n docosanol/herpes genitalis

The 22-carbon fatty alcohol, n-docosanol, exhibits in vitro antiviral activity against several lipid-enveloped viruses including herpes simplex viruses 1 and 2 by a mechanism that interferes with normal viral entry into target cells. We previously reported that mammalian cells incorporate

n-Docosanol has been shown to have antiviral activity. To demonstrate the efficacy of n-docosanol 10% cream in the treatment of recurrent herpes labialis, a randomised, double-blind, parallel group, placebo-controlled study was undertaken in 63 patients. In a crossover extension, 22 of the patients

BACKGROUND There are 3 new topical treatments for herpes labialis that have either been approved by the US Food and Drug Administration (penciclovir cream [Denavir] and n-docosanol cream [Abreva]) or recently undergone extensive clinical evaluation (acyclovir cream). The relative efficacy of these

BACKGROUND Recurrent herpes labialis (RHL) is a significant disorder with social and health consequences that affects upwards of 20 - 40% of the adult population. Docosanol is the only FDA-approved topical agent that is available over the counter for management of RHL. Its mechanism of action is

n-Docosanol-treated cells resist infection by a variety of lipid-enveloped viruses including the herpesviruses. Previous studies of the mechanism of action demonstrated that n-docosanol inhibits an event prior to the expression of intermediate early gene products but subsequent to HSV attachment.

Of the large number of agents under development for the treatment of herpes virus infections [herpes simplex virus types 1 and 2 (HSV-1 and HSV-2), varicella zoster virus (VZV), cytomegalovirus (CMV), Epstein-Barr virus (EBV)], only ten have apparently reached clinical development. Aciclovir was

Interactions between docosanol (n-docosanol, behenyl alcohol) and nucleoside or pyrophosphate analogs were investigated in vitro. The anti-HSV activity of acyclovir (ACV) was synergistically enhanced by treatment of cells with docosanol as judged by inhibition of progeny virus production and plaque