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.

The novel compounds clamikalant (HMR 1883) or its sodium salt HMR 1098) have been shown to block selectively Kir6.2/SUR1-composed K(ATP) channels. Clamikalant is under development by Aventis Pharma (formerly Hoechst Marion Roussel) for the potential treatment of heart arrest and ventricular arrhythmias. Nevertheless, clamikalant and its sodium salt did not pass the clinical trials

Quinazosin is a diaminoquinazoline derivative patented by Pfizer, Chas., and Co., Inc. as a hypotensive agent. Quinazosin acts as adrenoreceptor antagonist and in preclinical studies lowered systolic blood pressure in conscious hypertensive dogs, without having any significant effect on their heart rate. Quinazosin lowered blood pressure and reduced total peripheral vascular resistance, while the duration of these effects was dose-dependent. In cats, Quinazosin reduced or reversed the pressor effects of epinephrine, but did not alter those of angiotensin amide.

Ipazilide is an antiarrhythmic agent that prolongs ventricular refractoriness and possesses antiectopic activity. In clinical trials ipazilide administrations leads to dose- and time-dependent in decrease cardiac index and arterial pressure. Left ventricular filling pressure, right atrial pressure, and heart rate were not altered by ipazilide. Plasma concentrations of ipazilide peaked 90 minutes after administration of 100 or 200 of the drug, but peak concentrations were noted 3 hours after administration of 400 mg. The hemodynamic response correlated with the plasma concentration of ipazilide determined contemporaneously.

Cariporide is a selective sodium-hydrogen antiporter inhibitor patented by a pharmaceutical company Hoechst A.-G. for treatment myocardial ischemia-reperfusion injury. The sodium-hydrogen exchanger is an important player in the pathophysiology of myocardial ischemia-reperfusion injury. The accumulation of hydrogen ions in the myocyte cytosol; during ischemia creates a proton gradient that promotes the efflux of hydrogen ions in exchange for the influx of sodium ions. This sodium buildup can secondary activates the sodium-calcium exchanger to operate in the reverse mode, resulting in a net calcium accumulation in myocyte cytosol, which leads to dysfunction and cell death. By inhibiting sodium-hydrogen exchange, Cariporide can prevent the accumulation of calcium in the cytosol, therefore reduce the infarct size. In clinical trials, Cariporide shows a statistically significant decline in myocardial infarction but increases mortality. Due to the increase in mortality, cariporide did not pass clinical trials.

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.

Troxonium tosylate is a triethylcholine ester which resembles hemicholinium in some of its pharmacological effects. In animal pharmacological studies, it was noted that troxonium tosylate had a marked antitremorine activity with an associated hypotensive effect. This antitremorine activity, which is a common characteristic of antiparkinsonian agents, was found to be combined with an inhibitory function on acetylcholine synthesis and with a reduction of brain catecholamines. Troxonium tosylate was found to be an effective antiparkinsonian medication for drug-induced extrapyramidal manifestations. Troxonium tosylate caused a pronounced fall in the blood pressure in both normotensive and hypertensive animals. It produced this depressor effect mainly by antagonism of both central and peripheral autonomic ganglia. Troxonium did not possess atropine-like properties and was not active as an adrenergic blocker. Despite the potent effect upon the blood pressure, it did not significantly inhibit renal function and cardiac output. Because of its unique properties, it was postulated that troxonium might be of value in the management of hypertension of various etiologies.

Tipropidil designed for the treatment of cerebral and peripheral vascular diseases. Tipropidil has been investigated because of its expected antihyperviscosity properties. The increase in plasma free fatty acid levels and decrease in lipolytic response were found to be dependent on the amount of Tipropidil administered. Addition of Tipropidil to the in vitro lipolysis system inhibited norepinephrine- and theophylline-induced fatty acid release in a dose-dependent manner. These results suggest a potent inhibitory action for Tipropidyl on fatty acid mobilization in rat adipose tissue.

Trethinium is tetrahydroisoquinoline derivative. It is an antihypertensive agent.

Azamethonium (known in Europe as pendiomid), a substance with the ganglia-blocking effect that was used in Europe to treat patients with acute pulmonary embolism. Information about the nowadays application of this drug is not available.