Synopsis:Omeprazole is a proton pump inhibitor used in the treatment of peptic ulcer and gastroesophageal reflux disease. It can specifically act on the site of proton pump in gastric parietal cells and convert into the active form of sulphonamide. Then it can irreversibly combine with the sulfhydryl group of proton pump through disulfide bond to form a complex of sulphonamide and proton pump (H + - K + - ATPase), Therefore, inhibiting the activity of the enzyme can prevent the H + in parietal cells from being transported to the gastric cavity, and block the last step of gastric acid secretion, which can greatly reduce the amount of gastric acid in gastric juice. Therefore, this product has a strong and lasting inhibitory effect on gastric acid secretion caused by various reasons (such as basic gastric acid secretion, gastric acid secretion caused by histamine, pentagastrin and stimulation of vagus nerve, including gastric acid secretion caused by dibutyl camp, which cannot be inhibited by H2 receptor blockers). This is related to the irreversibility of the inhibitory effect of the product on proton pump. Only after the formation of a new proton pump can the acid secretion recover.
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Summary
Omeprazole is a proton pump inhibitor used in the treatment of peptic ulcer and gastroesophageal reflux disease. It can specifically act on the site of proton pump in gastric parietal cells and convert into the active form of sulphonamide. Then it can irreversibly combine with the sulfhydryl group of proton pump through disulfide bond to form a complex of sulphonamide and proton pump (H + - K + - ATPase), Therefore, inhibiting the activity of the enzyme can prevent the H + in parietal cells from being transported to the gastric cavity, and block the last step of gastric acid secretion, which can greatly reduce the amount of gastric acid in gastric juice. Therefore, this product has a strong and lasting inhibitory effect on gastric acid secretion caused by various reasons (such as basic gastric acid secretion, gastric acid secretion caused by histamine, pentagastrin and stimulation of vagus nerve, including gastric acid secretion caused by dibutyl camp, which cannot be inhibited by H2 receptor blockers). This is related to the irreversibility of the inhibitory effect of the product on proton pump. Only after the formation of a new proton pump can the acid secretion recover.