Current Knowledge of Buprenorphine and Its Unique Pharmacological Profile

Abstract

Despite the increasing clinical use of transdermal buprenorphine, questions have persisted about the possibility of a ceiling effect for analgesia, its combination with other μ-opioid agonists, and the reversibility of side effects. In October 2008, a consensus group of experts met to review recent research into the pharmacology and clinical use of buprenorphine. The objective was to achieve consensus on the conclusions to be drawn from this work. It was agreed that buprenorphine clearly behaves as a full μ-opioid agonist for analgesia in clinical practice, with no ceiling effect, but that there is a ceiling effect for respiratory depression, reducing the likelihood of this potentially fatal adverse event. This is entirely consistent with receptor theory. In addition, the effects of buprenorphine can be completely reversed by naloxone. No problems are encountered when switching to and from buprenorphine and other opioids, or in combining them. Buprenorphine exhibits a pronounced antihyperalgesic effect that might indicate potential advantages in the treatment of neuropathic pain. Other beneficial properties are the compound's favorable safety profile, particularly in elderly patients and those with renal impairment, and its lack of effect on sex hormones and the immune system. The expert group agreed that these properties, as well as proven efficacy in severe pain and favorable tolerability, mean that buprenorphine can be considered a safe and effective option for treating chronic cancer and noncancer pain.

The Therapeutic Potential of Nociceptin/Orphanin FQ Receptor Agonists as Analgesics without Abuse Liability

“…Buprenorphine is well known as a MOP partial agonist that has been used for both pain management and opioid abuse/addiction and it has less rewarding property compared to other MOP agonists in primates. 51,93 When a NOP agonist (either Ro 64-6198 or SCH 221510) is combined with systemic buprenorphine, the NOP agonist dose-dependently potentiated buprenorphine-induced analgesia. 52 It is worth noting that NOP antagonists potentiated the antinociceptive effects of buprenorphine in rodents, indicating that buprenorphine's own NOP agonist activity attenuated its own MOP agonist activity.…”

Epigenetics in the perioperative period

“…The risk of inducing chronic hyperalgesia seems to vary with the opiate used, and is assumed to be highest for remifentanil (van Gulik et al, 2012), while the partial μ receptor agonist and κ receptor antagonist, buprenorphine has even been associated with an antihyperalgesic effect (Pergolizzi et al, 2010). OIH is prevented by the administration of the NMDA receptor antagonist, ketamine (Laulin et al, 2002).…”

Buprenorphine does not impact the inflammatory response in haemophilia A mice with experimentally-induced haemarthrosis

“…Buprenorphine is the most commonly used analgesic in laboratory rodents 33 and the drug of choice for analgesia in this model but the impact on inflammatory response is unknown. Buprenorphine is a semi-synthetic opioid and has been found to function as a full m-agonist for analgesia 34 and its analgesic potency has been found to be 25-40 times that of morphine in mice when administered parenterally. 35 Most research on opioids and their effect on the inflammatory response concern morphine and heroin and describe increased production of pro-inflammatory cytokines.…”