Fantridone is an antidepressant.

Amelubant, its metabolite BIIL 260 (formed by removal of the ethoxycarbonyl protecting group), and its major metabolite BIIL 315 (formed by removal of the protecting group and glucuronidation) had potent in vitro and in vivo Leukotriene B4 receptor antagonistic properties. Amelubant has been in phase II clinical trials by Boehringer Ingelheim for the treatment of cystic fibrosis, chronic obstructive pulmonay disease, bronchial asthma and rheumatoid arthritis. However, this research has been discontinued. In 2002, orphan drug designation was received in E.U. for the treatment of cystic fibrosis. Serious adverse events of Amelubant were characterized by increased presentation of respiratory signs and/or symptoms associated with pulmonary exacerbation and resulted in admission to a hospital and/or administration of IV antibiotics.

Flurantel is an anthelmintic agent. Information about the current use of this compound is not available.

Cirazoline is an agonist of alpha1A adrenergic receptor, a partial agonist of alpha1B and alpha1D receptors, and an antagonist of alpha2 adrenergic receptors. Cirazoline was used to study the biologic function of adrenergic receptors. Injection of cirazoline into to the paravenricular hypothalamic nucleus of rats suppressed food and water intake. Cirazoline caused a large renal vasopressor response in rats. Systemic administration of cirazoline impaired spatial working memory in monkeys.

Guamecycline, a tetracycline derivative was studied in patients with broncho-pulmonary diseases and for the treatment of acute pneumopathies. However, information about the current use of this compound is not available.

Etocarlide (4,4'-dihydroxythiocarbanilide) is an antibiotic active against Mycobacterium tuberculosis.

Dimiracetam is a nootropic drug of the racetam family. Dimiracetam inhibited the NMDA-induced increase of [3H]D-Asp release from hippocampal synaptosomes. The increased potency and longer duration of action of dimiracetam, together with the potential cognition enhancing property makes it a very promising and safe for the treatment of neuropathic pain conditions for which there are very limited therapeutic options. Dimiracetam is in Phase II clinical trials for the treatment of HIV-associated pain and in phase I clinical trials for the treatment of osteoarthritis pain.

Lysergide (LSD) is a semi-synthetic hallucinogen and is one of the most potent drugs known. Recreational use became popular between the 1960s to 1980s, but is now less common. LSD was first synthesized by Albert Hoffman while working for Sandoz Laboratories in Basel in 1938. Some years later, during a re-evaluation of the compound, he accidentally ingested a small amount and described the first ‘trip’. During the 1950s and 1960s, Sandoz evaluated the drug for therapeutic purposes and marketed it under the name Delysid®. It was used for research into the chemical origins of mental illness. Recreational use started in the 1960s and is associated with the ‘psychedelic period’. LSD possesses a complex pharmacological profile that includes direct activation of serotonin, dopamine and norepinephrine receptors. In addition, one of its chief sites of action is that of compound-specific (“allosteric”) alterations in secondary messengers associated with 5HT2A and 5HT2C receptor activation and changes in gene expression. The hallucinogenic effects of LSD are likely due to agonism at 5HT2A and 5HT2C receptors. LSD is also an agonist at the majority of known serotonin receptors, including 5HT1A, 5HT1B, 5HT1D, 5HT5A, 5HT6 and 5HT7 receptors. During the 1960s, LSD was investigated for a variety of psychiatric indications, including the following: as an aid in treatment of schizophrenia; as a means of creating a "model psychosis"; as a direct antidepressant; and as an adjunct to psychotherapy. LSD is listed in Schedule I of the United Nations 1971 Convention on Psychotropic Substances.

Roletamide is a hypnotic. No information on current use of this compound is available.

Dexnafenodone is a dual of adrenergic receptor antagonist and serotonin uptake inhibitor potentially for the treatment of major depressive disorder. Drug induced a rapid and marked suppression of REM sleep, and in parallel an increase in chin muscle tone during NREM sleep. Dexnafenodone produced a frequency- and voltage-dependent inhibition of the fast sodium channels similar to that exhibited with imipramine. It inhibited voltage- and agonist-stimulated Ca2+ entry in isolated rat aortas. In addition, it decreased Ca2+ content in both resting and noradrenaline-stimulated muscles, suggesting that it may deplete noradrenaline-sensitive intracellular Ca2+ stores. As a consequence, dexnafenodone would reduce the concentration of intracellular free Ca2+ available at the contractile apparatus for vascular smooth muscle contraction. Dexnafenodone exerted fewer cardiodepressant effects than imipramine and desipramine in isolated guinea-pig atrial and ventricular muscle fibres less.