| Celecoxib to prevent restenosis--results from the COREA-TAXUS trial. | |
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MedLine Citation:
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PMID: 18201156 Owner: NLM Status: MEDLINE |
Abstract/OtherAbstract:
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Celecoxib inhibits Akt, which is stimulated during restenosis. Cell and animal studies showed that celecoxib inhibited Akt stimulation and restenosis. Recently, the COREA-TAXUS (Effect of Celecoxib on Restenosis after Coronary Angioplasty with Taxus stent) trial was performed in subjects with angina or a positive-stress test receiving paclitaxel-eluting stents. The primary end point at 6 months was the in-stent, late luminal loss, which was 0.49 mm in the celecoxib-treated group; less than the 0.75 mm in the group not treated with celecoxib. The rate of revascularisation of the target lesion was lower in celecoxib-treated subjects (5%) than in the untreated subjects (15%). In conclusion, this is an excellent demonstration of translating a mechanism of action of a drug into a clinical use. |
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Authors:
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Sheila A Doggrell |
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Publication Detail:
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Type: In Vitro; Journal Article; Review |
Journal Detail:
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Title: Expert opinion on pharmacotherapy Volume: 9 ISSN: 1744-7666 ISO Abbreviation: Expert Opin Pharmacother Publication Date: 2008 Feb |
Date Detail:
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Created Date: 2008-01-18 Completed Date: 2008-04-08 Revised Date: - |
Medline Journal Info:
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Nlm Unique ID: 100897346 Medline TA: Expert Opin Pharmacother Country: England |
Other Details:
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Languages: eng Pagination: 339-41 Citation Subset: IM |
Affiliation:
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RMIT University, Discipline of Pharmaceutical Sciences, School of Medical Sciences, Bundoora, Victoria 3083, Australia. sheila.doggrell@bigpond.com |
Export Citation:
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APA/MLA Format Download EndNote Download BibTex |
| MeSH Terms | |
Descriptor/Qualifier:
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Adult Coronary Restenosis / drug therapy, prevention & control* Female Humans Male Pyrazoles / standards*, therapeutic use* Randomized Controlled Trials as Topic / methods, trends* Sulfonamides / standards*, therapeutic use* |
| Chemical | |
Reg. No./Substance:
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0/Pyrazoles; 0/Sulfonamides; 169590-42-5/celecoxib |
From MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine
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