Microbiology

Mechanism of Antiviral Action: Famciclovir undergoes rapid biotransformation to the active antiviral compound penciclovir, which has demonstrated inhibitory activity against herpes simplex virus types 1 (HSV-1) and 2 (HSV-2) and varicella zoster virus (VZV). In cells infected with HSV-1, HSV-2 or VZV, the viral thymidine kinase phosphorylates penciclovir to a monophosphate form that, in turn, is converted to penciclovir triphosphate by cellular kinases. In vitro studies demonstrate that penciclovir triphosphate inhibits HSV-2 DNA polymerase competitively with deoxyguanosine triphosphate. Consequently, herpes viral DNA synthesis and, therefore, replication are selectively inhibited.

Penciclovir triphosphate has an intracellular half-life of 10 hours in HSV-1-, 20 hours in HSV-2- and 7 hours in VZV-infected cells grown in culture; however, the clinical significance is unknown.

Antiviral Activity: In cell culture studies, penciclovir is inhibitory to the following herpes viruses (listed in decreasing order of potency): HSV-1, HSV-2 and VZV. Sensitivity test results, expressed as the concentration of the drug required to inhibit the growth of the virus by 50% (EC50) or 99% (EC99) in cell culture, vary greatly depending upon a number of factors, including the assay protocols, and in particular the cell type used. See Table 1.

Table 1

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