Vincantril is a vinca alkaloid. It is antianoxia agent.

Suricainide (also known as AHR 10718) is an aminoalkylurea derivative patented by A. H. Robins Co., Inc. as an antiarrhythmic agent. Suricainide induces a use-dependent decrease in Vmax and significantly decreased Purkinje fiber conduction velocity and action potential duration. Suricainide had no effect on slow response action potentials induced by isoproterenol but ventricular muscle action potentials were significantly prolonged by Suricainide. Suricainide significantly decreased normal automaticity, catecholamine-enhanced automaticity, and abnormal automaticity induced by barium or myocardial infarction. In preclinical modes, Suricainide suppresses the aconitine-induced canine atrial arrhythmia.

Celivarone is a benzofuran derivative with a multifactorial mode of action including class IV Vaughan Williams’ electrophysiological as well as anti-adrenergic properties. It has no iodine and has a limited tissue accumulation compared with amiodarone. Celivarone exhibits effective anti-arrhythmic properties in several ventricular ischemia- or reperfusioninduced arrhythmia models as well as in in vitro and in vivo atrial fibrillation (AF) models. Its electrophysiological properties are similar to amiodarone (multifactorial mode of action) but with different relative effects on the ion channels. At the ventricular level, celivarone shows anti-arrhythmic activities by suppressing reperfusion-induced arrhythmias (i.v. and oral routes) and reducing the early mortality due to myocardial infarction (oral route) in rats models. At the atrial level, celivarone is effective in atrial fibrillation models with restoration of sinus rhythm or prevention of AF induction and AF recurrence.

Eproxindine (KC 3791) is an antiarrythmic. It is able to inactivate voltage-dependent sodium channels. Eproxindine also proved to be capable of blocking open potassium channels at outwardly directed potassium currents

Brufacaine was developed as an antiarrhythmic drug that has never been marketed.

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.

Idrapril is an inhibitor of the angiotensin-converting enzyme the last is responsible for recurrent myocardial infarction in patients with left ventricular dysfunction. Idrapril participated in phase II clinical trials in essential hypertensive patients, where was shown that the drug was well tolerated. In addition, it was involved in preclinical studies as a potential drug to treat heart failure and postmyocardial infarction. However, the development of the drug was discontinued.

Carcainium is phenylcarbamoylmethyl derivative with local anesthetic and potent anti-tussive activity. In preclinical studies Carcainium significantly reduced the spontaneous and histamine-evoked discharges in Aδ-fibres originating from airway, rapidly adapting stretch receptors (RARs) without affecting histamine-evoked bronchoconstriction. Acute pre-treatment of guinea-pigs with aerosols of Carcainium prevent of capsaicin-evoked and citric acid-induced coughs.

Capadenoson (BAY 68-4986) is a nonnucleoside agonist for the A1 Adenosine Receptor (A1AR) and the A2BAR. Capadenoson has undergone two Phase IIa clinical trials, initially in patients with atrial fibrillation and subsequently in patients with stable angina. Capadenoson has also been shown to decrease cardiac remodeling in an animal model of advanced heart failure and a capadenoson derivative, neladenoson bialanate, recently entered clinical development for the treatment of chronic heart failure. The therapeutic effects of capadenoson are currently thought to be mediated through the A1AR.

Aprikalim [RP 52891, RPG 52891] is a potent, specific, and selective opener of ATP-sensitive K+ (KATP) channels. By virtue of this pharmacological property, aprikalim affords cardioprotection in experimental models of ischemia/reperfusion injury, and, at higher doses, also causes peripheral or coronary vasodilatation. It is undergoing phase II clinical trials with Aventis Pharma for the treatment of asthma; heart failure; hypertension; myocardial ischaemia.