Clinical Information

Clinically, buprenorphine is utilized as a substitution therapy for opioid dependence and as an analgesic. Buprenorphine is a partial agonist of the mu-opioid receptor. These mu binding sites are discretely distributed in the human brain, spinal cord, and other tissue. The clinical effects of mu receptor agonists are sedation, euphoria, respiratory depression, and analgesia. As a partial mu receptor agonist, buprenorphine's clinical effects are decreased, giving buprenorphine a wider safety margin.(1) Buprenorphine has a prolonged duration of activity. The combination of decreased clinical effects and prolonged activity gives buprenorphine the added advantage of a delayed and decreased withdrawal syndrome, compared to other opioids.(1) Compared to morphine, buprenorphine is 25 to 40 times more potent.(1) As with any opioid, abuse is always a concern. To reduce illicit use of buprenorphine, it is available mixed with naloxone in a ratio of 4:1. When the combination is taken as prescribed, only small amounts of naloxone will be absorbed. However, if the combination is transformed into the injectable form, naloxone then acts as an opioid receptor antagonist.

Buprenorphine is metabolized through N-dealkylation to norbuprenorphine through cytochrome P450 3A4 (CYP 3A4). Both parent and metabolite then undergo glucuronidation. Norbuprenorphine is an active metabolite possessing one fifth of the potency of its parent. The glucuronide metabolites are inactive.(1)

This procedure uses immunoassay reagents that are designed to produce a negative result when no drugs are present in a natural (ie, unadulterated) specimen of urine; the assay is designed to have a high true-negative rate. Like all immunoassays, it can produce a false-positive result due to cross-reactivity with natural chemicals and drugs other than those they were designed to detect. The immunoassay also can produce a false-negative result due to the antibody's ability to cross-react with different drugs in the target class.