vidarabine

Vidarabine, also known as adenine arabinoside (ara-A), is a purine nucleoside analogue used as an antiviral agent. It was one of the early antiviral drugs developed for herpesviruses and was once widely used for systemic and ophthalmic infections caused by herpes simplex virus (HSV) and varicella-zoster virus (VZV).

Mechanism of action is based on phosphorylation to its active triphosphate form (ara-ATP) by cellular kinases. Ara-ATP inhibits viral DNA polymerase more effectively than host polymerases, interfering with viral DNA synthesis and, in high concentrations, can cause chain termination.

Clinical use has included treatment of severe HSV and VZV infections, including mucocutaneous disease and HSV keratitis. Ophthalmic preparations were used for herpetic eye infections, and systemic vidarabine was employed in certain neonatal and disseminated HSV cases when other options were limited. It is not active against cytomegalovirus and is generally not the preferred therapy today.

Administration and pharmacokinetics: vidarabine is given intravenously for systemic infections, and exists in topical ophthalmic formulations. Oral bioavailability is poor. After administration, the drug is phosphorylated to ara-ATP and distributed widely; it is largely renally excreted. Pharmacokinetic parameters can be affected by renal function.

Adverse effects are dose- and route-dependent and can include fever, malaise, nausea, vomiting, phlebitis with IV use, nephrotoxicity, and central nervous system effects such as confusion or seizures. Bone marrow suppression has also been reported in some cases.

History and status: vidarabine was among the first antivirals effective against HSV but has been largely supplanted by acyclovir and related agents due to better tolerability and safety profiles. It remains available in limited settings and for specific indications where alternatives are unsuitable.