For research use only.
Licensed by Pfizer Catalog No.S1733
CAS No. 83-43-2
Methylprednisolone (NSC-19987) is a synthetic glucocorticoid receptor agonist, used to achieve prompt suppression of inflammation. Methylprednisolone activates ACE2 and reduces IL-6 levels, thus improves severe or critical COVID-19. Methylprednisolone markedly reduces autophagy and apoptosis.
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Choose Selective Glucocorticoid Receptor Inhibitors
|Description||Methylprednisolone (NSC-19987) is a synthetic glucocorticoid receptor agonist, used to achieve prompt suppression of inflammation. Methylprednisolone activates ACE2 and reduces IL-6 levels, thus improves severe or critical COVID-19. Methylprednisolone markedly reduces autophagy and apoptosis.|
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. 
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)|
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Clinical Trial Information
|NCT Number||Recruitment||interventions||Conditions||Sponsor/Collaborators||Start Date||Phases|
|NCT04796493||Recruiting||--||Mesenteric Traction Syndrome||Rigshospitalet Denmark||March 11 2021||--|
|NCT04780581||Recruiting||Drug: Dexamethasone|Drug: Methylprednisolone||Corona Virus Infection||Fundación Instituto de Estudios de Ciencias de la Salud de Castilla y León|Instituto de Investigación Biomédica de Salamanca||February 1 2021||Phase 4|
|NCT04560582||Not yet recruiting||Procedure: Blood Draw||Kidney Transplant; Complications|Kidney Transplant Rejection|Kidney Transplant Failure||University of Minnesota||October 2020||--|
|NCT04477993||Terminated||Drug: Janus Kinase Inhibitor (ruxolitinib)|Other: Placebo||Severe Acute Respiratory Syndrome Coronavirus 2|SARS-CoV2||Vanderson Geraldo Rocha|University of Sao Paulo General Hospital||August 14 2020||Phase 2|Phase 3|
|NCT04509219||Recruiting||Drug: Methylprednisolone Injection||Mucocutaneous Lymph Node Syndrome||Chang Gung Memorial Hospital||April 15 2020||Phase 1|
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