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Famvir (Famciclovir)

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Famvir is the medication of high quality, which is taken in treatment of infections, which are caused by herpes viruses. It is also used in the treatment of cold sores, shingles, chicken pox, genital herpes. Famvir is acting by slowing the growth and spread of the herpes virus so that the body can fight off the infection. It is antiviral medicine.

Other names for this medication:
Ancivin, Famciclovirum, Famtrex, Lizhufeng, Oravir, Pentavir, Ziravir

Similar Products:
Zovirax , Valtrex , Combivir , Retrovir

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Also known as: Famciclovir.


The target of Famvir is the treatment of infections, which are caused by herpes viruses, cold sores, shingles, chicken pox, genital herpes.

Famvir is acting by slowing the growth and spread of the herpes virus so that the body can fight off the infection. It is antiviral medicine.

Famvir is also known as Famciclovir.

Generic name of Famvir is Famciclovir (oral).

Brand name of Famvir is Famvir.


Take Famvir tablets orally at the same time with water, with or without food.

The tablet should not be chewed.

Do not stop taking it suddenly.


If you overdose Famvir and you don't feel good you should visit your doctor or health care provider immediately.


Store at room temperature between 15 and 30 degrees C (59 and 86 degrees F) away from moisture and heat. Throw away any unused medicine after the expiration date. Keep out of reach of children.

Side effects

The most common side effects associated with Famvir are:

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Side effect occurrence does not only depend on medication you are taking, but also on your overall health and other factors.


Do not take Famvir while you are pregnant or have nurseling. Famvir can pass in breast milk and harm your baby.

Do not use Famvir if you are allergic to Famvir components.

Do not take probenecid (Benemid).

Be careful with Famvir if you have history of galactose intolerance, glucose-galactose malabsorption, kidney disease, severe lactase deficiency.

Avoid dehydrating.

It is forbidden to take Famvir if you are under 18.

Do not stop taking it suddenly.

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There was no difference in the parameters representing blocking of viral production (epsilon = 93%, 95% and 86%, respectively), turnover of free virus (half-life of 16 h, 10 h and 12 h, respectively) and turnover of infected hepatocytes (half-life of 9 days, 7 days and 4 days, respectively) between the lamivudine, lamivudine-famciclovir and lamivudine-ganciclovir treatment groups.

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Famciclovir has been shown to have potent and selective activity against herpesviruses. The possibility of a pharmacokinetic interaction between the anti-viral agent, famciclovir and allopurinol has been investigated in twelve healthy male volunteers following a single oral dose of famciclovir (500 mg) in the presence and absence of steady-state levels of allopurinol (300 mg). Similarly, the pharmacokinetic profiles of allopurinol and oxypurinol prior to and following a single dose of famciclovir were compared. Mean values of Cmax, AUC and terminal-phase half-life for penciclovir following administration of famciclovir alone at 3.3, 8.8 and 2.1 h, respectively were unchanged by co-administration of allopurinol. Similarly, mean urinary recovery and renal clearance values of penciclovir following famciclovir alone were 56.8% and 27 l.h-1, and when given with allopurinol 59.7% and 27.5 l.h-1, respectively. No evidence of accumulation of the inactive precursor to penciclovir, BRL 42359, was noted as a result of co-administration of the two drugs. Mean steady-state Cmax, AUC and terminal-phase half-life values for allopurinol after co-administration of allopurinol with famciclovir also appeared unchanged from values obtained after dosing of allopurinol alone, at 2.12, 5.73 and 1.38 h, respectively. Mean Cmax and AUC values of the active metabolite of allopurinol, oxypurinol were 11.2 and 96.0, respectively, and these were also unaltered by co-administration of famciclovir with allopurinol, with values of 10.6 micrograms/ml and 89.8 micrograms.h/ml, respectively.(ABSTRACT TRUNCATED AT 250 WORDS)

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Two-stage treatment was given to 100 patients suffering from GH with severe regular recurrences. One-stage treatment included famvir in combination with interferon (viferon) or interferon inductors (amixin, cycloferon) and antioxidants. Stage two treatment consisted of vaccine therapy of patients who failed prophylactic standard vaccination by allergometric technique.

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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]. The groups were comparable in time to complete healing (median 7 days for both groups; hazard ratio, 1.01; 95% CI, 0.79-1.29; P = 0.95), cessation of viral shedding (median of 2 days [hazard ratio = 0.93; 95% C.I. 0.68, 1.27; p = 0.64]), and loss of lesion-associated symptoms (median 4 days; hazard ratio, 0.99; 95% CI, 0.75-1.30; P = 0.93). Similar numbers in each group withdrew because of treatment failure. There were no differences between groups in the incidence of adverse events.

