Conversely, buprenorphine behaves like a partial agonist of the MOR with respect to respiratory depression.Buprenorphine is also known to bind to with high affinity and antagonize the putative ε-opioid receptor.Full analgesic efficacy of buprenorphine requires both exon 11- and exon 1-associated μ-opioid receptor splice variants.The active metabolites of buprenorphine are not thought to be clinically important in its CNS effects.In positron emission tomography (PET) imaging studies, buprenorphine was found to decrease whole-brain MOR availability due to receptor occupancy by 41% (i.e., 59% availability) at 2 mg, 80% (i.e., 20% availability) at 16 mg, and 84% (i.e., 16% availability) at 32 mg.

Other actions
Unlike some other opioids and opioid antagonists, buprenorphine binds only weakly to and possesses little if any activity at the sigma receptor.Buprenorphine also blocks voltage-gated sodium channels via the local anesthetic binding site, and this underlies its potent local anesthetic properties.Similarly to various other opioids, buprenorphine has also been found to act as an agonist of the toll-like receptor 4, albeit with very low affinity. Pharmacokinetics
Buprenorphine is metabolized by the liver, via CYP3A4 (also CYP2C8 seems to be involved) isozymes of the cytochrome P450 enzyme system, into norbuprenorphine (by N-dealkylation). The glucuronidation of buprenorphine is primarily carried out by UGT1A1 and UGT2B7, and that of norbuprenorphine by UGT1A1 and UGT1A3. These glucuronides are then eliminated mainly through excretion into bile. The elimination half-life of buprenorphine is 20 to 73 hours (mean 37 hours).
Buprenorphine/samidorphan, a combination product of buprenorphine and samidorphan (a preferential μ-opioid receptor antagonist), appears useful for treatment-resistant depression. Cocaine dependence
In combination with samidorphan or naltrexone (μ-opioid receptor antagonists), buprenorphine is under investigation for the treatment of cocaine dependence, and recently demonstrated effectiveness for this indication in a large-scale (n = 302) clinical trial (at a high buprenorphine dose of 16 mg, but not a low dose of 4 mg). Neonatal abstinence
Buprenorphine has been used in the treatment of the neonatal abstinence syndrome, a condition in which newborns exposed to opioids during pregnancy demonstrate signs of withdrawal. In the United States, use currently is limited to infants enrolled in a clinical trial conducted under an FDA-approved investigational new drug (IND) application. Preliminary research suggests that buprenorphine is associated with shorter time in hospital for neonates, compared to methadone. An ethanolic formulation used in neonates is stable at room temperature for at least 30 days. Obsessive–compulsive disorder
In one study, buprenorphine was found to be effective in a subset of individuals with treatment-refractory obsessive–compulsive disorder. References
External links
"Buprenorphine". Drug Information Portal. U.S. National Library of Medicine. U.S. Federal government buprenorphine program for opioid addiction
Australian national buprenorphine policy
"The bitter pill": A Wired article on Suboxone
"Subu Must Die – How a nation of junkies went cold turkey": A New Republic article on Subutex abuse in the nation of Georgia