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Buprenorphine (Subutex®, Buprenorphine mepha®)
Buprenorphine (Subutex®, buprenorphine mepha®) may offer advantages over methadone in certain situations for pharmacological reasons. Basically, clarification/status and approval procedures are the same as with methadone, see “SBG: Start in 1 Consultation” (best practice, suitable for experienced doctors) or “SGB Start in 2 Consultations”. An aid for the differentiated indication for buprenorphine can be found here. Buprenorphine is much more expensive than methadone but is also compulsory health insurance.
Sublingual administration with rapid absorption (pronounced first-pass effect, therefore hardly bioavailable after swallowing and low risk of intoxication). After 3-5 minutes the tablets dissolve under the tongue (to fully allow the effect of the tablets, do not swallow for 5 minutes).
sublingual bioavailability = 31-52%
Time to reach a clinical effect approx. 30 (-60) minutes
Time to reach maximum plasma levels about 90-150 minutes
Time to reach maximum clinical effect about 1-4 hours
Rapid absorption from the plasma and redistribution into various tissues (e.g., adipose tissue). Out of the different tissues, there is a time-delayed, slow redistribution, which ensures constant buprenorphine plasma levels (“depot effect”). Effective plasma levels: between 0.7 and 12 ng / ml; dose-dependent duration of action Steady state: about after 5-8 days; no significant daily fluctuations with regular intake. Most of the metabolism is via cytochrome P450 3A4. Since other enzymes are involved in the degradation of buprenorphine (CYP 2C8), the degradation metabolism of buprenorphine and its metabolites is relatively insensitive to interactions. Elimination half-life: 20-25 / 37hours. The elimination is predominantly hepatic by glucuronidation and N-dealkylation. The excretion is about 70-80% of the feces, the rest, 20-30%, renal.
Mechanism of action
Buprenorphine is a partial agonist on the mu opioid receptor (mediating effects such as euphoria, analgesia, respiratory depression, and dependence) and an antagonist on the kappa receptor (mediating effects such as dysphoria and sedation). Compared to methadone and heroin, buprenorphine shows important differences due to its special properties at the opioid receptors: Buprenorphine has a higher receptor affinity (heroin and methadone are displaced) and a moderate intrinsic agonistic activity with only partial stimulation of the mu opioid receptors (high doses of buprenorphine result in a lighter, less euphoric and less sedating central nervous effect than high doses of other opioids such as heroin, methadone). Ceiling Effect: There is no linear dose-response relationship. With increasing dosage, it comes to reaching a Wirkplateaus. Buprenorphine, in combination with other central depressants, may contribute to a limited respiratory depressive effect. Buprenorphine shows a long receptor half-life with slow receptor dissociation and less receptor-down regulation.
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