Famciclovir microbiology
Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]
Microbiology
Antiviral activity: In cell culture studies, Penciclovir is inhibitory to the following herpes viruses: HSV-1, HSV-2 and ZVZ. The antiviral activity of Penciclovir against wild type strains grown on human foreskin fibroblasts was assessed with a plaque reduction assay and staining with crystal violet 3 days postinfection for HSV and 10 days postinfection for ZVZ. The median EC50 values of Penciclovir against laboratory and clinical isolates of HSV-1, HSV-2, and ZVZ were 2 µM (range 1.2 to 2.4 µM, n=7), 2.6 µM (range 1.6 to 11 µM, n=6), and 34 µM (range 6.7 to 71 µM, n=6), respectively.
Resistance: Penciclovir-resistant mutants of HSV and ZVZ can result from mutations in the viral thymidine kinase (TK) and DNA polymerase genes. Mutations in the viral TK gene may lead to complete loss of TK activity (TK negative), reduced levels of TK activity (TK partial), or alteration in the ability of viral TK to phosphorylate the drug without an equivalent loss in the ability to phosphorylate thymidine (TK altered). The median EC50 values observed in a plaque reduction assay with Penciclovir resistant HSV-1, HSV-2, and ZVZ were 69 µM (range 14 to 115 µM, n=6), 46 µM (range 4 to >395 µM, n=9), and 92 µM (range 51 to 148 µM, n=4), respectively. The possibility of viral resistance to Penciclovir should be considered in patients who fail to respond or experience recurrent viral shedding during therapy.
Cross-resistance: Cross-resistance has been observed among HSV DNA polymerase inhibitors. The most commonly encountered acyclovir resistant mutants that are TK negative are also resistant to Penciclovir.[1]
References
- ↑ "http://www.accessdata.fda.gov/drugsatfda_docs/label/2011/020363s037lbl.pdf" (PDF). External link in
|title=(help)
Adapted from the FDA Package Insert.