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The treatment decreased the duration of outbreaks in 87 % of participants and decreased the mean duration of outbreaks from 8.77 days and 6.7 days in the control groups to 2.87 days in the treatment group (P < 0.001, both groups). All participants reported no adverse experiences.

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The anti-herpesvirus activity of (1'S,2'R)-9-[[1',2'-bis(hydroxymethyl)cycloprop-1'-yl]methyl]guani ne (A-5021) was evaluated in murine cells and in several murine models of herpes simplex virus (HSV) infection. Against HSV type 1 (HSV-1), A-5021 was 15-30- and 30-60-fold more active, and against HSV type 2 (HSV-2), it was 2- and 8-fold more active than acyclovir and penciclovir in Balb/3T3 cells, respectively. When antiviral compounds were administered orally (once daily) to mice infected intraperitoneally with HSV-1 (Tomioka), A-5021 was more active than acyclovir or famciclovir in spite of its relatively low oral bioavailability. A-5021 was as active as penciclovir when the antiviral compounds were given intravenously (three times daily) to mice infected intraperitoneally with HSV-2 (186). In mice with a cutaneous HSV-1 (KOS) infection, three times daily oral therapy with A-5021 at 25 mg/kg per day produced more significant reduction in severity of skin lesions than equivalent treatment with acyclovir or famciclovir. In mice infected intracerebrally with HSV-1 (Tomioka), complete survival was observed in the group treated intravenously with A-5021 at 25 mg/kg per day (three times daily), while more than 50% of mice died in the groups treated intravenously with acyclovir of up to 100 mg/kg per day (three times daily). Moreover, A-5021 was more effective than acyclovir in clearing infectious virus from the brain. These findings demonstrate that A-5021 has potent anti-HSV activity in several murine models.

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Genital herpes is a chronic infection characterized by periodic reactivation. It can produce symptomatic disease in the host although asymptomatic viral excretion can also occur. It is currently the main cause of genital ulceration and an important public health problem that has substantial clinical, psychological, and economic repercussions. This review analyzes the currently available therapeutic options and regimens, which are based mainly on systemic use of antiviral agents such as aciclovir, valacyclovir, and famciclovir. In addition, special emphasis is placed on the prevention and management of this infection in specific situations, such as pregnant, pediatric, and immunocompromised patients.

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Data regarding antiviral activity were included if accepted and widely used methods were followed. Clinical trials in which a comparison with acyclovir or placebo was performed were given the highest priority.

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A series of 2-amino-9-(3-hydroxymethyl-4-alkoxycarbonyloxybut-1-yl)purines (4-10) and 2-amino-9-(2-(2-oxo-1,3-dioxan-5-yl)ethyl)purine (1) were synthesized as potential prodrugs of penciclovir and evaluated for their oral penciclovir bioavailability in mice and rats. Treatment of 2-(2-benzyloxyethyl)propane-1,3-diol (11) with 1,1'-carbonyldiimidazole in THF followed by hydrogenolytic removal of the benzyl group of the resulting cyclic carbonate 12 gave 5-(2-hydroxyethyl)-1,3-dioxan-2-one (13). Mesylation of the alcohol 13 and then a coupling reaction of the resulting mesylate 14 with 2-amino-6-chloropurine using anhydrous Cs2CO3 in DMF afforded 2-amino-6-chloro-9-(2-(2-oxo-1,3-dioxan-5-yl)ethyl)purine (16) after purification by flash column chromatography on silica gel using EtOAc/MeCN/Et3N as eluent. Hydrogenation of the 6-chloro cyclic carbonate 16 followed by a ring-opening reaction of the 6-deoxy cyclic carbonate 1 in a mixture of an appropriate alcohol and CHCl3 using activated SiO2 as a Lewis acid afforded the corresponding alkyl monocarbonate derivatives 3-10 in fair to good yields. Of the prodrugs tested in mice, the isopropyl monocarbonate 6 achieved the highest mean urinary recovery of penciclovir (53%), followed in order by the propyl monocarbonate 5 (51%), the isopentyl monocarbonate 10 (51%), the ethyl monocarbonate 4 (50%), and famciclovir (48%). In rats, the methyl monocarbonate 3, 4, 6, the n-butyl monocarbonate 7, and 10 (39-41%) showed levels of mean urinary recovery of penciclovir similar to that from famciclovir (40%). The alkyl monocarbonates 4-10 were found to be quite stable in the aqueous buffer solutions, and among them, 6 was the most stable with the half-lives (t1/2) of 88, >200, 61, and 26 days at pH 1.2, 6.0, 7.4, and 8.0, respectively. In addition, 6 was highly soluble in H2O (138.8 mg/mL, 20 degrees C).

