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.

Synthetic nucleoside antiviral drugs have 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.

Synthetic nucleoside antiviral drugs have 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.

This product is a disinfectant and preservative. Its mechanism of action is to denature and kill bacterial proteins, and it has a killing effect on bacteria, fungi, and viruses.

This product has strong anti-inflammatory, liver cell membrane protection and liver function improvement effects. Pharmacological experiments have shown that oral administration of this product to mice can reduce the increase of serum alanine aminotransferase and aspartate aminotransferase caused by carbon tetrachloride, thioacetamide and D-galactosamine. It can also significantly reduce the morphological damage of D-galactosamine to the liver and improve the chronic damage of immune factors to the liver morphology.