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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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The results of a considerable number of recent prospective studies have demonstrated that greater acute pain severity in herpes zoster patients is associated with a significantly greater risk of developing postherpetic neuralgia (PHN). Only a few studies have examined the relationships between acute pain severity and demographic characteristics and clinical features of patients with herpes zoster, however, and the results of these studies have been inconsistent. To clarify these relationships, data from 1778 herpes zoster patients studied within 72 h of rash onset in four clinical trials of the antiviral agent famciclovir were examined. Univariate and multivariate analyses indicated that greater acute pain severity was significantly associated with greater age, female sex, greater rash severity, the presence of a prodrome, and primary involvement of non-trigeminal dermatomes. These results demonstrate that three of the established risk factors for PHN - older age, greater rash severity, and the presence of a prodrome - are also associated with more severe acute pain assessed soon after rash onset in patients with herpes zoster. The results of this study are consistent with the recommendation that herpes zoster patients who are older, who have had a prodrome, or who have severe rash or severe acute pain should be targeted for interventions designed to prevent PHN.

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Persons 50 years of age and older are not only at increased risk of developing herpes zoster, they are also more likely to suffer the long-term morbidity of postherpetic neuralgia (PHN). PHN is pain persisting after the rash of herpes zoster has healed. PHN affects at least 40% of all herpes zoster patients over age 50 and over 75% of herpes zoster patients over age 75; PHN is the single most common neurologic condition in elderly patients.

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384 subjects were randomized. There was a highly statistically significant difference between treatments in time to first recurrence of symptoms in favor of suppressive treatment (p<0.0001). There was no significant difference between treatments in total score of the RGHQoL or in subject satisfaction with treatment.

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Perioperative application of famciclovir is not recommendable, whereas lamivudine seems to lower recurrence rates significantly. Whether the observed effect is due to pre- or postoperative application remains to be addressed in further studies. In addition the long-term course has to be awaited.

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Randomized, double-blinded placebo-controlled clinical trial in a tertiary referral center, with 12 subjects in the active treatment arm and 11 subjects in the placebo arm.

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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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Herpes simplex virus (HSV) infections are very common in the general population and can be treated with the nucleoside analogue acyclovir. Acyclovir is initially phosphorylated intracellularly in HSV-infected cells by a viral-specific thymidine kinase to acyclovir-monophosphate. The monophosphate is subsequently di- and triphosphorylated by host cellular kinases to the active form of the drug, which inhibits HSV DNA polymerase and incorporates into the elongating viral DNA and causes chain termination. Acyclovir resistance has been increasingly described and is caused by mutations in either the thymidine kinase or the DNA polymerase genes. These mutations result in decreased or absent HSV thymidine kinase production, altered affinity of the thymidine kinase for acyclovir-triphosphate, or altered affinity of the HSV DNA polymerase for acyclovir-triphosphate. Thymidine kinase deficiency accounts for approximately 95% of acyclovir-resistant isolates. Clinical disease due to acyclovir-resistant HSV occurs primarily in immunocompromised patients and is usually characterized by a chronic, progressive ulcerative mucocutaneous disease with prolonged shedding of virus. Several large surveys have been done in an effort to determine the incidence of in vitro and clinical acyclovir resistance. Among immunocompetent hosts, even those who have received > or = 6 years of continuous acyclovir, the prevalence of acyclovir-resistant isolates has remained stable at approximately 3%. Only three cases of clinical resistance of HSV to acyclovir have been reported. However, the incidence in immunocompromised patients, particularly those with AIDS and those who have had bone marrow transplants, is increasing. Transmission of acyclovir-resistant isolates from person to person has not been documented, but due to the increased use of acyclovir and newer drugs, such as famciclovir, there is great concern that this transmission might occur in the future. Continued surveillance in both immunocompetent and immunocompromised hosts for the development of clinical acyclovir-resistant HSV disease is necessary.

