VIDARABINE (200 MG)G-2939UG/MG(AI)

Absorption

Systemetic absorption of vidarabine should not be expected to occur following ocular administration and swallowing lacrimal secretions.

Toxicity

Acute massive overdosage by oral ingestion of the ophthalmic ointment has not occurred. However, the rapid deamination to arabinosylhypoxanthine should preclude any difficulty. The oral LD50 for vidarabine is greater than 5020 mg/kg in mice and rats. No untoward effects should result from ingestion of the entire contents of the tube. Overdosage by ocular instillation is unlikely because any excess should be quickly expelled from the conjunctival sac.

The Uses of VIDARABINE (200 MG)G-2939UG/MG(AI)

Antiviral.

Background

A nucleoside antibiotic isolated from Streptomyces antibioticus. It has some antineoplastic properties and has broad spectrum activity against DNA viruses in cell cultures and significant antiviral activity against infections caused by a variety of viruses such as the herpes viruses, the vaccinia VIRUS and varicella zoster virus.

Indications

For treatment of chickenpox - varicella, herpes zoster and herpes simplex

Definition

A biologically active pharmaceu- tical product having both antitumor and antiviral properties. It was originally prepared (1959) by chemical synthesis at Stanford Research Institute, and later isolated from a fermentation beer of Strep- tomyces antibioticus.

brand name

Vira-A (Parkdale).

Pharmacokinetics

Vidarabine is a synthetic purine nucleoside analogue with in vitro and in vivo inhibitory activity against herpes simplex virus types 1 (HSV-1), 2 (HSV-2), and varicella-zoster virus (VZV). The inhibitory activity of Vidarabine is highly selective due to its affinity for the enzyme thymidine kinase (TK) encoded by HSV and VZV. This viral enzyme converts Vidarabine into Vidarabine monophosphate, a nucleotide analogue. The monophosphate is further converted into diphosphate by cellular guanylate kinase and into triphosphate by a number of cellular enzymes. In vitro, Vidarabine triphosphate stops the DNA replication of herpes virus by being incorporated into the DNA strand and preventing the formation of phosphodiester bridges between bases. This ultimately leads to destabilization of the viral DNA strands.

Metabolism

In laboratory animals, vidarabine is rapidly deaminated in the gastrointestinal tract to Ara-Hx.