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Re: Temgesic; Addendum

Posted by Neal on July 24, 2001, at 1:20:09

In reply to Re: Temgesic;Elizabeth;ShelliR, posted by Neal on July 23, 2001, at 23:43:37

I found this government report about buprenorphine to be informative and interesting, even though it is about bup's use in heroin addiction mainly, and using very large doses.

General Information
What is Buprenorphine?
Buprenorphine is a derivative of the morphine alkaloid, thebaine, and is a partial opioid
agonist at the m opioid receptors in the nervous system. It is also a k (kappa) opioid receptor
antagonist. It has low intrinsic agonist activity, only partially activating m opioid receptors, thus
producing a milder, less euphoric and less sedating effect than full opioid agonists such as
heroin, morphine and methadone. Nevertheless, its activity is usually sufficient to diminish
cravings for heroin, and prevent or alleviate opioid withdrawal in dependent heroin users.
Buprenorphine also has a high affinity for m opioid receptors, binding more tightly to these
receptors than full opioid agonists. It therefore reduces the impact of additional heroin (or
other opioid) use, by preventing heroin from occupying these receptors. By its dual effects of
producing opioid responses while blocking the effects of additional heroin use, buprenorphine
reduces the self-administration of heroin.
What form does it come in?
The buprenorphine product registered in Australia for treating opioid dependence is Subutex®,
a sublingual tablet preparation of buprenorphine hydrochloride in 0.4, 2, and 8 mg strengths.
Buprenorphine is also registered in Australia for the management of short term (not more than
one week) relief of moderate to severe pain, including post –operative and terminaland chronic
pain pain as Temgesic® sublingual tablets and ampoules for intramuscular or subcutaneous
injection. Sublingual buprenorphine tablets have approximately 30-35% of the bioavailability of
intravenous buprenorphine preparations 1 . Buprenorphine undergoes extensive first pass
metabolism when taken orally.
How is it metabolised?
Peak plasma concentrations are achieved 1 - 2 hours after sublingual administration.
Buprenorphine has a distribution half-life of 2 - 5 hours. It is principally metabolised by two
hepatic pathways: conjugation with glucuronic acid and N-de-alkylation. The metabolites
areexcreted in the biliary system, with enterohepatic cycling of buprenorphine and its
metabolites. Most of the drug is excreted in the faeces and urine.

Buprenorphine has an elimination half-life of 24 - 37 hours. It is long-acting, relative to the
dose administered. Peak clinical effects occur 1 - 4 hours after sublingual administration, with
continued effects for up to 12 hours at low doses (2 mg), but as long as 48 - 72 hours at higher
doses (16 or 32 mg). The extended duration of action of buprenorphine is thought to relate to
three factors:
· its very high affinity for opioid m receptors (once bound to these receptors it is
dislodged only slowly);
· its high lipophilicity (low levels of buprenorphine are released slowly from fat
stores, particularly with chronic dosing).
· Reabsorption of buprenorphine after intestinal hydrolysis of the conjugated
The prolonged duration of effect at high doses enables alternate-day, and even 3-
days-a-week dispensing regimes.
Onset of effects 30 - 60 minutes
Peak clinical effects 1 - 4 hours
Duration of effects 8 - 12 hours at low dose (e.g. < 4 mg)
24 - 72 hours at high dose (e.g. >16 mg)

Buprenorphine also exhibits antagonist effects at the k opioid receptor. The role of these
receptors in humans is still poorly understood, but excess endogenous k agonist activity
appears to be implicated in both affective and psychotic conditions. Buprenorphine’s
antagonist effects at the k receptor are thought to produce anti-depressant and anti-psychotic
effects in some people. However, as further research is needed into these effects,
buprenorphine is not currently indicated for these conditions.

Withdrawal syndrome from buprenorphine
Its partial agonist properties, along with its slow dissociation from opioid receptors, are thought
to explain why opioid withdrawal syndrome is milder with the cessation of buprenorphine
treatment, than with heroin, morphine or methadone. Typically, the withdrawal syndrome
following the abrupt cessation of long-term buprenorphine treatment emerges within 3 – 5
days of the last dose, and mild withdrawal features continue for up to several weeks.




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