Profadol is a pyrrolidine derivative patented in the 1960s by pharmaceutical company Parke-Davis as opioid analgesic. Profadol acts as a mixed agonist-antagonist of the μ-opioid receptor and in preclinical studies, Profadol precipitates abstinence in morphine-dependent monkeys and can reverse pethidine- induced narcosis in nondependent monkeys. In morphine-dependent human subjects, Profadol was also found to pre¬cipitate acute abstinence syndromes, with a potency 40 to 50 times less than that of nalorphine. Profadol, unlike other morphine-antagonists, does not produce nalorphine-like subjective effects. Over a fourfold range of doses, this drug was found to produce subjective effects indistinguishable from those of morphine. Also unlike other morphine-antagonists, profadol is quite active on the "classical" rodent tests for analgesia. It is about 1.3 times as potent as pethidine on the mouse hot-plate test, and about four times as potent on the rat tail-pressure test.

LEVOFENFLURAMINE is a levorotatory enantiomer of fenfluramine, a substituted amphetamine which was formerly used to treat obesity. LEVOFENFLURAMINE has dopamine-antagonistic properties and, at high doses, increases dopamine concentrations in rat striatal dialysates. It is essentially inactive to reduce food intake in human subjects.

m-Chlorophenylpiperazine (meta-chlorophenylpiperazine or mCPP) is a psychoactive substance, which is illegal in many countries but can be found on the black market. It induces endocrine, neurological and psychiatric effects. mCPP is a partial agonist at the 5-HT2C receptor but antagonized the 5-HT2B and 5-HT3 receptors. mCPP is also an active metabolite of the drug trazodone, which is used as an effective antidepressant drug with a broad therapeutic spectrum, including anxiolytic efficacy. It is known, that mCPP induces migraine attacks and that the decrease of food intake induced by the mCPP depends on its ability to act as a serotonin agonist is a brain.

Acetorphine is a synthetic narcotic analgesic. Acetorphine was reported to have uses in veterinary medicine with pronounced advantages in the immobilization of the giraffe in which toxic effects were reduced as compared to the effects of etorphine. In July 1966, the Director-General of the World Health Organization informed the Secretary-General that WHO had arrived at the conclusion that etorphine and acetorphine should be included in Schedule I of the Convention, since they could give rise to similar abuse, and produce similar ill effects as the substances already listed therein. Acetorphine is a Schedule I controlled substance in the United States.

Profadol is a pyrrolidine derivative patented in the 1960s by pharmaceutical company Parke-Davis as opioid analgesic. Profadol acts as a mixed agonist-antagonist of the μ-opioid receptor and in preclinical studies, Profadol precipitates abstinence in morphine-dependent monkeys and can reverse pethidine- induced narcosis in nondependent monkeys. In morphine-dependent human subjects, Profadol was also found to pre¬cipitate acute abstinence syndromes, with a potency 40 to 50 times less than that of nalorphine. Profadol, unlike other morphine-antagonists, does not produce nalorphine-like subjective effects. Over a fourfold range of doses, this drug was found to produce subjective effects indistinguishable from those of morphine. Also unlike other morphine-antagonists, profadol is quite active on the "classical" rodent tests for analgesia. It is about 1.3 times as potent as pethidine on the mouse hot-plate test, and about four times as potent on the rat tail-pressure test.

Suxethonium is a depolarising muscle relaxant, with low incidence of postoperative muscle pain.

There is no much available information related to the biological and pharmacological application of imidoline, but this compound has been found to be as potent as chlorpromazine in increasing striatal DOPA accumulation and prolactin secretion in vivo. Imidoline exhibited only weak inhibitory activity towards dopamine-sensitive adenylate cyclase and 3H-spiroperidol binding to striatal membranes in vitro. A proposed active conformation involves intramolecular hydrogen bonding between the protonated dimethylamino group and the oxygen of the imidazolidinone ring. The spatial relationship between the amine nitrogen and phenyl ring in this conformation allows proper fit of imidoline with key dimensions described for the dopamine receptor.

Nolpitantium (SR-140333) is a highly selective nonpeptide antagonist of neurokinin-1 (NK1) receptor. Nolpitantium potently, selectively and competitively inhibited substance P binding to NK1 receptors from various animal species, including humans. In vitro, it was a potent antagonist in functional assays for NK1 receptors such as [Sar9, Met(O2)11]substance P-induced endothelium-dependent relaxation of rabbit pulmonary artery and contraction of guinea-pig ileum. Up to 1 mkM, Nolpitantium had no effect in bioassays for NK2 and NK3 receptors. The antagonism exerted by Nolpitantium toward NK1 receptors was apparently non-competitive, with pD2' values between 9.65 and 10.16 in the different assays. Nolpitantium also blocked in vitro [Sar9, Met(O2)11]substance P-induced release of acetylcholine from rat striatum. In vivo, Nolpitantium exerted highly potent antagonism toward [Sar9, Met(O2)11]substance P-induced hypotension in dogs, bronchoconstriction in guinea-pig) and plasma extravasation in rats. Nolpitantium was found to be effective in the modulation of the inflammatory response and airway remodeling in mice. Nolpitantium is reported to cause antagonism of the SP-induced relaxations of human isolated intralobar pulmonary arterial rings. Nolpitantium also blocked the activation of rat thalamic neurons after nociceptive stimulation. Nolpitantium has been shown to reduce the severity of inflammation in trinitrobenzene sulfonic acid-induced colitis in the rat colon. Nolpitantium inhibited mustard oil-induced plasma protein extravasations in the dorsal skin of the rat hind paw. Nolpitantium had been in some phase II clinical trials but further studies were discontinued.