MK-0557, trans-N-[1-(2-fluorophenyl)-3-pyrazolyl]-3-oxospiro [6 azaisobenzofuran-1(3H),10-cyclohexane]-40-carboxamide, is an orally available Neuropeptide Y (NPY5) receptor antagonist. MK-0557 was studied in the clinical trials for the treatment of obesity, however, MK-0557 did not significantly increase the weight loss efficacy. MK-0557 safety and effectiveness were studied in a trial for the treatment of cognitive impairment in patients with schizophrenia. It seems MK-0557 development was discontinued.

IVOQUALINE, a quinoline derivative, is a potent and selective inhibitor of the uptake of serotonin, being about 20 times as active as clomipramine.

Quinacillin is semisynthetic penicillase-resistant penicillin patented by Boots Pure Drug Co. Ltd. For the treatment of bacterial infection. Quinacillin binds to and inactivates penicillin-binding proteins (PBPs) located on the inner membrane of the bacterial cell wall. Inactivation of PBPs interferes with the cross-linkage of peptidoglycan chains necessary for bacterial cell wall strength and rigidity. This interrupts bacterial cell wall synthesis and results in the weakening of the bacterial cell wall, eventually causing cell lysis. In clinical trials Staph. aureus was eradicated from all but two patients during treatment but recurred in 4 after withdrawal. The antibiotic was especially useful in the treatment of staphylococcal respiratory infections, as it has little effect on the normal bacterial flora of the chest.

Persilic acid is a virucide, hemostatic, capillary protective agent. 0.1% aqueous solution of K salt is used as a fluorescent acid-base indicator.

Pentiapine is a dopamine release inhibitor. It is a tranquiliser. Pentiapine produces a dose-dependent decrease in spontaneous motor activity and blocks the morphineinduced hyperactivity. Moreover, this drug in itself has no effect on place conditioning but blocks the acquisition of morphine-induced conditioned place preference.

Etamocycline is a broad-spectrum antibiotic. It was studied in the treatment of bronchopulmonary and gastrointestinal infectious diseases.

Etaqualone (Aolan, Athinazone) is an analog of the hypnotic methaqualone, a non-barbiturate sedative it was developed and marked in France. Etaqualone possesses sedative and hypnotic properties and was used to treat insomnia resulting from its agonist activity at the β subtype of the GABAa receptor.

Prothixene is a thioxanthene derivative patented by Swiss multinational healthcare F. Hoffmann-La Roche & Co. as an antiemetic and neuroleptic agent. In preclinical models, prothixene shows patent antihistaminic activity. The central depressant activity of prothixene in the rotating rod test and the potentiation of thiopental narcosis and hypothermia in white mice (H strain) is one order lower than in the case of chlorprothixene. Prothixene has a higher protective effect in the supramaximal electric shock test with mice than promethazine and chlorprothixene. However, it has no effect on the reserpine ptosis in mice nor on the ulcerogenic action of reserpine in rats (Wistar strain). Its anti-serotonin activity is higher in vivo and in vitro than that of promethazine. The local irritation, tested on rabbits, is lower by 52% after prothixene application than after promethazine. Prothixene applied parenterally is more toxic to mice than promethazine. In oral administration, to mice, no differences in toxicity were found.

Pumafentrine is benzonaphthyridine derivative patented by BYk Gulden Lomberg Chemische Fabrik G.m.b.H. as phosphodiesterase (PDE) inhibitor useful for bronchial treatment. In preclinical trials, Pumafentrine acts as a mixed selective PDE-3/4 inhibitor. Treatment with pumafentrine from week 4 to 6 after a single injection of monocrotaline (partially reversed pulmonary hypertension and right heart hypertrophy in rats. In addition, small pulmonary arterial muscularization, medial hypertrophy and decrease in lumen area were largely reversed. Inhibition of smooth muscle proliferation under pumafentrine was demonstrated in vivo as was a pro-apoptotic effect of pumafentrine on vascular cells. Moreover, pumafentrine dose-dependently increased cyclic adenosine monophosphate levels and inhibited proliferation of cultured pulmonary arterial smooth muscle cells. Pumafentrine was used in phase 2 clinical trials for the treatment of asthma but was discontinued in 2002, reportedly due to a short duration of action. An active metabolite of pumafentrine, hydroxypumafentrine, has also been described, although there have been no published clinical data on this compound