Licensed by Pfizer Catalog No.S1733 Synonyms: NSC-19987
Molecular Weight(MW): 374.47
Methylprednisolone is a synthetic glucocorticoid receptor agonist, used to achieve prompt suppression of inflammation.
Purity & Quality Control
Choose Selective Glucocorticoid Receptor Inhibitors
|Description||Methylprednisolone is a synthetic glucocorticoid receptor agonist, used to achieve prompt suppression of inflammation.|
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 vivo||Methylprednisolone 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. |
|In vitro||DMSO||75 mg/mL (200.28 mM)|
|Ethanol||2 mg/mL (5.34 mM)|
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Clinical Trial Information
|NCT Number||Recruitment||Conditions||Sponsor/Collaborators||Start Date||Phases|
|NCT02960555||Recruiting||Myeloma||M.D. Anderson Cancer Center|Sanofi||February 8, 2017||Phase 2|
|NCT02798523||Recruiting||Normal Physiology||National Institute of Allergy and Infectious Diseases (NIAID)|National Institutes of Health Clinical Center (CC)||June 7, 2016||Phase 1|
|NCT01875237||Active, not recruiting||Leukemia|Myeloma|Myeloproliferative Diseases||M.D. Anderson Cancer Center|Bellicum Pharmaceuticals||December 27, 2013||Phase 1|Phase 2|
|NCT01331018||Recruiting||Fanconi Anemia||Fred Hutchinson Cancer Research Center|National Cancer Institute (NCI)|National Heart, Lung, and Blood Institute (NHLBI)||February 22, 2012||Phase 1|
|NCT02867904||Not yet recruiting||Arthroscopic Shoulder Surgery|Intra-articular Debridement|Subacromial Decompression|Acromioplasty|Acromioclavicular Joint Resection||Peter Chang|University of South Dakota||August 2017||Phase 4|
|NCT03007147||Not yet recruiting||B Acute Lymphoblastic Leukemia With t(9;22)(q34.1;q11.2); BCR-ABL1|BCR-ABL1 Fusion Protein Expression|Minimal Residual Disease|Philadelphia Chromosome Positive|T Acute Lymphoblastic Leukemia|Untreated Adult Acute Lymphoblastic Leukemia|Untreated Childhood Acute Lymphoblastic Leukemia||Childrens Oncology Group|National Cancer Institute (NCI)||July 2017||Phase 3|
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