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. 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 remission of peptic ulcer disease, thereby reducing complications such as gastrointestinal bleeding and the need for long-term treatment with anti-acid drugs.

It can improve the limb motor dysfunction caused by toxic peripheral neuropathy in rats caused by hexadione and acrylamide, shorten the latency of nerve-muscle action potential, and increase the amplitude of nerve-muscle action potential. It can reduce the incidence of myelin swelling in animal tibial nerves and reduce the number of degenerated tibial nerve fibers. It suggests that it may promote the recovery of damaged nerves.

This product is a synthetic nucleoside antiviral drug, which has inhibitory effects on herpes simplex virus type I (HSV-1), type H (HSV-2) and varicella-zoster virus (VZV) in vivo and in vitro. Cell culture results show that this product has the strongest inhibitory effect on HSV-1 virus, followed by HSV-2 and VZV virus. Because this product has affinity for thymidine kinase (TK) encoded by HSV and VZV, it has a highly selective inhibitory effect. This type of viral enzyme converts acyclovir into acyclovir monophosphate, a nucleoside analog. The monophosphate is further converted into diphosphate by guanylate kinase in the cell, and then converted into triphosphate by multiple enzymes in the cell. In vitro, acyclovir triphosphate stops herpes virus DNA replication.

It transmits specific cellular immune information of hepatitis B, regulates and enhances the body's specific cellular immune function against hepatitis B virus infection. It can transform the patient's normal T cells into specific sensitized T cells, including killer sensitized T cells (TC) and delayed-type hypersensitivity T cells (TDTH). TC can specifically kill liver cells parasitized by hepatitis B virus and expel the virus; TDTH releases a variety of lymphokines (such as interferon, interleukin, etc.), enhances the killing of viruses, and sensitizes other lymphocytes in the body to form more effector lymphocytes to expand the immune effect. At the same time, it has the function of a common transfer factor and can regulate other aspects of the body's immune function.

It achieves antibacterial effect by inhibiting the activity of bacterial DNA gyrase and hindering the replication of bacterial DNA. It has good antibacterial effect on most Enterobacteriaceae, Gram-negative bacteria, some Gram-positive bacteria, Legionella, Mycoplasma, Chlamydia, but has poor effect on anaerobic bacteria and enterococci.