How stuff works—Buprenorphine
Buprenorphine was discovered in 1966, at a home products company Reckitt and Colman. They believed that “opioids with structures substantially more complex than morphine could selectively retain the desirable actions whilst shedding the undesirable side effects,” and their main goal was to find such an opioid. They had two failed attempts before finally putting buprenorphine into clinical studies. When presented at major conferences, buprenorphine was attractive to many pharmacologists because it was seen as an effective pain killer that didn’t have a high abuse potential, and it also had potential as a drug treatment for narcotic addiction. Despite this realization it took almost three decades for it to be used therapeutically.
This sublingual form of buprenorphine was manufactured by Reckitt and was released in 1995, first in France, in response to the AIDS epidemic among heroin injection users. In 2002, it received FDA approval in the United States. Subutex contains just buprenorphine, so it was prone to diversion.
Buprenorphine + Naloxone = Suboxone
In 1993, the National Institute on Drug Abuse approached Reckitt about developing a combination tablet that could help prevent the problem of buprenorphine and methadone diversion. In 2003, Suboxone, the response to the request, received FDA approval. Suboxone contains both buprenorphine and naloxone, a full agonist that can help prevent users from injecting Suboxone to get high.
Buprenorphine is a partial μ-opioid receptor agonist and κ-opioid receptor antagonist with a ceiling effect, which reduces both abuse potential and accidental respiratory depression. Naloxone is an opioid receptor antagonist, which causes withdrawal effects if used intravenously by opioid-dependent patients.