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    Methylprednisolone
    Methylprednisolone

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    This product is for research use only, not for human use. We do not sell to patients.
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    InvivoChem Cat #: V1703
    CAS #: 83-43-2 Purity ≥98%

    Description: Methylprednisolone (also known as NSC-19987) is a synthetic and potent glucocorticoid receptor agonist, used to achieve prompt suppression of inflammation. It is used in arthritis therapy and short-term treatment of bronchial inflammation or acute bronchitis due to various respiratory diseases. It is also used both in the treatment of acute periods and long-term management of autoimmune diseases, most notably systemic lupus erythematosus.

    References: Clin Exp Immunol. 1996 Oct;106(1):91-6; J Neurosci. 2003 Aug 6;23(18):6993-7000.

    Related CAS#: 2375-03-3 (Methylprednisolone sodium succinate; U-9088); 2921-57-5 (Methylprednisolone succinate); 2375-03-3 (6α-Methylprednisolone 21-hemisuccinate sodium)

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    Molecular Weight (MW)374.47
    FormulaC22H30O5
    CAS No.83-43-2(Methylprednisolone);
    Storage-20℃ for 3 years in powder form
    -80℃ for 2 years in solvent
    Solubility (In vitro)DMSO: 75 mg/mL (200.3 mM)
    Water:<1 mg/mL
    Ethanol: 2 mg/mL (5.3 mM)
    SMILES
    O=C1C=C[[email protected]]2(C)[[email protected]@]3([H])[[email protected]@H](O)C[[email protected]]4(C)[[email protected]@](O)(C(CO)=O)CC[[email protected]@]4([H])[[email protected]]3([H])C[[email protected]](C)C2=C1
    SynonymsNSC-19987; U-7532; NSC 19987; U 7532; NSC19987; U7532;


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    In Vitro

    In vitro activity: Methylprednisolone (2-10 mg/kg) markedly inhibits TNF production but does not affect serum levels of IL-10, while a high methylprednisolone dose (50 mg/kg) increases LPS-induced IL-10 levels. Methylprednisolone(from 0.01 to 100 mg/mL) also increases the biosynthesis of IL-10 by LPS-activated mouse peritoneal macrophages.  

    In VivoMethylprednisolone decreases RGC survival in rats with electrophysiologically diagnosed optic neuritis. Methylprednisolone decreases RGC survival by a nongenomic, calcium-dependent mechanism. Methylprednisolone-induced enhancement of RGC degeneration depends on calcium influx through voltage-gated calcium channels. Methylprednisolone treatment leads to a significant decrease in the number of ED1-positive cells in both rostral and caudal stumps. Methylprednisolone treatment results in a significant reduction in tissue loss in both cord stumps at 2, 4 and 8 week post-injury. Methylprednisolone leads to a long-term reduction of ED1-positive cells and spinal tissue loss, reduced dieback of vestibulospinal fibres, and a transient sprouting of vestibulospinal fibres near the lesion at 1 and 2 weeks post-lesion. Methylprednisolone at a dose of 30 mg/kg which has been shown to be effective in improving functional outcomes in rat SCI models, suppresses TNF-α expression and NF-kB activation. Methylprednisolone inhibition of NF-kB function is likely mediated by the induction of IkB, which traps NF-kB in inactive cytoplasmic complexes.
    Animal model Rats
    Formulation & Dosage 30 mg/kg
    ReferencesClin Exp Immunol. 1996 Oct;106(1):91-6; J Neurosci. 2003 Aug 6;23(18):6993-7000.


    These protocols are for reference only. InvivoChem does not independently validate these methods.

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