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The unique clinical and pathological findings in nine Asian (Elephas maximus) and two African (Loxodonta africana) elephants from North American Zoos with a highly fatal disease caused by novel endotheliotropic herpesviruses are described. Identification of the viruses by molecular techniques and some epidemiological aspects of the disease were previously reported. Consensus primer polymerase chain reaction (PCR) combined with sequencing yielded molecular evidence that confirmed the presence of two novel but related herpesviruses associated with the disease, one in Asian elephants and the second in African elephants. Disease onset was acute, with lethargy, edema of the head and thoracic limbs, oral ulceration and cyanosis of the tongue followed by death of most animals in 1 to 7 days. Pertinent laboratory findings in two of three clinically evaluated animals included lymphocytopenia and thrombocytopenia. Two affected young Asian elephants recovered after a 3 to 4 wk course of therapy with the anti-herpesvirus drug famciclovir. Necropsy findings in the fatal cases included pericardial effusion and extensive petechial hemorrhages in the heart and throughout the peritoneal cavity, hepatomegaly, cyanosis of the tongue, intestinal hemorrhage, and ulceration. Histologically, there were extensive microhemorrhages and edema throughout the myocardium and mild, subacute myocarditis. Similar hemorrhagic lesions with inflammation were evident in the tongue, liver, and large intestine. Lesions in these target organs were accompanied by amphophilic to basophilic intranuclear viral inclusion bodies in capillary endothelial cells. Transmission electron microscopy of the endothelial inclusion bodies revealed 80 to 92 nm diameter viral capsids consistent with herpesvirus morphology. The short course of the herpesvirus infections, with sudden deaths in all but the two surviving elephants, was ascribed to acute cardiac failure attributed to herpesvirus-induced capillary injury with extensive myocardial hemorrhage and edema.

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Famciclovir is the prodrug of penciclovir, a guanosine analogue that inhibits viruses of the alpha sub-family of the Herpesviridae, as well as hepatitis B virus. It is indicated for management of mucocutaneous herpes simplex virus disease and acute herpes zoster, and has been investigated for management of hepatitis B virus infection.

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To describe the clinical characteristics, treatment, and outcomes of herpes simplex virus (HSV) infections of the cornea and adnexae to raise awareness and to improve management of this important eye disease in children.

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Orally administered antiviral therapy for genital herpes improves the time to lesion healing and resolves symptoms during an outbreak. Although traditional therapy for a recurrent episode for healthy adults has consisted of twice-daily dosing for 5 days, recent studies have indicated that shorter courses of antiviral therapy are effective. This study was conducted to assess the efficacy and safety of a patient-initiated, single-day regimen of famciclovir therapy, compared with placebo, in immunocompetent adult patients with recurrent genital herpes.

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The nucleoside analogues acyclovir (ACV) and famciclovir (FCV) reduce the frequency and severity of herpes simplex virus 2 (HSV-2) genital shedding, yet despite their high potency in vitro and a lack of induced drug resistance, frequent episodes of breakthrough mucosal shedding occur. We tested a published stochastic, spatial mathematical model of HSV-2 replication and spread, in concert with pharmacokinetic and pharmacodynamic equations, against virologic data from clinical trials of twice-daily acyclovir and famciclovir suppression. The model reproduced the key features of clinical trial data, including genital shedding episode rate, expansion and decay dynamics, and heterogeneous peak viral production and duration. In simulations, these agents shortened episode duration by limiting the extent of viral production by 1 to 2 log units and limiting the formation of secondary ulcers by ∼50%. However, drug concentrations were noninhibitory during 42% of the dosing cycle. Even if drug concentrations were high at episode initiation, prolonged episodes often ensued due to drug decay over ensuing hours and subsequent rebound of rapidly replicating HSV-2. The local CD8(+) T-cell density was more predictive of episode viral production (R(2) = 0.42) and duration (R(2) = 0.21) than the drug concentration at episode onset (R(2) = 0.14 and 0.05, respectively), though the model projected that an agent with an equivalent potency but a two times longer half-life would decrease shedding by 80% compared to that of standard twice-daily regimens. Therefore, long half-life is a key characteristic of any agent that might fully suppress HSV-2 reactivations.

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Hepatitis B virus replicates inside the hepatocyte through an intermediate step of reverse transcription mediated by the viral polymerase. We describe five nucleoside/nucleotide analogues that interfere with the replication mechanisms of the hepatitis B virus. The resemblance of nucleoside analogues to natural nucleosides may lead to direct cytotoxicity. Therefore, antiviral activity should always be interpreted in the light of cellular toxicity. In addition, prolonged therapy with a nucleoside analogue may induce mutations in the viral polymerase, causing structural and configurational changes of the polymerase resulting in a decreased affinity for the nucleoside analogue. Subsequently, the mutated virus is capable of renewed replication during continued antiviral pressure of the nucleoside analogue. The best antiviral strategy in the future is probably combination therapy, either with several nucleoside analogues or with a nucleoside analogue and interferon.

