Disease relevance of Famvir

• Famciclovir for genital herpes [1].
• CONCLUSIONS: Oral famciclovir, 500 mg or 750 mg three times daily for 7 days, is an effective and well-tolerated therapy for herpes zoster that decreases the duration of the disease's most debilitating complication, postherpetic neuralgia [2].
• Famciclovir for the suppression of symptomatic and asymptomatic herpes simplex virus reactivation in HIV-infected persons. A double-blind, placebo-controlled trial [3].
• Famciclovir and postherpetic neuralgia [4].
• Breakthrough reactivations that occurred while patients were receiving famciclovir were infrequent, short, and often asymptomatic, HSV-2 isolates from these reactivations were susceptible to penciclovir in vitro [3].

High impact information on Famvir

• Oral famciclovir for the suppression of recurrent genital herpes: a randomized controlled trial. Collaborative Famciclovir Genital Herpes Research Group [5].
• Patients who initiated famciclovir prior to viral shedding were more likely to not shed virus throughout [6].
• Acyclovir has been the mainstay for treating severe varicella-zoster virus infections; however, newer antiviral agents, including valacyclovir and famciclovir, have expanded therapeutic options for treating adults with herpes zoster [7].
• CONCLUSIONS: Antiviral chemotherapy with famciclovir results in clinically and statistically significant reductions in the symptoms associated with HSV infection and the symptomatic and asymptomatic shedding of HSV among HIV-positive persons [3].
• Famciclovir for the treatment of acute herpes zoster: effects on acute disease and postherpetic neuralgia. A randomized, double-blind, placebo-controlled trial. Collaborative Famciclovir Herpes Zoster Study Group [2].

Chemical compound and disease context of Famvir

• Combination therapy with lamivudine and famciclovir for chronic hepatitis B-infected Chinese patients: a viral dynamics study [8].
• OBJECTIVE: To compare the efficacy and safety of 7 days' treatment with famciclovir 500 mg twice a day versus acyclovir 400 mg five times a day, for mucocutaneous herpes simplex virus (HSV) infection in HIV-infected individuals [9].
• In this article, we review modeling and interpretation of kinetics data obtained from patients with chronic hepatitis B virus infection that has been treated with lamivudine, adefovir dipivoxil, and lamivudine plus famciclovir combination therapy [10].
• Brivudin was as effective as oral famciclovir 250mg three times daily in terms of the prevalence of PHN, the time to last vesicular eruption and lesion healing in another large, 7-day, phase III study in immunocompetent patients with herpes zoster [11].
• We describe our first experience with the new antiviral agent famciclovir in combination with a short course of prostaglandin E in a patient with severe hepatitis B after liver transplantation [12].

Biological context of Famvir

• Pharmacokinetics of famciclovir in subjects with varying degrees of renal impairment [13].
• Recently, nucleoside analogues, such as famciclovir, were found to have a direct suppressive effect on hepatitis B virus replication in both in vitro and in vivo studies [14].
• Viral persistence after anti-HBe seroconversion induced by interferon, lamivudine or famciclovir, was often associated with circulating HBV genomes harboring mutations in the precore promoter [15].
• To gain insight into the mechanism involved in the virus's resistance to famciclovir, the amino acid sequences of the terminal protein and reverse-transcriptase (RT) domains of the viral polymerase were determined during therapy among 28 patients [16].
• The antiviral response was independent of viral genotypes, and nonresponse to famciclovir was associated with a complex variability of the RT domain [16].

Anatomical context of Famvir

• Clinical and serological outcomes in these patients were compared with 24 HBsAg-positive recipients of allogeneic bone marrow transplantation who did not receive famciclovir (historical controls) [14].
• The two compounds differed in their effects on the acute neural infection, and ganglia explanted from famciclovir-treated mice were markedly reduced in their ability to reactivate virus, although neither drug affected latency if treatment was delayed for several months [17].
• This suggests that FCV is phosphorylated in Sertoli cells, and thereafter, leaks to neighboring spermatogonia, apparently through cell-cell junctions present, enabling trafficking of phosphorylated FCV [18].
• When adult transgenic (TG) mice were treated with famciclovir (FCV) for 4 wk, their spermatogenesis was totally abolished, with only Sertoli cells and few spermatids remaining in the seminiferous tubules [18].
• Thymosin-alpha1 and famciclovir combination therapy activates T-cell response in patients with chronic hepatitis B virus infection in immune-tolerant phase [19].

Associations of Famvir with other chemical compounds

• The sensitivity of the V542I mutant to penciclovir, the active metabolite of famciclovir, was further studied in tissue culture [20].
• All 5 famciclovir-associated mutations were sensitive to adefovir diphosphate (ADVDP) in in vitro enzymatic assays (<2.3-fold decreased sensitivity) [21].
• RESULTS: Equivalence was defined prospectively and famciclovir was equivalent to acyclovir in preventing new lesion formation: new lesions occurred in 16.7% and 13.3% of patients, respectively [difference, 3.4%; 95% confidence interval (CI), -4.8-11.5] [9].
• Here we report the functional characterization of a third polymerase mutation (rtV173L) associated with resistance to lamivudine and famciclovir. rtV173L was observed at baseline in 9 to 22% of patients who entered clinical trials of adefovir dipivoxil for the treatment of lamivudine-resistant HBV [22].
• In the last 2.5 years of famciclovir treatment, an increase in serum HBV DNA levels and a reduced sensitivity of the virion-associated DNA polymerase to penciclovir triphosphate were observed [23].

Gene context of Famvir

• In vitro evaluation of hepatitis B virus polymerase mutations associated with famciclovir resistance [21].
• Efficacy trials of combination therapy with famciclovir and IFN-alpha are warranted [24].
• The 6-deoxy derivative of penciclovir (BRL 42359) and the corresponding diacetyl and dipropionyl 6-deoxy derivatives (BRL 42810 [famciclovir; British approved name] and BRL 43599) were tested as oral prodrugs [25].
• RESULTS: Famciclovir induced rapid, dose-dependent suppression of viral replication and reduction in alanine aminotransferase (ALT), with greatest efficacy in the 500-mg tid treatment group [26].
• Efficacy of famciclovir treatment in chronic hepatitis B patients with different mutations at position 552 of the DNA polymerase gene [27].

Analytical, diagnostic and therapeutic context of Famvir

• Famciclovir (FCV) and lamivudine (LAM) reduce viral replication in patients with recurrent hepatitis B virus (HBV) infection after orthotopic liver transplantation (OLT) [28].
• Efficacy against chronic hepatitis B virus (HBV) infection has been demonstrated in an animal model and in recent clinical trials of famciclovir, the oral form of PCV [29].
• Potential influence factors (HBV-DNA and HBeAg pretransplant, HDV coinfection, pretreatment with famciclovir and immunosuppression) on treatment response were analyzed by log [30].
• Following oral administration famciclovir undergoes extensive first pass metabolism to penciclovir and essentially no parent compound is recovered from plasma or urine [31].
• Liver biopsies were obtained before starting famciclovir and within 1 month of completion of treatment.RESULTS: HBV DNA levels decreased in nine of the 15 patients and levels rose again after treatment (P<0.05) [32].

References