Anatomical Therapeutic Chemical Classification System
Alginic acid is a polysaccharide distributed widely in the cell walls of brown algae which is hydrophilic and forms a viscous gum when hydrated. Its salts with metals such as sodium and calcium are known as alginates. It is a significant component of the biofilms produced by the bacterium Pseudomonas aeruginosa, a major pathogen found in the lungs of some people who have cystic fibrosis. The biofilm and P. aeruginosa have a high resistance to antibiotics and are susceptible to inhibition by macrophages. Its colour ranges from white to yellowish-brown. It is sold in filamentous, granular or powdered forms.
Under the effect of gastric acid, a precipitate is formed from tripotassium dicitrato bismuthate, which adheres primarily to the ulcerated area and inhibits the activity of pepsin. Tripotassium dicitrato bismuthate contributes to the healing of a high percentage of gastric and duodenal ulcers.
Carbenoxolone is a derivative of enoxolone with anti-inflammatory and anti-diuretic properties.
Cimetidine is a histamine H2-receptor antagonist which rapidly inhibits both basal and stimulated gastric secretion of acid and reduces pepsin output. It is a reversible, competitive antagonist, and is used as an anti-ulcer drug.
Esomeprazole is the S-isomer of omeprazole and reduces gastric acid secretion through a specific targeted mechanism of action. Esomeprazole is a weak base and is concentrated and converted to the active form in the highly acidic environment of the secretory canaliculi of the parietal cell, where it inhibits the enzyme H+ K+ -ATPase – the acid pump and inhibits both basal and stimulated acid secretion.
Famotidine is a potent competitive H2-receptor antagonist. Famotidine has a rapid onset of action and, at the recommended doses, has a long duration of action and is highly effective at relatively low blood concentrations.
Lansoprazole is a gastric proton pump inhibitor. It inhibits the final stage of gastric acid formation by inhibiting the activity of H+/K+ ATPase of the parietal cells in the stomach. The inhibition is dose-dependent and reversible, and the effect applies to both basal and stimulated secretion of gastric acid.
Misoprostol is an analogue of naturally occurring prostaglandin E1 which promotes peptic ulcer healing and symptomatic relief. Misoprostol protects the gastroduodenal mucosa by inhibiting basal, stimulated and nocturnal acid secretion and by reducing the volume of gastric secretions, the proteolytic activity of the gastric fluid, and increasing bicarbonate and mucus secretion.
Nizatidine is a potent, selective, competitive and fully reversible histamine H2-receptor antagonist. Nizatidine significantly decreased basal and stimulated gastric acid and pepsin concentration, in addition to the volume of gastric secretion.
Omeprazole, a racemic mixture of two enantiomers reduces gastric acid secretion through a highly targeted mechanism of action. It is a specific inhibitor of the acid pump in the parietal cell. It is rapidly acting and provides control through reversible inhibition of gastric acid secretion with once daily dosing.
Pantoprazole is a substituted benzimidazole which inhibits the secretion of hydrochloric acid in the stomach by specific blockade of the proton pumps of the parietal cells.
Rabeprazole belongs to the class of anti-secretory compounds, the substituted benzimidazoles, that do not exhibit anticholinergic or H2 histamine antagonist properties, but suppress gastric acid secretion by the specific inhibition of the H+/K+ -ATPase enzyme (the acid or proton pump).
Ranitidine is a specific rapidly acting histamine H2-antagonist. It inhibits basal and stimulated secretion of gastric acid, reducing both the volume and the acid and pepsin content of the secretion. Ranitidine has a relatively long duration of action and so a single 150 mg dose effectively suppresses gastric acid secretion for twelve hours.
Sucralfate forms an ulcer adherent complex with the proteinaceous exudate of the ulcer site. This property enables sucralfate to form a protective barrier over the ulcer lesion giving sustained protection against the penetration and action of gastric acid, pepsin and bile.