Vonoprazan (Vonoprazan fumarate or TAK-438) under brand name Takecab, discovered by Takeda, is a new medicine for treating acid-related diseases with a novel mechanism of action called potassium-competitive acid blockers (P-CABs) which competitively inhibits the binding of potassium ions to H+,K+-ATPase (also known as the proton pump) in the final step of gastric acid secretion in gastric parietal cells. The drug is approved in Japan for the treatment of acid-related diseases, including gastric ulcer, duodenal ulcer, reflux esophagitis and Adjunct to Helicobacter pylori eradication in the case of Helicobacter pylori gastritis.

Rabeprazole sodium was discovered by Eisai Co., Ltd. Janssen Pharmaceutica N.V. and Eisai Co., Ltd. have a strategic alliance in which Eisai and Janssen-Cilag co-promote the drug in Germany and the U.K. In the US rabeprazole sodium is co-promoted under the brand name AcipHex by Eisai Inc. and Janssen Pharmaceutica Inc. Pariet is available through Janssen-Cilag in most other countries excluding Japan and some Asian countries. Rabeprazole is an antiulcer drug in the class of proton pump inhibitors. Rabeprazole is a prodrug and is converted to the active sulphenamide form in the acid environment of the parietal cells. Rabeprazole is used to heal and maintain the healing of Erosive or Ulcerative Gastroesophageal Reflux Disease (GERD), for healing Duodenal Ulcers, and for treatment of pathological hypersecretory conditions such as Zollinger-Ellison Syndrome. Rabeprazole suppresses gastric acid secretion by inhibiting the gastric H+, K+ATPase at the secretory surface of the gastric parietal cell and does not exhibit anticholinergic or histamine H2-receptor antagonist properties. Because this enzyme is regarded as the acid (proton) pump within the parietal cell, rabeprazole has been characterized as a gastric proton-pump inhibitor which blocks the final step of gastric acid secretion. In gastric parietal cells, rabeprazole is protonated, accumulates, and is transformed to an active sulfonamide.

Omeprazole belongs to a class of antisecretory compounds, which suppress gastric acid secretion by specific inhibition of the H+ /K+ ATPase enzyme system at the secretory surface of the gastric parietal cell. Because this enzyme system is regarded as the acid (proton) pump within the gastric mucosa, omeprazole has been characterized as a gastric acid-pump inhibitor, in that it blocks the final step of acid production. This effect is dose-related and leads to inhibition of both basal and stimulated acid secretion irrespective of the stimulus. Omeprazole is used under brand names Prilosec and Losec for treatment of duodenal ulcer in adults, gastric ulcer in adults, Gastroesophageal Reflux Disease. In addition it used for maintenance of healing of erosive esophagitis in pediatric patients and adults and for treatment of pathological hypersecretory conditions in adults (eg, Zollinger-Ellison syndrome, multiple endocrine adenomas and systemic mastocytosis). The most frequent significant adverse effects occurring in at least of patients include headache; upper respiratory tract infection, abdominal pain, diarrhea, back pain, weakness and rash.

Nizatidine, chemically N-[2-[[[2- [(dimethylamino)methyl]-4-thiazolyl]methyl]thio]ethyl]-N’ -methyl-2-nitro-1,1-ethenediamine, is a histamine H2-receptor antagonist. Nizatidine reduced gastric acid secretion for up to 8 h suggesting that this compound could be used in with a once or twice daily dosage regime. Nizatidine was rapidly and well-absorbed orally, was widely distributed in tissues and the majority of the dose was excreted in the urine within 24 h. Nizatidine is indicated for duodenal and gastric ulcer as well as for the treatment of endoscopically diagnosed esophagitis, including erosive and ulcerative esophagitis, and associated heartburn due to gastroesophageal reflux disease.

Famotidine, a competitive histamine H2-receptor antagonist, is used to treat gastrointestinal disorders such as gastric or duodenal ulcer, gastroesophageal reflux disease, and pathological hypersecretory conditions. Famotidine inhibits many of the isoenzymes of the hepatic CYP450 enzyme system. Other actions of Famotidine include an increase in gastric bacterial flora such as nitrate-reducing organisms. Famotidine binds competitively to H2-receptors located on the basolateral membrane of the parietal cell, blocking histamine affects. This competitive inhibition results in reduced basal and nocturnal gastric acid secretion and a reduction in gastric volume, acidity, and amount of gastric acid released in response to stimuli including food, caffeine, insulin, betazole, or pentagastrin.

Ranitidine, a histamine H2-receptor antagonist, is now well established as a potent inhibitor of gastric acid secretion effective in the treatment and prophylaxis of gastrointestinal lesions aggravated by gastric acid secretion.

Aldioxa is the generic name for the metal complex, dihydroxyaluminum allantoinate, which is hydrolyzed to allantoin and aluminium hydrate at the gastric mucosa. Aldioxa was approved in Japan to improve subjective symptoms or objective of gastric/duodenal ulcer and gastritis. It was discovered, that aldioxa ameliorates delayed gastric emptying through its antagonistic activity on the α-2 adrenergic receptor. The most commonly reported adverse reactions include constipation.

Zaltidine (CP-57,361) is a guanidinothiazolylimidazole compound which is a highly specific H2-receptor antagonist. It potently inhibits gastric acid secretion. Zaltidine appears to be an effective treatment of duodenal ulcer in human studies. However, the incidence of hepatic damage (8%) seems higher than with commonly used H2-receptor antagonists.

Metiamide is an antagonist of histamine H2-receptors synthesized at Smith Kline & French Laboratories. It potently inhibited gastric acid secretion. Metiamide demonstrated promising clinical effects in patients with duodenal ulcers but questionable safety.

L-365,260 is an antagonist of gastrin and brain CCK-B receptor. In vivo, oral administration of L-365,260 antagonized gastrin-stimulated acid secretion. L-365,260 is used as a tool compound to investigate gastrin and brain CCK-B and their role in psysiology and disease. In a double-blind placebo-controlled study L-365,260 did not augment the analgesic effect of morphine in subjects with chronic neuropathic pain. Preclinical studies demonstrated modes activity of L-365,260 in models of anxiety and ulcers.