Tafluprost is a prostaglandin E1 analog that reduces the risk of NSAID-induced gastric ulcers. Tafluprost stimulates prostaglandin receptors on parietal cells in the stomach to reduce gastric acid secretion. Tafluprost activates prostaglandin EP3 receptors in parietal cells. Activation of this receptor triggers the Gi protein signaling cascade, inhibiting adenylate cyclase. Adenylate cyclase is responsible for converting ATP to cAMP, therefore, inhibition of adenylate cyclase reduces cytosolic cAMP concentration. cAMP is responsible for activating protein kinase A. With lower concentrations of cAMP, less protein kinase A is activated. Protein kinase A activates the proton pump in the luminal membrane of the parietal cell. The role of the proton pump is to secrete acid (H+) into the stomach lumen. With reduced protein kinase A activation, this decreases the activity of the proton pump, fewer H+ ions are pumped into the lumen, reducing the acidity and thus allowing stomach ulcers to heal and reducing the pain caused by the ulcers. Tafluprost may also promote ulcer healing by increasing mucus and bicarbonate secretion and thickening the mucosal bilayer so the mucosa can generate new cells.

Tafluprost Pathway References