Details
Stereochemistry | ABSOLUTE |
Molecular Formula | C22H28O5 |
Molecular Weight | 372.4547 |
Optical Activity | UNSPECIFIED |
Defined Stereocenters | 7 / 7 |
E/Z Centers | 0 |
Charge | 0 |
SHOW SMILES / InChI
SMILES
[H][C@@]12C[C@H](C)[C@](O)(C(=O)CO)[C@@]1(C)CC(=O)[C@@]3([H])[C@@]2([H])CCC4=CC(=O)C=C[C@]34C
InChI
InChIKey=PIDANAQULIKBQS-RNUIGHNZSA-N
InChI=1S/C22H28O5/c1-12-8-16-15-5-4-13-9-14(24)6-7-20(13,2)19(15)17(25)10-21(16,3)22(12,27)18(26)11-23/h6-7,9,12,15-16,19,23,27H,4-5,8,10-11H2,1-3H3/t12-,15-,16-,19+,20-,21-,22-/m0/s1
Meprednisone, also known as NSC-63278 and Betapar, is a glucocorticoid receptor agonist.It has anti-inflammatory and immunosuppressive activity. It was approved since 1978, but its marketing in USA was discontinied since. Meprednisone is marketed in Argentina under trade name Copytren for treatment of rheumatic diseases, diseases of collagen, dermatological, gastrointestinal, respiratory and ophtalmological diseases.
Approval Year
Targets
Primary Target | Pharmacology | Condition | Potency |
---|---|---|---|
Target ID: CHEMBL2034 Sources: http://medkoo.com/products/10909 |
Conditions
Condition | Modality | Targets | Highest Phase | Product |
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Palliative | BETAPAR Approved UseMeprednisone (16-β-methylprednisone) is a steroid anti-inflammatory with poor mineralocorticoid action due to the methylation of prednisone at the carbon 16 level. Corticosteroids have anti-inflammatory and immunosuppressive activity. The mechanism of anti-inflammatory action is due to the decrease of the tissue response to the inflammatory processes, without modifying the underlying causes. Steroids diffuse through the cell membrane and bind to specific cytoplasmic receptors. Then, this complex enters the nucleus, where it binds to other transcriptional factors and to DNA producing induction and repression of genes that lead to its anti-inflammatory, immunosuppressive and mild mineralocorticoid effect. Other effects are: suppression of pituitary corticotropin production leading to secondary adrenal insufficiency, decreased absorption and increased calcium excretion, increased surfactant factor production in type 2 pneumocytes, protein catabolism in lymphoid, muscle, Connective tissue and skin, hepatic gluconeogenesis with decreased peripheral glucose utilization, decreased formation and increased bone resorption. The mechanism by which corticosteroids decrease immunity involves inhibition of cell-mediated immune reactions, reduction of T lymphocyte, monocyte and eosinophil concentration, decreased binding of immunoglobulins to cell-surface receptors, and release and / or synthesis of interleukins. Launch Date1978 |
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Palliative | BETAPAR Approved UseMeprednisone (16-β-methylprednisone) is a steroid anti-inflammatory with poor mineralocorticoid action due to the methylation of prednisone at the carbon 16 level. Corticosteroids have anti-inflammatory and immunosuppressive activity. The mechanism of anti-inflammatory action is due to the decrease of the tissue response to the inflammatory processes, without modifying the underlying causes. Steroids diffuse through the cell membrane and bind to specific cytoplasmic receptors. Then, this complex enters the nucleus, where it binds to other transcriptional factors and to DNA producing induction and repression of genes that lead to its anti-inflammatory, immunosuppressive and mild mineralocorticoid effect. Other effects are: suppression of pituitary corticotropin production leading to secondary adrenal insufficiency, decreased absorption and increased calcium excretion, increased surfactant factor production in type 2 pneumocytes, protein catabolism in lymphoid, muscle, Connective tissue and skin, hepatic gluconeogenesis with decreased peripheral glucose utilization, decreased formation and increased bone resorption. The mechanism by which corticosteroids decrease immunity involves inhibition of cell-mediated immune reactions, reduction of T lymphocyte, monocyte and eosinophil concentration, decreased binding of immunoglobulins to cell-surface receptors, and release and / or synthesis of interleukins. Launch Date1978 |
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Primary | BETAPAR Approved UseMeprednisone (16-β-methylprednisone) is a steroid anti-inflammatory with poor mineralocorticoid action due to the methylation of prednisone at the carbon 16 level. Corticosteroids have anti-inflammatory and immunosuppressive activity. The mechanism of anti-inflammatory action is due to the decrease of the tissue response to the inflammatory processes, without modifying the underlying causes. Steroids diffuse through the cell membrane and bind to specific cytoplasmic receptors. Then, this complex enters the nucleus, where it binds to other transcriptional factors and to DNA producing induction and repression of genes that lead to its anti-inflammatory, immunosuppressive and mild mineralocorticoid effect. Other effects are: suppression of pituitary corticotropin production leading to secondary adrenal insufficiency, decreased absorption and increased calcium excretion, increased surfactant factor production in type 2 pneumocytes, protein catabolism in lymphoid, muscle, Connective tissue and skin, hepatic gluconeogenesis with decreased peripheral glucose utilization, decreased formation and increased bone resorption. The mechanism by which corticosteroids decrease immunity involves inhibition of cell-mediated immune reactions, reduction of T lymphocyte, monocyte and eosinophil concentration, decreased binding of immunoglobulins to cell-surface receptors, and release and / or synthesis of interleukins. Launch Date1978 |
|||
