Penciclovir: Difference between revisions
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==Mechanism of Action== | ==Mechanism of Action== | ||
The antiviral compound penciclovir has inhibitory activity against [[herpes simplex virus]] types 1 ([[HSV]]-1) and 2 ([[HSV]]-2). In cells infected with [[HSV]]-1 or [[HSV]]-2, the viral thymidine kinase phosphorylates penciclovir to a monophosphate form that, in turn, is converted by cellular kinases to the active form penciclovir triphosphate. Biochemical studies demonstrate that penciclovir triphosphate inhibits [[HSV]] 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 and 20 hours in [[HSV]]-2 infected cells grown in culture. However, the clinical significance of the intracellular half-life is unknown. | |||
==References== | ==References== | ||
Revision as of 15:59, 6 January 2014
Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]
Overview
Penciclovir (INN) (IPA: Template:IPA) is a guanine analogue antiviral drug used for the treatment of various herpesvirus infections. It is a nucleoside analogue which exhibits low toxicity and good selectivity. Because penciclovir is absorbed poorly when given orally (by mouth) it is used more as a topical treatment, and is the active ingredient in the cold sore medications Denavir and Fenistil. Famciclovir is a prodrug of penciclovir with improved oral bioavailability.
Category
Anticiral
US Brand Names
DENAVIR®
FDA Package Insert
Description | Clinical Pharmacology | Microbiology | Indications and Usage | Contraindications | Warnings and Precautions | Adverse Reactions | Drug Interactions | Overdosage | Clinical Studies | Dosage and Administration | Labels and Packages
Mechanism of Action
The antiviral compound penciclovir has inhibitory activity against herpes simplex virus types 1 (HSV-1) and 2 (HSV-2). In cells infected with HSV-1 or HSV-2, the viral thymidine kinase phosphorylates penciclovir to a monophosphate form that, in turn, is converted by cellular kinases to the active form penciclovir triphosphate. Biochemical studies demonstrate that penciclovir triphosphate inhibits HSV 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 and 20 hours in HSV-2 infected cells grown in culture. However, the clinical significance of the intracellular half-life is unknown.