Glycyclamide (Tolcyclamide) isn a cyclohexyl-containing sulfonylurea compound with antihyperglycemic activity. Tolcyclamide is closely related to tolbutamide, with a cyclohexyl ring in place of the butyl group. It is much less potent than glipizide, being active at a daily dose of 1000 mg.

Troxipide is a gastric cytoprotective agent used for the treatment of gastritis and gastric uclers in Japan, India, China and South Korea. Troxipide has a mode of action different from that for other anti-gastric agents: it does not inhibit acid secretion and does not have acid neutralizing activity. It exerts its activity by increasing mucus production, cytoprotective prostaglandin secretion, regeneration of collagen fibers, reducing inflammatory mediator induced neutrophil migration and reactive oxygen species generation in gastric mucosa, enhancing gastric mucosal metabolism and microcirculation.

Nepaprazole is a proton pump inhibitor of substituted 2-(2-pyridinylmethylsulfinyl)-1H-benzimidazole class evaluated as useful drug for the clinical treatment of peptic ulcer diseases. The effects of the TY-11345 (nepaprazole sodium salt) on gastric mucosal proton pump (H+/K(+)-ATPase) activity, gastric acid secretion and gastro-duodenal lesions were investigated in experimental animals. TY-11345 potently inhibited H+/K(+)-ATPase activity in isolated rabbit gastric mucosal microsomes and the inhibitory effect was enhanced under weak acid conditions. In Ghosh & Schild rats, intravenous injection of TY-11345 significantly inhibited gastric acid secretion stimulated by tetragastrin; the effect of TY-11345 was twice as potent as that of omeprazole. In pylorus ligated rats, TY-11345 inhibited basal gastric acid secretion by both the intraduodenal and oral routes with 9 and 5 times more greater potency than those of omeprazole, respectively. The antisecretory effect of TY-11345 persisted for more than 24 h in pylorus ligated rats. In experimental ulcer models, TY-11345 prevented the formation of water-immersion stress, ethanol or indomethacin-induced gastric lesions and mepirizole-induced duodenal lesions in rats. The antiulcer effects of TY-11345 were 3 to 15 times more potent than those of omeprazole. These results suggested that TY-11345 had potent antisecretory and antiulcer effects which are exerted by suppression of H+/K(+)-ATPase activity in gastric parietal cells. Nepaprazole sodium had been studied in phase II clinical trials for treatment of gastric ulser but this research has been discontinued.

Bezafibrate is a lipid-lowering fibric acid derivative. Bezafibrate directly bound to and activated all three peroxisome proliferator-activated receptor (PPAR) subtypes respectively in PPAR binding and transactivation assays. However, from a biochemical point of view, bezafibrate is a PPAR ligand with a relatively low potency. Bezafibrate leads to considerable raising of HDL cholesterol and reduces triglycerides, improves insulin sensitivity and reduces blood glucose level, significantly lowering the incidence of cardiovascular events and new diabetes in patients with features of metabolic syndrome. It is the only pan-PPAR activator with more than a quarter of a century of therapeutic experience with a good safety profile.

Tegoprazan is an oral, selective, reversible inhibitor of gastric H+/K+-ATPase that has a fast onset of action and can control gastric pH for a prolonged period. It was developed for the treatment of acid-related gastrointestinal diseases such as gastroesophageal reflux disease (GERD) and peptic ulcers. Tegoprazan has received a license from the Ministry of Food and Drug Safety in Korea for the treatment of gastroesophageal reflux disease and erosive oesophagitis. In addition, the drug is involved in phase III clinical trial to evaluate the triple therapy (tegoprazan, amoxicillin, and clarithromycin) in H. Pylori positive patients. This trial is on the stage of recruiting the patients.

Gliclazide (BILXONA®) is an oral sulfonylurea hypoglycemic agent which is used in type 2 diabetes to stimulate insulin production. It differs from other related compounds by an N-containing heterocyclic ring with an endocyclic bond. Gliclazide (BILXONA®) reduces blood glucose levels by stimulating insulin secretion from the beta-cells of the islets of Langerhans. Increase in postprandial insulin and C-peptide secretion persists after two years of treatment. In addition to these metabolic properties, Gliclazide (BILXONA®) has haemovascular properties. It is not available for sale in the United States.

Zaldaride is a calmodulin antagonist known to produce inhibition of calmodulin-dependent voltage-gated ion channels including those of Ca2 , Na , and K . Zaldaride was also observed to inhibit nicotinic acetylcholine receptor (nAChR) channel currents. Zaldaride has been studied in clinical trials as a potential treatment for travelers diarrhea.

Roxatidine is an histamine H2-receptor antagonist. Roxatidine is a potent and selective inhibitor of basal and stimulated gastric acid secretion through competitive blockade of H2-receptors. Total pepsin secretion is reduced in a dose-dependent manner. There is an independent mucosal protection action. Roxatidine is indicated for the treatment of peptic ulcer, gastro-oesophageal reflux disease, gastritis, upper gastrointestinal haemorrhage and Zollinger-Ellison syndrome also it can be used as a premedication before anaesthesia. Roxatidine possessed a robust estrogenic activity.

Parmidin (pyridinol carbamate) is a Soviet drug, has anti-arteriosclerotic (increased vascular resistance) activity, reduces the permeability of blood vessels, it helps to restore disturbed microcirculation in pathological processes. This is mainly due to the influence on kinin system, especially with a decrease in the activity of bradykinin receptors. It also reduces the aggregation of platelets. It’s used to treat: the brain vascular atherosclerosis, heart, limbs; diabetic retinopathy (non-inflammatory lesion of the retina associated with increased levels of sugar in the blood); thrombosis (violation of patency) retinal vein; occlusive disease (inflammation of the inner lining of arteries with a decrease in their lumen); trophic leg ulcers (slow-healing skin defects caused by malnutrition). Ointment is used in neurodermatitis (skin disease caused by disturbance of the central nervous system), Lichen sclerosus (teardrop scleroderma) genital organs of children, as well as a prophylactic and therapeutic agent against radiation skin lesions.

Fenoctimine is a nonanticholinergic inhibitor of gastric acid secretion in dogs and rats. Fenoctimine was more potent than cimetidine in the reduction of basal acid secretion in the gastric fistula rat and inhibited the production of gastric acid stimulated by histamine, gastrin tetrapeptide or bethanechol in the chronic gastric fistula dog. This compound is not an H2-antagonist but does inhibit the H+/K+-ATPase of hog gastric mucosa. The in vitro metabolism of fenoctimine by rat liver homogenates resulted in the oxidation of the aliphatic chain at the seven carbon, initially to an alcohol and then to a ketone. The unexpectedly weak effect of fenoctimine as a gastric antisecretory agent in humans, as well as anticholinergic effects, may be due to its extensive metabolism, which is different from that seen in dog and rat. The development of fenoctimine has been discontinued for unspecified reason.