Foscarnet: Difference between revisions
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==Mechanism of Action== | ==Mechanism of Action== | ||
FOSCAVIR is an organic analogue of inorganic pyrophosphate that inhibits replication of herpes viruses in vitro including cytomegalovirus (CMV) and herpes simplex virus types 1 and 2 (HSV-1 and HSV-2). | |||
FOSCAVIR exerts its antiviral activity by a selective inhibition at the pyrophosphate binding site on virus-specific DNA polymerases at concentrations that do not affect cellular DNA polymerases. FOSCAVIR does not require activation (phosphorylation) by thymidine kinase or other kinases and therefore is active in vitro against HSV TK deficient mutants and CMV UL97 mutants. Thus, HSV strains resistant to acyclovir or CMV strains resistant to ganciclovir may be sensitive to FOSCAVIR. However, acyclovir or ganciclovir resistant mutants with alterations in the viral DNA polymerase may be resistant to FOSCAVIR and may not respond to therapy with FOSCAVIR. The combination of FOSCAVIR and ganciclovir has been shown to have enhanced activity in vitro. | |||
==References== | ==References== | ||
Revision as of 21:51, 5 January 2014
Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]
Overview
Foscarnet is the conjugate base of the chemical compound with the formula HO2CPO3H2. This phosphonic acid derivative is (marketed by AstraZeneca as foscarnet sodium under the trade name Foscavir®) is an antiviralmedication used to treat herpes viruses, including cytomegalovirus (CMV) and herpes simplex viruses types 1 and 2 (HSV-1 and HSV-2). It is particularly used to treat CMV retinitis.
Category
Antiviral
US Brand Names
FOSCAVIR®
FDA Package Insert
Description | Clinical Pharmacology | Microbiology | Indications and Usage | Contraindications | Warnings and Precautions | Adverse Reactions | Drug Interactions | Overdosage | Clinical Studies | Dosage and Administration | How Supplied | Labels and Packages
Mechanism of Action
FOSCAVIR is an organic analogue of inorganic pyrophosphate that inhibits replication of herpes viruses in vitro including cytomegalovirus (CMV) and herpes simplex virus types 1 and 2 (HSV-1 and HSV-2).
FOSCAVIR exerts its antiviral activity by a selective inhibition at the pyrophosphate binding site on virus-specific DNA polymerases at concentrations that do not affect cellular DNA polymerases. FOSCAVIR does not require activation (phosphorylation) by thymidine kinase or other kinases and therefore is active in vitro against HSV TK deficient mutants and CMV UL97 mutants. Thus, HSV strains resistant to acyclovir or CMV strains resistant to ganciclovir may be sensitive to FOSCAVIR. However, acyclovir or ganciclovir resistant mutants with alterations in the viral DNA polymerase may be resistant to FOSCAVIR and may not respond to therapy with FOSCAVIR. The combination of FOSCAVIR and ganciclovir has been shown to have enhanced activity in vitro.