Palliative | BETAPAR Approved UseMeprednisone (16-β-methylprednisone) is a steroid anti-inflammatory with poor mineralocorticoid action due to the methylation of prednisone at the carbon 16 level. Corticosteroids have anti-inflammatory and immunosuppressive activity. The mechanism of anti-inflammatory action is due to the decrease of the tissue response to the inflammatory processes, without modifying the underlying causes. Steroids diffuse through the cell membrane and bind to specific cytoplasmic receptors. Then, this complex enters the nucleus, where it binds to other transcriptional factors and to DNA producing induction and repression of genes that lead to its anti-inflammatory, immunosuppressive and mild mineralocorticoid effect. Other effects are: suppression of pituitary corticotropin production leading to secondary adrenal insufficiency, decreased absorption and increased calcium excretion, increased surfactant factor production in type 2 pneumocytes, protein catabolism in lymphoid, muscle, Connective tissue and skin, hepatic gluconeogenesis with decreased peripheral glucose utilization, decreased formation and increased bone resorption. The mechanism by which corticosteroids decrease immunity involves inhibition of cell-mediated immune reactions, reduction of T lymphocyte, monocyte and eosinophil concentration, decreased binding of immunoglobulins to cell-surface receptors, and release and / or synthesis of interleukins. Launch Date1978 |
|||
Palliative | BETAPAR Approved UseMeprednisone (16-β-methylprednisone) is a steroid anti-inflammatory with poor mineralocorticoid action due to the methylation of prednisone at the carbon 16 level. Corticosteroids have anti-inflammatory and immunosuppressive activity. The mechanism of anti-inflammatory action is due to the decrease of the tissue response to the inflammatory processes, without modifying the underlying causes. Steroids diffuse through the cell membrane and bind to specific cytoplasmic receptors. Then, this complex enters the nucleus, where it binds to other transcriptional factors and to DNA producing induction and repression of genes that lead to its anti-inflammatory, immunosuppressive and mild mineralocorticoid effect. Other effects are: suppression of pituitary corticotropin production leading to secondary adrenal insufficiency, decreased absorption and increased calcium excretion, increased surfactant factor production in type 2 pneumocytes, protein catabolism in lymphoid, muscle, Connective tissue and skin, hepatic gluconeogenesis with decreased peripheral glucose utilization, decreased formation and increased bone resorption. The mechanism by which corticosteroids decrease immunity involves inhibition of cell-mediated immune reactions, reduction of T lymphocyte, monocyte and eosinophil concentration, decreased binding of immunoglobulins to cell-surface receptors, and release and / or synthesis of interleukins. Launch Date1978 |
Doses
Dose | Population | Adverse events |
---|---|---|
5 mg 1 times / day multiple, oral Recommended Dose: 5 mg, 1 times / day Route: oral Route: multiple Dose: 5 mg, 1 times / day Sources: Page: p.142 |
unhealthy, 16-31 n = 12 Health Status: unhealthy Condition: Hyperandrogenism Age Group: 16-31 Sex: F Population Size: 12 Sources: Page: p.142 |
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40 mg 2 times / day multiple, oral Studied dose Dose: 40 mg, 2 times / day Route: oral Route: multiple Dose: 40 mg, 2 times / day Sources: Page: p.2 |
unhealthy, 71 n = 1 Health Status: unhealthy Condition: Lupus nephropathy Age Group: 71 Sex: F Population Size: 1 Sources: Page: p.2 |
Other AEs: Osteoporosis... |
AEs
AE | Significance | Dose | Population |
---|---|---|---|
Osteoporosis | 40 mg 2 times / day multiple, oral Studied dose Dose: 40 mg, 2 times / day Route: oral Route: multiple Dose: 40 mg, 2 times / day Sources: Page: p.2 |
unhealthy, 71 n = 1 Health Status: unhealthy Condition: Lupus nephropathy Age Group: 71 Sex: F Population Size: 1 Sources: Page: p.2 |
Overview
CYP3A4 | CYP2C9 | CYP2D6 | hERG |
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OverviewOther
Other Inhibitor | Other Substrate | Other Inducer |
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Drug as perpetrator
Target | Modality | Activity | Metabolite | Clinical evidence |
---|---|---|---|---|
Sources: https://go.drugbank.com/drugs/DB09383 |
yes | |||
Sources: https://go.drugbank.com/drugs/DB09383 |
yes |
Drug as victim
Target | Modality | Activity | Metabolite | Clinical evidence |
---|---|---|---|---|
Sources: https://go.drugbank.com/drugs/DB09383 |
yes |
PubMed
Title | Date | PubMed |
---|---|---|
[Drug-induced lichenoid eruptions]. | 2006 Apr |
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Henoch-Schönlein Purpura in adults. | 2008 Apr |
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Screening of 397 chemicals and development of a quantitative structure--activity relationship model for androgen receptor antagonism. | 2008 Apr |
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[Fulminating sclerosant peritonitis. Spectacular response to treatment with steroids]. | 2010 |
Patents
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Classification Tree | Code System | Code | ||
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WHO-VATC |
QH02AB15
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WHO-ATC |
H02AB15
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NCI_THESAURUS |
C521
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SUB08756MIG
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29523
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100000081480
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DB09383
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527579
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CHEMBL1201148
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C008352
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MEPREDNISONE
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m7198
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C66096
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DTXSID8023260
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67U96J8P35
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1247-42-3
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1967
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214-996-1
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1388005
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ACTIVE MOIETY