World Library  
Flag as Inappropriate
Email this Article

Penciclovir

Article Id: WHEBN0005662960
Reproduction Date:

Title: Penciclovir  
Author: World Heritage Encyclopedia
Language: English
Subject: Famciclovir, Thymidine kinase from herpesvirus, Edoxudine, Imiquimod, Resiquimod
Collection: Anti-Herpes Virus Drugs, Purines
Publisher: World Heritage Encyclopedia
Publication
Date:
 

Penciclovir

Penciclovir
Systematic (IUPAC) name
2-amino-9-[4-hydroxy-3-(hydroxymethyl)butyl]-1H-purin-6(9H)-one
Clinical data
Trade names Denavir
AHFS/Drugs.com
MedlinePlus
Pregnancy
category
  • AU: B1
  • US: B (No risk in non-human studies)
Legal status
Routes of
administration
Topical
Pharmacokinetic data
Bioavailability 1.5% (oral), negligible (topical)
Protein binding <20%
Metabolism Viral thymidine kinase
Biological half-life 2.2–2.3 hours
Excretion Renal
Identifiers
CAS Registry Number  Y
ATC code D06 J05
PubChem CID:
DrugBank  Y
ChemSpider  Y
UNII  Y
KEGG  Y
ChEBI  Y
ChEMBL  Y
Chemical data
Formula C10H15N5O3
Molecular mass 253.258 g/mol
 Y   

Penciclovir (INN) is a guanosine 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 (NDC 0135-0315-52), Vectavir and Fenivir. Famciclovir is a prodrug of penciclovir with improved oral bioavailability.[1]

Contents

  • Efficacy 1
  • Mode of action and selectivity 2
  • See also 3
  • References 4

Efficacy

In herpes labialis, the duration of healing, pain and detectable virus is reduced by up to one day,[2] compared with the total duration of 2–3 weeks of disease presentation.

Mode of action and selectivity

Penciclovir is inactive in its initial form. Within a virally infected cell a viral thymidine kinase adds a phosphate group to the penciclovir molecule; this is the rate-limiting step in the activation of penciclovir. Cellular (human) kinases then add two more phosphate groups, producing the active penciclovir triphosphate. This activated form inhibits viral DNA polymerase, thus impairing the ability of the virus to replicate within the cell.

The selectivity of penciclovir may be attributed to two factors. First, cellular thymidine kinases phosphorylate the parent form significantly less rapidly than does the viral thymidine kinase, so the active triphosphate is present at much higher concentrations in virally infected cells than in uninfected cells. Second, the activated drug binds to viral DNA polymerase with a much higher affinity than to human DNA polymerases. As a result, penciclovir exhibits negligible cytotoxicity to healthy cells.

The structure and mode of action of penciclovir are very similar to that of other nucleoside analogues, such as the more widely used aciclovir. A difference between aciclovir and penciclovir is that the active triphosphate form of penciclovir persists within the cell for a much longer time than the activated form of aciclovir, so the concentration within the cell of penciclovir will be higher given equivalent cellular doses.

See also

References

  1. ^ "Instead of my cold sores, people now notice my lipstick".  
  2. ^ Farmaceutiska Specialiteter i Sverige - the Swedish official drug catalog. [http://www.fass.se Fass.se --> Vectavir. Retrieved on August 12, 2009. Translated from "Tiden för läkning, smärta och påvisbart virus förkortas med upp till ett dygn."
This article was sourced from Creative Commons Attribution-ShareAlike License; additional terms may apply. World Heritage Encyclopedia content is assembled from numerous content providers, Open Access Publishing, and in compliance with The Fair Access to Science and Technology Research Act (FASTR), Wikimedia Foundation, Inc., Public Library of Science, The Encyclopedia of Life, Open Book Publishers (OBP), PubMed, U.S. National Library of Medicine, National Center for Biotechnology Information, U.S. National Library of Medicine, National Institutes of Health (NIH), U.S. Department of Health & Human Services, and USA.gov, which sources content from all federal, state, local, tribal, and territorial government publication portals (.gov, .mil, .edu). Funding for USA.gov and content contributors is made possible from the U.S. Congress, E-Government Act of 2002.
 
Crowd sourced content that is contributed to World Heritage Encyclopedia is peer reviewed and edited by our editorial staff to ensure quality scholarly research articles.
 
By using this site, you agree to the Terms of Use and Privacy Policy. World Heritage Encyclopedia™ is a registered trademark of the World Public Library Association, a non-profit organization.
 


Copyright © World Library Foundation. All rights reserved. eBooks from Project Gutenberg are sponsored by the World Library Foundation,
a 501c(4) Member's Support Non-Profit Organization, and is NOT affiliated with any governmental agency or department.