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Famciclovir is an antiviral with efficacy and safety comparable to aciclovir, but famciclovir's more favorable pharmacokinetic profile enables a less frequent dosing regimen. Future trials will likely determine famciclovir's role in the suppression of HBV.

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Acyclovir was the first antiviral drug approved for the treatment of herpes zoster. Several new antiviral agents have since been introduced, one of which is famciclovir. The pharmacokinetics of famciclovir allow a more convenient dosing schedule than the schedule used with acyclovir. Famciclovir is metabolized in the liver, but the P450 cytochrome system is not involved. Both acyclovir and famciclovir accelerate cutaneous healing, but studies suggest that famciclovir may reduce the severity of postherpetic neuralgia when compared with placebo. Famciclovir is currently approved only for use in immunocompetent patients, but clinical trials involving immunocompromised patients are in progress.

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The current evidence demonstrates that long-term use of oral antiviral agents can prevent HSL, but the clinical benefit is small. We did not find evidence of an increased risk of adverse events. On the other hand, the evidence on topical antiviral agents and other interventions either showed no efficacy or could not confirm their efficacy in preventing HSL.

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famvir cost canada 2017-03-20

Daily acyclovir (or a suitable alternative) appears to be effective at preventing herpes Botox Injections Cost zoster virus in patients with myeloma who are receiving bortezomib, with or without corticosteroids.

famvir generic name 2015-02-01

The selective estrogen receptor modulator, raloxifene, has been demonstrated as a potent uncompetitive inhibitor of human liver aldehyde oxidase-catalyzed oxidation of phthalazine, vanillin, and nicotine-Delta1'(5')-iminium ion, with K(i) values of 0.87 to 1.4 nM. Inhibition was not time-dependent. Raloxifene has also been Celebrex Cost Cvs shown to be a noncompetitive inhibitor of an aldehyde oxidase-catalyzed reduction reaction of a hydroxamic acid-containing compound, with a K(i) of 51 nM. However, raloxifene had only small effects on xanthine oxidase, an enzyme related to aldehyde oxidase. In addition, several other compounds of the same therapeutic class as raloxifene were examined for their potential to inhibit aldehyde oxidase. However, none were as potent as raloxifene, since IC(50) values were orders of magnitude higher and ranged from 0.29 to 57 micro M. In an examination of analogs of raloxifene, it was shown that the bisphenol structure with a hydrophobic group on the 3-position of the benzthiophene ring system was the most important element that imparts inhibitory potency. The relevance of these data to the mechanistic understanding of aldehyde oxidase catalysis, as well as to the potential for raloxifene to cause drug interactions with agents for which aldehyde oxidase-mediated metabolism is important, such as zaleplon or famciclovir, is discussed.

famvir cost ireland 2017-06-26

Evidence from quality trials have shown significant reduction in risk of pain with valaciclovir and famciclovir for management of herpes zoster including ophthalmicus. Valaciclovir or famciclovir should be preferred treatment options in patients with herpes zoster as they both provide significant reduction in risk of herpes-zoster-associated pain. Furthermore, the superior pharmacokinetics and more convenient dosing regimens with the use Cymbalta Generic Price of valaciclovir and famciclovir clearly make them the preferred treatment option.

generic famvir 2015-04-01

To develop a population pharmacokinetic model for penciclovir (famciclovir is a prodrug of penciclovir) in adults and children and suggest an appropriate dose for children. Furthermore, to develop a limited sampling design based on Generic Avodart Cheap sampling windows for three different paediatric age groups (1-2, 2-5 and 5-12 years) using an adequate number of subjects for future pharmacokinetic studies.

famvir generic for 2015-09-29

We evaluated serum samples from 18 chronic hepatitis B virus ( Avapro Generic Date HBV) patients who underwent liver transplantation for the presence of HBV polymerase and S gene mutations and HBV genotype using a new commercially available sequencing assay. All three patients with hepatitis B immune globulin (HBIG) treatment failure followed by nucleoside analogue treatment failure were infected with HBV genotype C; a pre-existing HBV S antigen (HBsAg) mutation (sD144A) was identified in one patient pretransplant, while sG145R mutations emerged in the other two patients post-transplant. These HBsAg mutations persisted for the duration of the study (5-6 years), despite the absence of HBIG administration for a 4-5-year period. Significant viral polymerase mutations (rtL180M and rtM204I/V) also emerged in all of these patients following treatment with lamivudine and/or famciclovir. Four of six patients with HBIG breakthrough without nucleoside analogue treatment failure yielded potentially significant HBsAg mutations post transplant. These data do not support previous reports highlighting the disappearance of HBsAg mutants in liver transplant recipients after discontinuation of HBIG. Determination of HBV genotype, as well as identification of HBV polymerase and S gene mutations in liver transplant candidates may be warranted to optimize HBV management strategies post transplant.

