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Oxymorphone Extended Release Does Not Affect CYP2C9 or CYP3A4 Metabolic Pathways
Author(s) -
Adams Michael,
Pieniaszek Henry J.,
Gammaitoni Arnold R.,
Ahdieh Harry
Publication year - 2005
Publication title -
the journal of clinical pharmacology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.92
H-Index - 116
eISSN - 1552-4604
pISSN - 0091-2700
DOI - 10.1177/0091270004271969
Subject(s) - oxymorphone , cyp3a4 , pharmacology , cyp2c9 , naltrexone , medicine , triazolam , chemistry , metabolism , antagonist , oxycodone , cytochrome p450 , opioid , benzodiazepine , receptor
Two 14‐day, randomized, open‐label, parallel‐group studies examined the effects of extended‐release (ER) oxymorphone on CYP2C9 or CYP3A4 metabolic activities in healthy subjects. On days −1, 7, and 14, subjects received either a CYP2C9 probe (tolbutamide 500 mg) or CYP3A4 probes (midazolam and [ 14 C N‐methyl]‐erythromycin for the erythromycin breath test). Subjects were randomized to 5 groups: high‐dose oxymorphone ER (3 × 20 mg q12h) + naltrexone (50 mg q24h); low‐dose oxymorphone ER (10–20 mg q12h); rifampin (2 × 300 mg q24h), an inducer of CYP2C9 and CYP3A4 activities; naltrexone (50 mg q24h); or CYP probes alone (controls). Probe metabolism was significantly altered by rifampin on days 7 and 14 ( P < .05), whereas probe metabolism was not significantly affected by low‐dose oxymorphone ER or by high‐dose oxymorphone ER plus naltrexone. Oxymorphone ER exhibits a minimal potential for causing metabolic drug‐drug interactions mediated by CYP2C9 or CYP3A4.