Fenivir Crème
Fenivir Crème Uses, Dosage, Side Effects, Food Interaction and all others data.
Fenivir Crème is a synthetic acyclic guanine derivative with antiviral activity used for the treatment of various herpes simplex virus (HSV) infections. Displaying low toxicity and good selectivity, penciclovir is a nucleoside analogue.
Fenivir Crème is the active metabolite of the oral product famciclovir. The more favorable results observed with topical penciclovir versus topical acyclovir for the treatment of herpes labialis may be due to the longer intracellular half-life of penciclovir in HSV-infected cells. The activated drug inhibits the viral DNA polymerase. This impairs the ability of the virus to replicate within the cell.
Trade Name | Fenivir Crème |
Availability | Prescription only |
Generic | Penciclovir |
Penciclovir Other Names | Penciclovir, Penciclovirum |
Related Drugs | acyclovir, valacyclovir, Valtrex, Zovirax, tetracaine topical |
Type | |
Formula | C10H15N5O3 |
Weight | Average: 253.2578 Monoisotopic: 253.117489371 |
Protein binding | Less than 20%. |
Groups | Approved |
Therapeutic Class | |
Manufacturer | |
Available Country | Switzerland |
Last Updated: | September 19, 2023 at 7:00 am |
Uses
Fenivir Crème is a topical nucleoside polymerase inhibitor used in the treatment of recurrent herpes labialis.
Used to treat recurrent cold sores on the lips and face from various herpesvirus invections.
Fenivir Crème is also used to associated treatment for these conditions: Cold Sore
How Fenivir Crème works
Fenivir Crème has in vitro activity against herpes simplex virus types 1 (HSV-1) and 2 (HSV-2). In cells infected with HSV-1 or HSV-2, viral thymidine kinase phosphorylates penciclovir to a monophosphate form. The monophosphate form of the drug is then converted to penciclovir triphosphate by cellular kinases. The intracellular triphosphate of penciclovir is retained in vitro inside HSV-infected cells for 10-20 hours, compared with 0.7-1 hour for acyclovir. in vitro studies show that penciclovir triphosphate selectively inhibits viral DNA polymerase by competing with deoxyguanosine triphosphate. Inhibition of DNA synthesis of virus-infected cells inhibits viral replication. In cells not infected with HSV, DNA synthesis is unaltered. Resistant mutants of HSV can occur from qualitative changes in viral thymidine kinase or DNA polymerase. The most commonly encountered acyclovir-resistant mutants that are deficient in viral thymidine kinase are also resistant to penciclovir.
Toxicity
Symptoms of overdose include headache, abdominal pain, increased serum lipase, nausea, dyspepsia, dizziness, and hyperbilirubinemia.
Food Interaction
No interactions found.Elimination Route
Measurable penciclovir concentrations were not detected in plasma or urine of healthy male volunteers (n= 12) following single or repeat application of the 1% cream at a dose of 180 mg penciclovir daily.
Half Life
2 hours
Innovators Monograph
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