famvir generic 2016-12-05

Twelve patients with a history of childhood malignancy and chronic hepatitis B were treated with prednisone for 4 weeks (0.6 mg/kg body weight per day orally for 3 weeks followed by 0.3 mg/kg body weight per day for 1 week) followed by IFN-alpha-2a (5 megaunits/m(2) body surface area, three times a week, subcutaneously) at least for 1 year. After 1 year of IFN-alpha monotherapy Seroquel Generic , treatment was discontinued in patients with HBeAg seroconversion as well as patients without HBeAg seroconversion and a decrease of serum hepatitis B virus (HBV) DNA level less than 0.5 logs of the basal level. Patients who had a decrease of the serum HBV DNA of more than 0.5 logs of the basal level underwent treatment continuation with IFN-alpha combined with famciclovir (FAM) (20 mg/kg body weight per day orally) for another year.

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The antiherpetic drugs acyclovir (ACV, valaciclovir) and penciclovir (famciclovir) are phosphorylated by viral thymidine kinase and terminate DNA synthesis. ASP2151 (amenamevir) and foscavir (PFA) directly inhibit viral helicase-primase and DNA polymerase, respectively, and inhibit replication of herpes simplex virus (HSV) and varicella-zoster virus. ACV, ASP2151, and PFA all Epivir Cost inhibit HSV with a different mechanism of action and as a consequence, the kinetics of viral DNA accumulation and progeny virus production differ. This study focused on how viral DNA synthesis and its related events in the replication cycle would influence anti-HSV action of ACV, ASP2151, and PFA. ASP2151 suppressed HSV replication more efficiently than ACV at 10 × 50% effective concentration of plaque formation (EC50), when treatments were started 0-24 h after infection. ASP2151 and PFA were more potent than ACV in suppressing viral DNA synthesis and infectious virus production when they were added up to 3 h following infection. The virus replicated in the presence of ACV was compared for the ratios of HSV DNA copy number to infectivity with that without ACV and infectivity of ACV-treated virus was less efficient than that without ACV-treatment. The EC50 of infected cells in the time course after infection was preserved in PFA, limited in ASP2151, and much increased for ACV, indicating that viral DNA synthesis had little effect on antiviral action of PFA and ASP2151 but reduced the susceptibility of ACV. ASP2151 showed a preferable profile as an anti-herpetic agent with a better pharmacokinetic profile than ACV.

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To evaluate the effects of famciclovir treatment of Generic Priligy 60mg patients with chronic hepatitis B virus (HBV) infection.

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Three patients are described who developed hepatitis B reactivation and liver decompensation after stopping therapy. One of the three patients was participating in a famciclovir trial and the other two were receiving lamivudine therapy for active hepatitis B infection. All three patients had documented hepatitis B flares, and all had hepatitis B virus DNA detected at Ventolin Inhaler Cheap that time. All patients developed decompensated liver disease despite one patient having had a prior liver biopsy showing absence of cirrhosis. Reintroduction of lamivudine therapy failed to halt progression of liver decompensation even after hepatitis B virus DNA had been demonstrated to be absent. Sequencing for lamivudine resistant mutants in two cases where serum was available failed to show evidence of mutations associated with lamivudine resistance.

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Three strategies of treatment had no different effects on the change of patients' ALT levels. The serum HBV DNA became negative after treatment in 89.3% (25/28) of patients treated with combination of lamivudine and famciclovir, 66.7% (20/30) of patients treated with lamivudine, and 40.6% (13/32) of patients treated with famciclovir. The rate of serum HBeAg loss in 3 Evista Generic Alternative groups were 28.6% (8/28), 23.3% (7/30) and 21.9% (7/32), respectively.

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A balanced crossover design was used. Phase I consisted of a single administration (62.5 mg, PO) of famciclovir. Phase II consisted of multiple doses of famciclovir (62.5 mg, PO) given every 8 or 12 hours for 3 days. Plasma penciclovir concentrations were assayed via liquid chromatography-mass spectrometry at fixed time points after famciclovir Priligy Buy Online administration.