Denavir

Topical Antivirals

Penciclovir is administered topically to lesions on the lips and face. Application to mucous membranes is not recommended.
Avoid application on or near the eyes.

erythema / Early / 50.0-50.0
edema / Delayed / 0-1.0

headache / Early / 5.3-5.3
skin irritation / Early / 1.3-1.3
parosmia / Delayed / 0-1.0
urticaria / Rapid / 0-1.0
skin discoloration / Delayed / 0-1.0
paresthesias / Delayed / 0-1.0
hypoesthesia / Delayed / 0.9-0.9
dysgeusia / Early / 0.2-0.2

Denavir

Rx

Topical antiviral medication; active metabolite of famciclovir
For treatment of herpes labialis in patients 12 years and older
More favorable results than with topical acyclovir

Apply cream every 2 hours while awake for 4 days beginning as soon as possible after onset of symptoms (during the prodrome or when lesions appear).[46977]

Apply cream every 2 hours while awake for 4 days beginning as soon as possible after onset of symptoms (during the prodrome or when lesions appear).

No dosage adjustment is recommended for topical therapy. The pharmacokinetics of penciclovir have not been evaluated in patients with severe uncompensated hepatic impairment.

No dosage adjustment needed for topical therapy.

There are no drug interactions associated with Penciclovir products.

Denavir/Penciclovir Sodium Topical Cream: 1%

No maximum dosage information is available.

No maximum dosage information is available.

No maximum dosage information is available.

 >= 12 years: No maximum dosage information is available.
 < 12 years: Safety and efficacy have not been established.

Safety and efficacy have not been established.

Penciclovir is a deoxynucleoside analog DNA polymerase inhibitor with 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 to 20 hours, compared with 0.7 to 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 cell culture studies, reduced susceptibility to penciclovir has been observed in HSV-1 and HSV-2 isolates with mutations in the viral thymidine kinase (TK) and DNA polymerase (POL) genes. These mutations lead to a decreased amount of viral thymidine kinase, and consequently a reduction in the initial phosphorylation of penciclovir. HSV resistance should be considered in patients who fail to respond or experience recurrent viral shedding during penciclovir therapy. Similar TK and POL mutations have been identified in HSV isolates from patients who have failed acyclovir therapy. Cross-resistance to penciclovir has been observed in acyclovir-resistant HSV-1 and HSV-2 isolates with TK and POL mutations and in foscarnet-resistant HSV-1 isolates with POL mutations.[46977]

Penciclovir cream is applied topically to the lips or face. Application to mucous membranes is not recommended.

In a study of healthy male volunteers, measurable penciclovir concentrations were not detected in plasma or urine following single or repeat application of the 1% cream at a dose of 180 mg penciclovir daily (about 67 times the estimated usual clinical dose).

No adequate and well-controlled studies have been conducted regarding the use of penciclovir during pregnancy; however, because penciclovir is not systemically absorbed following topical application, fetal drug exposure is not expected.[46977]

It is not known if penciclovir is excreted in human milk; however, because penciclovir is not systemically absorbed following topical application, fetal drug exposure is not expected. Potential alternatives to consider during breast-feeding include acyclovir and valacyclovir. However, patient factors, local susceptibility patterns, and specific microbial susceptibility should be assessed before choosing an alternative agent. Consider the benefits of breast-feeding, the risk of potential infant drug exposure, and the risk of an untreated or inadequately treated condition. If a breast-feeding infant experiences an adverse effect related to a maternally ingested drug, healthcare providers are encouraged to report the adverse effect to the FDA.