It is the L-valyl ester of acyclovir; the result of an effort to develop a prodrug to improve acyclovir oral bioavailability.

Valaciclovir Hydrochloride is rapidly converted to acyclovir, which inhibits DNA synthesis. Acyclovir must be phosphorylated intracellularly to be active. Acyclovir is converted to the monophosphate by viral thymidine kinase, then to diphosphate by cellular guanylate kinase, and finally to the triphosphate by various cellular enzymes. Acyclovir triphosphate competitively inhibits viral DNA polymerase, and to a lesser extent human DNA polymerase. Acyclovir triphosphate also competes with the natural substrate, deoxyguanosine triphosphate, for incorporation into viral DNA. Once incorporated, acyclovir triphosphate inhibits DNA synthesis by acting as a chain terminator. Formation of a complex at the end of the DNA strand may lead to irreversible inactivation of viral DNA polymerase. Herpes virus DNA polymerases differ in sensitivity to acyclovir. Uninfected cells show only minimal phosphorylation of acyclovir, and there is only a small amount of acyclovir taken up into these cells. Acyclovir is effective only against actively replicating viruses; it does not eliminate the latent herpes virus genome.