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.

Cizolirtine is a potent analgesic in mice and rats, with an efficacy superior to that of aspirin and other nonsteroid anti-inflammatory drugs. Recent studies have shown that the analgesic effect of cizolirtine could be related, at least partially, to an inhibition of spinal substance P and calcitonin gene-related peptide release. Cizolirtine has been in clinical trials for the treatment of pain and overactive bladder. Reported adverse events are: dry mouth, dizziness, nausea, vomiting, blurred vision.

Ufiprazole (Omeprazole sulfide) is a metabolite of Omeprazole, which is a proton pump inhibitor. Omeprazole sulfide has been shown to be a direct-acting inhibitor of CYP2C19 in pooled human liver microsomes. Ufiprazole is also a weak BRS-3 agonist.

Ciclafrine is azaspiroalkane derivative patented by pharmaceutical company Goedecke A.-G. for the low blood pressure treatment

Fenclonine, also known as p-chlorophenylalanine, is an inhibitor of tryptophan hydroxylase, the enzyme that plays a rate-limiting role in the biosynthesis of serotonin. Fenclonine was studied for the treatment of carcinoid syndrome, but the psychological side effects, prevented for the further development for this use.

Benzobarbital (under the brand name Benzona), a barbiturate derivative developed in Russia that is used to treat convulsive forms of epilepsy, newborn hemolytic disease, and insomnia.

Pranidipine is the calcium channel blocker. Pranidipine did not affect the sensitivity of the contractile proteins to calcium. Pranidipine also did not alter cyclic GMP-induced relaxation in alpha-toxin-skinned vascular preparations. Pranidipine also prolonged glyceryl trinitrate-induced relaxation in the endothelium denuded rat aorta. Pranidipine enhances cyclic GMP-independent NO-induced relaxation of smooth muscle by a mechanism other than through NO-induced hyperpolarization. These effects were in direct contrast to amlodipine, another new 1,4-dihydropyridine calcium antagonist. Pranidipine increased blood velocity and probably blood flow in the optic nerve head, choroid, and retina of rabbits. Pranidipine was not detrimental to global cardiac function in animals with dilated cardiomyopathy. Pranidipine enhances relaxation produced by endothelium-derived relaxing factor in carotid artery. Pranidipine was investigated as pharmacological agent for the treatment of angina pectoris and hypertension.

Rioprostil is a methylprostaglandin E1 analog. Rioprostil inhibits gastric acid secretion and enhances the gastric mucus-bicarbonate barrier. In peptic ulcer cases, it facilitates the healing process and the elimination of pain. Rioprostil can also be used to prevent recurrence of duodenal ulcers. However, its development has been discontinued in 2000.

Avoralstat, a small molecule inhibitor of plasma kallikrein, participated in clinical trials phase III to prevent hereditary angioedema, but these studied were discontinued due to insufficient efficacy study. Recently published article has described that avoralstat could improve the quality of life in C1‐INH‐HAE patients. Hereditary angioedema (HAE) with C1 inhibitor deficiency (C1‐INH‐HAE) is an autosomal dominant disorder characterized by recurrent episodes of swelling of the skin, pharynx, gastrointestinal tract, genitals, and is due primarily to mutations in the SERPING1 gene that results in insufficient production of the natural plasma kallikrein inhibitor, C1 inhibitor (C1‐INH).