It transforms into an active structure under acidic conditions and combines with the SH group of the (HK)-ATPase of the proton pump, thereby inhibiting the activity of the enzyme and inhibiting gastric acid secretion; it can inhibit the (HK)-ATPase activity of microsomes in dog gastric mucosa; it has an inhibitory effect on the acid secretion of dog gastric mucosal parietal cells stimulated by histamine, acetylcholine and gastrin; it can significantly inhibit the acid secretion, nocturnal gastric acid secretion and 24-hour gastric acid secretion caused by gastrin and insulin stimulation in healthy adults; it can promote the healing of chronic gastric and duodenal ulcers in rats, and has an inhibitory effect on the formation of various experimental ulcers.

Under acidic conditions, it transforms into an active structure and combines with the SH group of the (HK)-ATPase of the proton pump to inhibit the activity of the enzyme and thus inhibit gastric acid secretion. It can inhibit the (HK)-ATPase activity of microsomes in the gastric mucosa of dogs, the acid production of parietal cells, the acid secretion caused by gastrin or insulin stimulation in healthy adults, the nocturnal gastric acid secretion, the 24-hour gastric acid secretion, and promote ulcer healing and inhibit ulcer formation.

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.

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.

It promotes the conversion of fibrinogen into fibrin, which is applied to wounds to coagulate blood and stop bleeding.