Ganciclovir is an analog of 2'-deoxyguanine nucleotides that inhibits the replication of herpes viruses. Its mechanism of action is: ganciclovir is first phosphorylated into a monophosphate by a protein kinase homolog encoded by CMV (UL97 gene), and then further phosphorylated into a diphosphate and a triphosphate by cellular kinases. In CMV-infected cells, the level of triphosphate is 100 times higher than that in non-infected cells, suggesting that this product can be preferentially phosphorylated in infected cells. Once ganciclovir forms a triphosphate, it can persist for several days in CMV-infected cells. The triphosphate of ganciclovir is believed to inhibit viral DNA synthesis in the following ways: 1) competitively inhibiting viral DNA polymerase; 2) co-entering viral DNA, thereby leading to the termination of viral DNA elongation.

In the acidic environment of the stomach, it forms a diffuse protective layer covering the ulcer surface, preventing gastric acid, enzymes and food from invading the ulcer. It reduces the activity of pepsin, increases mucin secretion, and promotes the release of prostaglandins from the mucosa, thereby protecting the gastric mucosa. It has a killing effect on Helicobacter pylori (HP) and can promote the healing of gastritis.

Nucleoside antiviral drugs. After entering the cell, this product is rapidly phosphorylated to a monophosphate compound, and then becomes a triphosphate compound through the action of cellular kinase. Its phosphorylation in cells infected with cytomegalovirus is faster than that in normal cells. Ganciclovir can competitively inhibit DNA polymerase and incorporate into the DNA of viruses and host cells, thereby inhibiting DNA synthesis. This product has a stronger inhibitory effect on viral DNA polymerase than host cell polymerase. In animal experiments, this product has teratogenic, carcinogenic, immunosuppressive effects and reproductive system toxicity.

Nucleoside antiviral drugs. Competitively inhibit DNA polymerase and incorporate into the DNA of viruses and host cells, thereby inhibiting DNA synthesis. The inhibitory effect on viral DNA polymerase is stronger than that on host cell polymerase. In animal experiments, this product has teratogenic, carcinogenic, immunosuppressive effects and reproductive system toxicity.

This product has a broad-spectrum antibacterial effect and strong antibacterial effect. It has strong antibacterial activity against most Enterobacteriaceae, such as Escherichia coli, Klebsiella, Proteus, Salmonella, Shigella, and Gram-negative bacteria such as Haemophilus influenzae, Legionella pneumophila, and Neisseria gonorrhoeae. It also has antibacterial effects on Gram-positive bacteria such as Staphylococcus aureus, Streptococcus pneumoniae, Streptococcus pyogenes, and Mycoplasma pneumoniae and Chlamydia pneumoniae, but has poor effects on anaerobic bacteria and enterococci. Its mechanism of action is to inhibit the activity of bacterial DNA gyrase, prevent the synthesis and replication of bacterial DNA, and cause bacterial death.