A new type of drug that inhibits gastric acid secretion. It acts on the H-K-ATPase of gastric parietal cells, preventing the H of parietal cells from being transported to the stomach, resulting in a significant reduction in the amount of gastric acid in gastric juice. It is clinically used for the treatment of duodenal ulcer, gastric ulcer, reflux esophagitis, and Zollinger-Ellison syndrome (gastrinoma), with significant efficacy, and has an inhibitory effect on Helicobacter pylori.

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.

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Preventive administration experiments on hyperlipidemia rats and rabbits showed that this product has the effect of reducing animal serum triglycerides and cholesterol.

Liranabate is a thiocarbamate antifungal drug and a squalene epoxidase inhibitor. It exerts its antifungal effect by inhibiting the epoxidation reaction of squalene in fungal cell membranes and affecting the synthesis of ergosterol, a component of cell membranes. Liranabate has a strong antifungal effect on skin filamentous fungi (Trichophyton, Microsporum, Epidermophyton), and also shows antifungal effects on other filamentous fungi, dark fungi, and dimorphic fungi.