synthetase, and the biologically generated triphosphate competitively inhibits thymidine triphosphate incorporation into DNA by DNA polymerase. In addition, trifluridine in its triphosphate form is incorporated into viral and cellular DNA, creating fragile, poorly functioning DNA.
Trifluridine is approved in the United States for the treatment of primary keratoconjunctivitis and recurrent epithelial keratitis caused by HSV types 1 and 2. Topical trifluridine shows some efficacy in patients with acyclovir-resistant HSV cutaneous infections. Trifluridine solutions are heat sensitive and require refrigeration.
Chemically, vidarabine (Vira-A), is 9-jS-d-arabinofuranosy-ladenine. The drug is the 2' epimer of natural adenosine. Introduced in 1960 as a candidate anticancer agent, vidara-bine was found to have broad-spectrum activity against DNA viruses.34 The drug is active against herpesviruses, poxviruses, rhabdoviruses, hepadnavirus, and some RNA tumor viruses. Vidarabine was marketed in the United States in 1977 as an alternative to idoxuridine for the treatment of HSV keratitis and HSV encephalitis. Although the agent was initially prepared chemically, it is now obtained by fermentation with strains of Streptomyces antibioticus.
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