Source: Medicines & Healthcare Products Regulatory Agency (GB) Revision Year: 2020 Publisher: Indivior UK Limited, The Chapleo Building, Henry Boot Way, Priory Park, Hull, HU4 7DY, United Kingdom
Buprenorphine is a µ (mu) opioid partial agonist and k (kappa) antagonist. It is a strong analgesic of the partial agonist (mixed agonist/antagonist) class.
When taken orally, buprenorphine undergoes first-pass hepatic metabolism with N-dealkylation and glucuroconjungation in the small intestine. The use of this medication by oral route is therefore inappropriate.
Peak plasma concentrations are achieved 90 minutes after sublingual administration.
The absorption of buprenorphine is followed by a rapid distribution phase and a half-life of 2 to 5 hours.
Buprenorphine is oxidatively metabolised by 14-N-dealkylation to N-desalkyl-buprenorphine (also known as norbuprenorphine) via cytochrome P450 CYP3A4 and by glucuroconjungation of the parent molecule and the dealkylated metabolite. Norbuprenorphine is µ (mu) agonist with weak intrinsic activity.
Elimination of buprenorphine is bi- or tri- exponential, with a long terminal elimination phase of 20-25 hours, due in part to reabsorption of buprenorphine after intestinal hydrolysis of the conjugated derivative, and in part to the highly lipophilic nature of the molecule.
Buprenorphine is essentially eliminated in the faeces by biliary excretion of the glucuroconjugated metabolites (80%), the rest being eliminated in the urine.
None stated.
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