<unk>  is inactive in its initial form. Within a virally infected cell a viral thymidine kinase adds a phosphate group to the<unk>  molecule; this is the rate-limiting step in the activation of<unk> . Cellular (human) kinases then add two more phosphate groups, producing the active<unk>  triphosphate. This activated form inhibits viral DNA polymerase, thus impairing the ability of the virus to replicate within the cell. The selectivity of<unk>  may be attributed to two factors. First, cellular thymidine kinases phosphorylate the parent form significantly less rapidly than does the viral thymidine kinase, so the active triphosphate is present at much higher concentrations in virally infected cells than in uninfected cells. Second, the activated drug binds to viral DNA polymerase with a much higher affinity than to human DNA polymerases. As a result,<unk>  exhibits negligible cytotoxicity to healthy cells. The structure and mode of action of<unk>  are very similar to that of other nucleoside analogues, such as the more widely used aciclovir. A difference between aciclovir and<unk>  is that the active triphosphate form of<unk>  persists within the cell for a much longer time than the activated form of aciclovir, so the concentration within the cell of<unk>  will be higher given equivalent cellular doses.
Penciclovir
Aciclovir
Valganciclovir
Famciclovir
Ganciclovir
Alcaftadine
Letermovir
Amantadine