Diprenorphine is the strongest opioid antagonist that is commercially available (some 100 times more potent as an antagonist than nalorphine),[6] and is used for reversing the effects of very strong opioids for which the binding affinity is so high that naloxone does not effectively or reliably reverse the narcotic effects.[7] These super-potent opioids, with the single exception of buprenorphine (which has an improved safety-profile due to its partial agonism character[8]), are not used in humans because the dose for a human is so small that it would be difficult to measure properly [citation needed], so there is an excessive risk of overdose leading to fatal respiratory depression. However conventional opioid derivatives are not strong enough to rapidly tranquilize large animals, like elephants and rhinos, so drugs such as etorphine and carfentanil are available for this purpose.
Diprenorphine is considered to be the specific reversing agent/antagonist for etorphine and carfentanil,[9] and is normally used to remobilise animals once veterinary procedures have been completed.[10] Since diprenorphine also has partial agonistic properties of its own, it should not be used on humans if they are accidentally exposed to etorphine or carfentanil. Naloxone or naltrexone is the preferred human opioid receptor antagonist.[11]
In theory, diprenorphine could also be used as an antidote for treating overdose of certain opioid derivatives which are used in humans, particularly buprenorphine for which the binding affinity is so high that naloxone does not reliably reverse the narcotic effects. However, diprenorphine is not generally available in hospitals; instead a vial of diprenorphine is supplied with etorphine or carfentanil specifically for reversing the effects of the drug, so the use of diprenorphine for treating a buprenorphine overdose is not usually carried out in practice.
Because diprenorphine is a weak partial agonist of the opioid receptors rather than a silent antagonist, it can produce some opioid effects in the absence of other opioids at sufficient doses.[12] Moreover, due to partial agonism of the KOR, where it appears to possess significantly greater intrinsic activity relative to the MOR, diprenorphine can produce sedation as well as, in humans, hallucinations.[3][5][13][14][15]
References
^US 3433791, "Endoethano Nor Oripavines & Nor Thebaines"
^Lewis JW, Husbands SM (2004). "The orvinols and related opioids--high affinity ligands with diverse efficacy profiles". Current Pharmaceutical Design. 10 (7): 717–32. doi:10.2174/1381612043453027. PMID15032698.
^Furst S, Hosztafi S, Friedmann T (1995). "Structure-Activity Relationships of Synthetic and Semisynthetic Opioid Agonists and Antagonists". Current Medicinal Chemistry. 1 (6): 423–440. doi:10.2174/092986730106220216112120. S2CID99996951.
^Takemori AE, Hayashi G, Smits SE (October 1972). "Studies on the quantitative antagonism of analgesics by naloxone and diprenorphine". European Journal of Pharmacology. 20 (1): 85–92. doi:10.1016/0014-2999(72)90219-1. PMID4637947.
^Jessup DA, Clark WE, Jones KR, Clark R, Lance WR (December 1985). "Immobilization of free-ranging desert bighorn sheep, tule elk, and wild horses, using carfentanil and xylazine: reversal with naloxone, diprenorphine, and yohimbine". Journal of the American Veterinary Medical Association. 187 (11): 1253–4. PMID4077657.
^Alford BT, Burkhart RL, Johnson WP (April 1974). "Etorphine and diprenorphine as immobilizing and reversing agents in captive and free-ranging mammals". Journal of the American Veterinary Medical Association. 164 (7): 702–5. PMID4817959.
^Caulkett NA, Arnemo JM (2007). "Chemical Immobilization of Free-Ranging Terrestrial Mammals.". In Tranquilli WJ, Thurmon JC, Grimm KA (eds.). Lumb and Jones' Veterinary Anesthesia and Analgesia (4th ed.). Philadelphia: Lippincott, Williams and Wilkins. p. 815.
^Traynor JR, Corbett AD, Kosterlitz HW (May 1987). "Diprenorphine has agonist activity at opioid kappa-receptors in the myenteric plexus of the guinea-pig ileum". European Journal of Pharmacology. 137 (1): 85–9. doi:10.1016/0014-2999(87)90185-3. PMID3038579.