| Indication |
For the treatment of acute herpes zoster (shingles). Also for the
treatment or suppression of recurrent genital herpes in immunocompetent
patients and treatment of recurrent mucocutaneous herpes simplex
infections in HIV infected patients. |
| Pharmacodynamics |
Famciclovir is a prodrug that undergoes rapid biotransformation
to the active antiviral compound penciclovir. Penciclovir is an
anti-viral drug which has inhibitory activity against herpes simplex
virus types 1 (HSV-1) and 2 (HSV-2) and varicella zoster virus (VZV).
Therefore, herpes viral DNA synthesis and replication are selectively
inhibited. |
| Mechanism of action |
Famciclovir undergoes rapid biotransformation to the active
antiviral compound penciclovir, which has inhibitory activity against
herpes simplex virus types 1 (HSV-1) and 2 (HSV-2) and varicella zoster
virus (VZV). In cells infected with HSV-1, HSV-2 or VZV, viral thymidine
kinase phosphorylates penciclovir to a monophosphate form that, in
turn, is converted to penciclovir triphosphate by cellular kinases. In
vitro studies demonstrate that penciclovir triphosphate inhibits HSV-2
DNA polymerase competitively with deoxyguanosine triphosphate.
Consequently, herpes viral DNA synthesis and, therefore, replication are
selectively inhibited. |
| Absorption |
77 % |
| Volume of distribution |
- 1.08±0.17 L/kg [healthy male subjects following a single
intravenous dose of penciclovir at 400 mg administered as a 1-hour
intravenous infusion]
|
| Protein binding |
20-25% |
| Metabolism |
Hepatic |
| Route of elimination |
Active tubular secretion contributes to the renal elimination of penciclovir. |
| Half life |
10 hours |
| Clearance |
- 36.6 +/- 6.3 L/hr [healthy male]
- 0.48 +/- 0.09 L/hr/kg [healthy male]
|
| Toxicity |
Symptoms of overdose include constipation, diarrhea, dizziness, fatigue, fever, headache, nausea, and vomiting. |
