Comparative Pharmacology
Head-to-head clinical analysis: DURAGESIC 37 versus VICODIN.
Peer-Reviewed Evidence
Head-to-head clinical analysis: DURAGESIC 37 versus VICODIN.
DURAGESIC-37 vs VICODIN
Comparing the clinical profiles, pharmacokinetic behaviors, and safety indices of these two therapeutic agents.
Fentanyl binds to mu-opioid receptors, activating G-protein coupled receptor signaling, leading to inhibition of adenylate cyclase, decreased cAMP production, and modulation of ion channels (increased potassium efflux, decreased calcium influx). This results in reduced neuronal excitability, inhibition of nociceptive transmission, and altered pain perception. Additionally, fentanyl may interact with other opioid receptors (kappa, delta) with lower affinity.
VICODIN (hydrocodone/acetaminophen) is a combination opioid agonist and analgesic. Hydrocodone acts on mu-opioid receptors in the CNS to alter pain perception and response; acetaminophen inhibits cyclooxygenase (COX) activity, likely in the CNS, reducing prostaglandin synthesis and providing antipyretic effects.
Initial: 25 mcg/hour transdermal patch applied every 72 hours. Titrate based on opioid tolerance. For opioid-naive patients: 12 mcg/hour patch.
1-2 tablets (hydrocodone 5-10 mg and acetaminophen 300-325 mg) orally every 4-6 hours as needed for pain; maximum daily acetaminophen dose 4 g.
None Documented
None Documented
Terminal elimination half-life 20-27 hours (range 13-42 h) after transdermal removal; due to continuous absorption from skin depot, effective half-life is longer during patch wear.
Hydrocodone: 3.8-6.4 hours (terminal); Acetaminophen: 2-3 hours (terminal). Clinically, steady-state achieved in 1-2 days.
Primarily renal: 75% as metabolites (mostly norfentanyl) and <10% unchanged drug. Fecal: 9% via biliary elimination.
Hydrocodone: primarily renal (~60% as metabolites, 12% unchanged); minor biliary. Acetaminophen: renal (90-100% as metabolites, 2-4% unchanged).
Category C
Category C
Opioid Analgesic
Opioid Analgesic