Zamicastat (also known as BIA 5-1058) is a dopamine β-hydroxylase (DβH) inhibitor that decreases noradrenaline and increases dopamine levels in peripheral sympathetically innervated tissues. It is known that the use of DβH inhibitors is a promising approach to treat hypertension, heart failure and cardiovascular diseases where a reduction in the sympathetic tone has beneficial effects. Zamicastat participated in phase II clinical trials in pulmonary arterial hypertension as adjuvant therapy in Austria. In addition, the drug successfully completed phase I in patients with hypertension and chronic heart failure.

Trabodenoson is a potent (Ki = 0.97 nM) and selective (>10,000- fold vs. adenosine 2 receptor) adenosine 1 receptor agonist. Ex vivo, trabodenoson (100 nM to 3 uM) progressively prolonged A-V-nodal conduction without reducing left ventricular function or coronary resistance. In vivo, trabodenoson up to a dose of 50 ug/kg did not reduce the carotid arterial blood pressure. Twice-daily ocular doses of trabodenoson, from 50 to 500 ug, were well tolerated and showed a dose-related decrease in intraocular pressure that was statistically significant and clinically relevant at 500 ug in patients with ocular hypertension or primary open-angle glaucoma. Trabodenoson had been in phase III clinical trial for the treatment of glaucoma and ocular hypertension. However, this development was discontinued.

Ropitoin (TR2985) is a diphenylhydantoin derivative. It is an antiarrhythmic compound that causes a depression of the maximum upstroke velocity (used as a measure of cardiac function: an indirect index of the magnitude of the sodium current). Its effect was shown in several cardiac tissues and in guinea pig muscles and dog Purkinje fibers (myocardial cells). Ropitoin is believed to bind to the same receptor site in the sodium channel as mexiletine and quinidine. In an animal study, ropitoin was shown to be ineffective in preventing reentrant ventricular tachycardia (when the electric signal fails to die out after normal activation) or ventricular fibrillation. No information on the current use of this compound is available.

Risotilide is a Class III antiarrhythmic agent that inhibits the voltage-dependent potassium channel. Risotilide prolongs cardiac action potentials and refractory periods. It was shown to reduce ventricular vulnerability in a study on arrhythmogenic effects of left ventricular hypertrophy (LVH) in the intact heart in cats. Phase I and II trials have been conducted, but development of this drug has been discontinued.

Tipentosin is prazosin derivative. It is an angiotensin-converting enzyme inhibitor. Tipentosin was developed as an antihypertensive agent.

Saprisartan (formerly known as GR 138950) was developed as a potent long-lasting angiotensin II (AT1) receptor antagonist with high oral bioavailability. The drug was used for the treatment of hypertension and heart failure. However, these studies were discontinued.

Terlakiren (also known as CP80794) is a cysteinamide derivative patented by Pfizer Inc. as potent renin inhibitor. Terlakirens inhibitory potency against plasma renin of guinea pigs, dogs, and monkeys ranges from 0.3 to 0.7 nM. In preclinical models, Terlakiren caused significantly greater increases in renal blood flow and suppressed renin activity to a greater degree than captopril.

Sematilide (CK-1752) was developed as a novel class III antiarrhythmic agent for the arrhythmia treatment. Sematilide blocks the inward rectifier potassium channel (IK1). The further development of the drug was discontinued.

Trimoxamine hydrochloride is an antihypertensive agent.

Vincantril is a vinca alkaloid. It is antianoxia agent.