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.

This product is a proton pump inhibitor of gastric parietal cells. It can specifically inhibit the secretory microtubules and tubular vesicles in the cytoplasm of the parietal cell apical membrane, thereby effectively inhibiting the secretion of gastric acid. Since H, K-ATPase is the last process of acid secretion of parietal cells, this product has a strong acid inhibition ability. It can not only non-competitively inhibit gastric acid secretion caused by gastrin, histamine, choline, food, and stimulation of the vagus nerve, but also inhibit part of the basic gastric acid secretion that is not affected by choline or H2 receptor blockers. It also has a strong and lasting inhibitory effect on gastric acid secretion caused by dibutyl cyclic adenosine monophosphate (DCAMP) stimulation that cannot be inhibited by H2 receptor antagonists. In addition, this product also has an inhibitory effect on pepsin secretion, has no obvious change in gastric mucosal blood flow, and does not affect body temperature, gastric cavity temperature, arterial blood pressure, venous hemoglobin, arterial oxygen partial pressure, carbon dioxide partial pressure and arterial blood pH.

This product is a proton pump inhibitor of gastric parietal cells. It can specifically inhibit the secretory microtubules and tubular vesicles in the cytoplasm of the parietal cell apical membrane, thereby effectively inhibiting the secretion of gastric acid. Since H, K-ATPase is the last process of acid secretion of parietal cells, this product has a strong acid inhibition ability. It can not only non-competitively inhibit gastric acid secretion caused by gastrin, histamine, choline, food, and stimulation of the vagus nerve, but also inhibit part of the basic gastric acid secretion that is not affected by choline or H2 receptor blockers. It also has a strong and lasting inhibitory effect on gastric acid secretion caused by dibutyl cyclic adenosine monophosphate (DCAMP) stimulation that cannot be inhibited by H2 receptor antagonists. In addition, this product also has an inhibitory effect on pepsin secretion, has no obvious change in gastric mucosal blood flow, and does not affect body temperature, gastric cavity temperature, arterial blood pressure, venous hemoglobin, arterial oxygen partial pressure, carbon dioxide partial pressure and arterial blood pH.

This product acts specifically on the gastric mucosal parietal cells, reducing the activity of H/KATPase in the parietal cells, thereby inhibiting the secretion of gastric acid. Compared with omeprazole and lansoprazole, this product has a weaker inhibitory effect on cytochrome P450-dependent enzymes. No adverse effects were found in either short-term or long-term administration of pantoprazole. This drug is non-carcinogenic, does not impair fertility, and does not induce teratogenesis. After 2.5 years of continuous medication, there were no changes in various experimental parameters of liver enzymology and cholesterol metabolism.

It binds to the viral DNA polymerase, reducing its activity and inhibiting DNA synthesis. After phosphorylation, it generates adenosine arabinoside diphosphate (Ara-ADP) and adenosine arabinoside triphosphate (Ara-ATP), in which Ara-ATP competes with deoxyadenosine triphosphate (dATP) to bind to viral DNAP, thereby inhibiting the activity of the enzyme and the synthesis of viral DNA. At the same time, it inhibits the activity of viral nucleotide reductase and inhibits the synthesis of viral DNA. It can also inhibit the activity of viral DNA terminal deoxynucleotidyl transferase, allowing Ara-A to penetrate into the viral DNA and connect to the end of the DNA chain 3prime;-OH position, inhibiting the continued synthesis of viral DNA.