This product is a gastric mucosal protective agent. Under gastric acid conditions, it forms a diffuse protective layer covering the ulcer surface, preventing gastric acid, enzymes and food from invading the ulcer, and promoting the regeneration of the ulcer mucosa and the healing of the ulcer. This product also has the effects of reducing the activity of pepsin, increasing mucin secretion, and promoting the release of PGE2 from the mucosa, thereby protecting the gastric mucosa. In addition, this product has a killing effect on Helicobacter pylori (Hp), thus promoting the healing of gastritis.

It inhibits bacterial protein synthesis by hindering the bacterial transpeptidation process. It has antibacterial effects on a variety of Gram-positive aerobic bacteria, Gram-negative aerobic bacteria, anaerobic bacteria, sexually transmitted disease microorganisms and other microorganisms. The mechanism of action is the same as that of erythromycin, mainly binding to the 50S subunit of the bacterial ribosome to inhibit RNA-dependent protein synthesis.

This product is an antiviral drug. It has an inhibitory effect on herpes simplex virus, varicella zoster virus, cytomegalovirus, etc. in vitro. After entering the cells infected by herpes virus, this product competes with deoxynucleoside for viral thymidine kinase or cell kinase, and the drug is phosphorylated into activated acyclovir triphosphate, and then inhibits viral replication in two ways: ① Interfering with viral DNA polymerase and inhibiting viral replication; ② Under the action of DNA polymerase, it binds to the growing DNA chain, causing the extension of the DNA chain to be interrupted. This product has a special affinity for viruses, but has low toxicity to mammalian host cells.

The second generation of sulfonylurea hypoglycemic drugs has a strong effect. It selectively acts on pancreatic β cells, promotes insulin secretion, and improves the effect of glucose intake, inhibiting the production and output of glycogen. In addition, it can reduce the aggregation and adhesion of platelets, which helps prevent and treat diabetic microangiopathy.

In acute toxicity experiments, the LD50 in mice and rats was greater than 4000 mg/Kg. In subacute toxicity experiments, Wistar male and female rats were given 40 mg, 200 mg and 1000 mg/Kg per day for 5 weeks, and male and female rabbits were given 6 mg, 60 mg and 600 mg/Kg per day for 23 consecutive days. There were no special changes in the blood, urine and morphological observations of the test animals. In chronic toxicity experiments, Wistar male and female rats were given 6 mg, 60 mg and 600 mg/Kg per day for 26 consecutive weeks. There were no special changes in the general state, blood and urine examinations, and morphological observations of the test animals.