Ca2+ concentrations. The relaxation induced by Mesaconitine was abolished by N(omega)-nitro-L-arginine methyl ester (0.1 mM, an inhibitor of nitric-oxide synthase), as well as the relaxation induced by acetylcholine. Acetylcholine induced relaxation in two phases in our conditions; the initial phase was transient and external Ca2+ -independent, and the second phase was sustained and external Ca2+ -dependent. Treatment with 100 nM thapsigargin, which depleted intracellular Ca2+ stores, inhibited acetylcholine-induced, but not Mesaconitine-induced, relaxation. Mesaconitine increased the [Ca2+]i level in endothelial cells by influx of Ca2+ from extracellular spaces. These findings suggest that Mesaconitine-induced Ca2+ influx and activation of nitric-oxide synthase in endothelial cells and, thus, induced vasorelaxation in rat aorta.
    Citation [2]

    Xenobiotica. 2011 Jan;41(1):46-58.

    Characterization of metabolites and human P450 isoforms involved in the microsomal metabolism of mesaconitine.[Pubmed: 21105783]
    Results showed that the inhibitor of CYP3A had a strong inhibitory effect; the inhibitors of CYP2C8, CYP2C9, CYP2C19, and CYP2D6 had modest inhibitory effects, whereas inhibitors of CYP1A2 and CYP2E1 had no obvious inhibitory effects on Mesaconitine metabolism. Recombinant human cytochrome P450 isoforms CYP3A4 and CYP3A5 contributed greatly to the formation of MA metabolites, and CYP2C8, CYP2C9, and CYP2D6 played a minor role in the formation of Mesaconitine metabolites. Mesaconitine could be transformed into at least nine metabolites in MHLMs. Mesaconitine might be metabolized by CYP3A4, CYP3A5, CYP2C8, CYP2C9, and CYP2D6 in MHLMs.
    Citation [3]

    Planta Med. 1994 Oct;60(5):391-4.

    Antinociceptive mechanism of the aconitine alkaloids mesaconitine and benzoylmesaconine.[Pubmed: 7997462 ]
    We explored the possible role of the specific regions in the brain stem on the antinociceptive actions of Mesaconitine (MA) and benzoylmesaconine (BM) by the microinjection of MA and BM into nucleus reticularis paragigantocellularis (NRPG), nucleus raphe magnus (NRM), and periaqueductal gray (PAG). MA microinjected into NRPG, NRM, or PAG elicited a dose-dependent antinociceptive action, whereas BM injected into NRM or PAG elicited a dose-dependent antinociceptive action but not in NRPG. The NRM appeared to be the most sensitive region among the three tested locations.
    Citation [4]

    Eur J Pharmacol. 1998 Jan 26;342(2-3):183-91.

    Inhibition of stimulus-triggered and spontaneous epileptiform activity in rat hippocampal slices by the Aconitum alkaloid mesaconitine.[Pubmed: 9548384]
    The aim of the present study was to investigate if the plant alkaloid, Mesaconitine, which has been reported to have antinociceptive effects via stimulation of the noradrenergic system, inhibits epileptiform field potentials. The experiments were performed as extracellular recordings on rat hippocampal slices. Epileptiform activity was induced by omission of Mg2+ from the bathing medium or by addition of bicuculline and stimulus-evoked population bursts were recorded in the CA1 region. Spontaneous epileptiform activity was elicited by perfusing a nominally Mg2+-free bathing medium with high K+ concentration (5 mM). Both stimulus-triggered and spontaneous epileptiform activity was attenuated in a concentration-dependent manner by Mesaconitine (30 nM-1 microM). The inhibitory effect was rather variable in appearance when lower concentrations (30 and 100 nM) of Mesaconitine were applied. Pretreatment of the slices with the alpha-adrenoceptor antagonist yohimbine (1 microM) prevented the effect of Mesaconitine. It is concluded that the inhibitory action of Mesaconitine at low concentration is mediated via alpha-adrenoceptors.
    Citation [5]

    Eur J Pharmacol. 1982 Aug 13;82(1-2):65-71.

    Mechanism of inhibitory action of mesaconitine in acute inflammations.[Pubmed: 6127222]
    Mesaconitine (MA) inhibited carrageenin-induced hind-paw edema in sham-operated mice as well as adrenalectomized mice. Hind-paw edema produced by subplantar injection of histamine, serotonin and prostaglandin E1 was suppressed by MA, indicating that it elicits the antiinflammatory activity at the early exudative stage of inflammations. However, MA did not affect the biosynthesis of the prostaglandins. Trazoline and propranolol had no effect on the inhibitory activity of MA on carrageenin-induced hind-paw edema. MA when administered i.c. at the doses where it shows marked analgesic activity produced dose-dependent antiinflammatory responses on paw edema produced by carrageenin and on vascular permeability accelerated by acetic acid and agar. The inhibitory activity of morphine on carrageenin-induced paw edema failed to be potentiated by the concurrent administration of MA, demonstrating that the mechanism of the antiinflammatory activity of MA involves the central nervous system.