Carbazeran is a potent PDE-II and PDE-III inhibitor. Potently inhibits cAMP hydrolysis. Shows chronotropic and inotropic effect in vivo (EC50 = 100 μM, ionotropic effects, independent of adrenergic mechanisms). Carbazeran is a potent cardiac stimulant. Phosphodiesterase inhibition and elevation of intracellular cyclic AMP concentration may be involved, at least in part, in carbazeran`s cardiac effect.

Nesosteine is a mucoregulatory agent. Nesosteine reduced the viscosity of tracheobronchial mucus in rabbits made bronchitic by H2SO4 aerosol and markedly increased mucoproduction in healthy animals. Nesosteine was more active than the best known mucolytic/mucoregulatory drugs, such as sobrerol, N-acetylcysteine and mercaptopropionylglycine. The fluidifying activity of the drug was also demonstrated in vitro (pig's gastric mucin), although this proved to be less marked than in vivo. Nesosteine reduced the amount of total proteins of the tracheobronchial mucus, acting on albumin, alpha 1, alpha 2, beta and gamma mucoproteins.

Amiglumide [CR 1795] is an amino acid derivative with cholecystokinin A antagonist activity. It has potential use for treating gastrointestinal disorders, pancreatitis and biliary dyskinesia. Amiglumide was developed in preclinical trials with Rottapharm in Italy.

Ethonam is an antifungal compound. Its activity was evaluated in the treatment of chronic athlete's foot.

Detorubicin is a semi-synthetic derivative of the anthracycline antineoplastic antibiotic. It intercalates into DNA and interacts with topoisomerase II, thereby inhibiting DNA replication and repair and RNA and protein synthesis. This agent also produces toxic free-radical intermediates and interacts with cell membrane lipids causing lipid peroxidation. Detorubicin is less toxic than daunorubicin. Although it showed some clinical activity, the drug appeared to have no particular advantage over doxorubicin except for demonstrated activity against malignant melanoma. Unfortunately, detorubicin clearly has cardiac toxicity – in clinical trial, one patient developed congestive heart failure and other patients revealed endomyocardial biopsy evidence of cardiac toxicity.

Talviraline (HBY 097) was developed as a nonnucleoside inhibitor of human immunodeficiency virus type 1 (HIV-1) reverse transcriptase (NNRTI) for the treatment of HIV Infections. Talviraline participated in a phase II clinical trial. It was found that the drug caused pronounced acute suppression of HIV-1 replication both in combination with zidovudine and alone. However, further development of the drug has been discontinued.

Wyeth was developing the small molecule plasminogen activator inhibitor-1 (PAI-1) antagonist aleplasinin for the treatment of Alzheimer's disease in the US. PAZ-417 inhibits PAI-I (Plasminogen activator inhibitor-1), thereby increasing the activation of plasminogen to form plasmin. There is some evidence that plasmin can increase the cleavage of amyloid precursor protein at the alpha cleavage site, which could reduce the formation or increase the clearance of amyloid beta, a suspected culprit in Alzheimer's disease. However, it`s development for Alzheimer's disease treatment was discontinued.

Budiodarone is a chemical analog of amiodarone with mixed ion channel electrophysiological activity. Budiodarone was developed to capitalize on the proven efficacy of amiodarone and to avoid its side effects. Budiodarone has a short plasma half-life (7 h) and a lower volume of distribution (13 L/kg). It is cleared from the body in 48 h. Like amiodarone, Budiodarone has balanced, multiple cardiac ion channel inhibiting activity, giving it properties of all four Vaughan Williams antiarrhythmic drug classes. Budiodarone, unlike amiodarone, undergoes rapid metabolism by plasma and tissue esterases. In clinical trials, Budiodarone effectively reduces the number and duration of atrial tachycardia/atrial fibrillation episodes.

Nacartocin is synthetic oxytocin analogue patented by Ceskoslovenska Akademie as a specific natriuretic agent. The natriuretic effect is mainly due to the inhibitory action of the peptide on tubular sodium resorption. Nacartocin decreased the blood pressure of anesthetized rats by the decrease of the total peripheral resistance which was greater than that observed after oxytocin administration.