Medorinone is an inhibitor of cAMP phosphodiesterase activity. Inhibition of cAMP phosphodiesterase by medorinone in cardiac and vascular smooth muscle is a mechanism by which this agent produces both positive cardiac inotropy and vascular smooth muscle relaxation. It inhibits platelet aggregation.

FENGABINE, a benzylidene derivative, is a GABAmimetic compound with clinically proven antidepressant action. It inhibits neither monoamine uptake nor monoamine oxidase. It also lacks any sedative effect.

ISBOGREL is a specific thromboxane A2 synthetase inhibitor. Its clinical development was discontinued, although it was a suitable candidate for clinical trials in cardiovascular diseases in which imbalance between thromboxane and prostacyclin may be involved in the pathogenesis.

K-134, a 2(1H)-quinolinone derivative, is a phosphodiesterase 3 inhibitor. It has both anti-thrombotic and anti-hyperplastic activities. It was evaluated in a phase II trial in patients with peripheral artery disease and claudication.

Cipemastat (Ro 32-3555, tentative trade name Trocade) is a dipeptide, potent, competitive inhibitor of matrix metalloproteinases (MMP) 1, 8 and 13, which was under development by Roche for the potential treatment of rheumatoid arthritis. Cipemastat is a selective inhibitor of metalloproteinases 1, 8 and 13 over the related human matrix metalloproteinases stromelysin 1, and gelatinases A and B. Cipemastat mediated MMP inhibition leads to block the final common event in the destructive cascade resulting in the breakdown of cartilage and bone. Trocade has also been shown to inhibit cartilage destruction in vivo and to prevent structural joint damage in animal models of rheumatoid and osteoarthritis. Cipemastat was in phase II clinical trials for the treatment of rheumatoid arthritis. However, Roche discontinued the development of cipemastat because of an unfavorable risk-benefit profile.

Trecetilide is a class III antiarrhythmic agent developed for the treatment of atrial flutter and fibrillation. Trecetilide probably has effects on the cardiac myocyte membrane that are similar to ibutilide. It is being developed for both oral and intravenous administration. Unlike ibutilide, trecetilide has good oral bioavailability. Trecetilide has a good metabolic stability. As with ibutilide, its mechanism of class III action may involve both rectifier K+ current blockade and other mechanisms of prolonging repolarization.