This product can inhibit the synthesis of prostaglandins and has antipyretic and analgesic effects.

It has a high affinity for serotonin (5HT2) receptors, which is greater than its affinity for dopamine D1 and dopamine D2 receptors in the brain; it also has a high affinity for histamine receptors and adrenergic α1 receptors, a low affinity for adrenergic α1 receptors, but has little affinity for cholinergic receptors or benzodiazepine receptors. Quetiapine tablets do not produce a persistent increase in prolactin and are effective in treating both positive and negative symptoms of schizophrenia.

Proton pump inhibitor. This product is a fat-soluble weak alkaline drug that is easily concentrated in an acidic environment. After oral administration, it can be specifically distributed in the secretory tubules of the gastric mucosal parietal cells, and converted into the active form of sulfenamide in a high acid environment. It irreversibly combines with the residues of H, K-ATPase (also known as proton pump) in the secretory membrane of gastric cells through a sulfur bond to form a complex of sulfenamide and proton pump, thereby inhibiting the activity of the enzyme and blocking the final step of gastric acid secretion. It has a strong and lasting inhibitory effect on gastric acid secretion caused by various reasons.

Proton pump inhibitor. This product is a fat-soluble weakly alkaline drug that is easily concentrated in an acidic environment. Therefore, after oral administration, it can be specifically distributed in the secretory tubules of the gastric mucosal parietal cells and converted into the active form of sulfenamide in this high-acid environment. It then irreversibly combines with the sulfhydryl group of the H,K-ATPase (also known as the proton pump) in the secretory membrane of the parietal cells through a disulfide bond to form a complex of sulfenamide and the proton pump, thereby inhibiting the activity of the enzyme and blocking the final step of gastric acid secretion. Therefore, this product has a strong and lasting inhibitory effect on gastric acid secretion caused by various reasons.

Omeprazole is a racemic mixture of a pair of active optical enantiomers. It reduces gastric acid secretion through a highly targeted mechanism of action and is a special inhibitor of the acid pump in gastric parietal cells. This product acts rapidly, and a once-daily dose can reversibly inhibit gastric acid secretion. Omeprazole is a weakly alkaline substance that is concentrated and converted into active substances in the highly acidic environment of the tubules in gastric parietal cells, inhibiting H, K-ATPase (proton pump). This inhibitory effect on the final step of gastric acid formation is dose-related, and highly inhibits basal gastric acid secretion and irritant gastric acid secretion, but has nothing to do with irritants. Intravenous administration of omeprazole in humans inhibits gastric acid secretion in a dose-related manner. In order to quickly achieve the same effect of reducing gastric acidity as multiple oral administrations of 20 mg, it is recommended to give 40 mg of omeprazole intravenously for the first time. Intravenous injection of 40 mg of omeprazole rapidly reduces gastric acidity, with an average decrease of 90% within 24 hours. The inhibitory effect of omeprazole on gastric acid secretion is related to the area under the drug-time curve (AUC), but has nothing to do with the blood drug concentration at the time of administration. Helicobacter pylori is associated with acid peptic diseases, including duodenal ulcers and gastric ulcers, with 95% and 70% of duodenal ulcers and gastric ulcers, respectively, being associated with Helicobacter pylori infection. Helicobacter pylori is the main cause of gastritis. Helicobacter pylori and gastric acid together are the main causes of peptic ulcers. Omeprazole combined with antibiotics can eradicate Helicobacter pylori, which is associated with rapid relief of symptoms, high rates of gastric mucosal repair, and long-term relief of peptic ulcer disease, thereby reducing complications such as gastrointestinal bleeding, and also reducing the need for long-term treatment with anti-acid drugs. Any method, including the reduction of gastric acid caused by proton pump inhibitors, increases the number of normal flora in the gastrointestinal tract, and the risk of gastrointestinal infection with Salmonella and Campylobacter may be slightly increased with acid-suppressing drug treatment. In a study of rats given long-term omeprazole, enlargement of gastric ECL cells and benign tumors were observed, which is the result of persistent hypergastrinemia due to gastric acid suppression. Similar findings were also seen after treatment with H2 receptor antagonists, proton pump inhibitors, and partial fundus resection. Apparently, these changes were not a direct effect of the above drugs.