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Almost all of the approved antiviral drugs have become available during the past two decades. Approximately one half of these agents are for the treatment of human immunodeficiency virus (HIV) infections and comprise five classes. The first three classes all act to inhibit reverse transcriptase: nucleoside analogs; nonnucleoside analogs; and nucleotide analogs. The fourth class, protease inhibitors, prevent viral packaging; the fifth class, fusion inhibitors, prevent fusion between HIV and the target cell. Four nucleoside analogs, acyclovir, valacyclovir, famciclovir and penciclovir, are approved for the therapy of herpes simplex and varicella zoster infections. Interferon alpha is approved in the injectable form for condyloma acuminatum and Kaposi's sarcoma, but the more efficient method of delivering this agent is via interferon induction following topical use of imiquimod cream. Antiviral agents are also approved for infections with cytomegalovirus, hepatitis B and C, respiratory syncytial virus, and influenza viruses. Most of these antiviral drugs are virastatic and not viracidal. Vaccines and public health measures are much more effective and cost effective than antiviral drugs and must be promoted accordingly in the defense against viral infections.

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To assess time to next recurrence and development of antiviral resistance in patients with recurrent genital herpes treated with either single-day famciclovir (1 g twice-daily) or 3-day valacyclovir (500 mg twice-daily).

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famvir 250 dosage 2017-11-06

Although vidarabine was the first systemic antiviral drug for the treatment of acute herpes zoster, the agent now used most frequently is acyclovir, a far safer drug that became available a decade ago. However, even with widespread use of acyclovir, postherpetic neuralgia (PHN) remains a principal cause of postinfectious morbidity. Newer antiviral agents, such as famciclovir and valacyclovir, have recently been introduced for the treatment of uncomplicated herpes zoster. In a double-blind, randomized study, 500 mg of famciclovir three times daily for 7 days was compared with placebo; in a second study, 500 mg of famciclovir three times daily for 7 days was compared with 800 mg of acyclovir five times daily for 7 days. Famciclovir significantly reduced duration of viral shedding (P = 0.0001) and accelerated lesion resolution compared with placebo. Famciclovir was comparable to acyclovir for these acute parameters. Most importantly, famciclovir recipients Tab Minipress Dose lost PHN two times faster than those receiving placebo (P = 0.02 all patients; P = 0.004 patients > or = 50 years) resulting in a reduction in the median duration of PHN (56 days all patients; 100 days patients > or = 50 years). This reduction translated to a 3.5-month reduction in the median duration of PHN for patients 50 years or older, those at greatest risk for developing the most common complication of herpes zoster. Famciclovir 500 mg administered three times a day for 7 days is an effective and well-tolerated treatment for acute herpes zoster, and is the only oral antiviral agent proven to reduce the duration of PHN when administered during acute zoster infection.

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Agents available to treat herpesvirus infections include idoxuridine, trifluridine, vidarabine and acyclovir for the topical treatment of herpetic eye infections; vidarabine and acyclovir for the systemic (intravenous) treatment of herpes encephalitis; acyclovir for the topical and systemic (oral) treatment of genital herpes; acyclovir for the systemic (intravenous, oral) treatment of HSV or varicella-zoster (VZV) infections in immunosuppressed patients; brivudin for the systemic (oral) treatment of HSV-1 or VZV infections in immunosuppressed patients; and ganciclovir and foscarnet for the systemic (intravenous) treatment of cytomegalovirus (CMV) retinitis in AIDS patients. Brivudin is also effective in the treatment of herpetic eye infections that no longer respond to idoxuridine, trifluridine, vidarabine or acyclovir; and foscarnet is effective in the treatment Use Of Noroxin Tablet of infections with acyclovir-resistant, thymidine kinase-deficient (TK-) HSV or VZV mutants. Other antiviral agents considered for use in herpesvirus infections include brovavir, penciclovir (and its prodrug famciclovir), desciclovir (a prodrug of acyclovir), bishydroxymethylcyclobutylguanine (BHCG) and, in particular, 1-(3-hydroxy-2-phosphonylmethoxypropyl)cytosine (HPMPC). The latter is more active than either acyclovir or ganciclovir in the chemotherapy and prophylaxis of various HSV-1, HSV-2, TK- HSV, VZV or CMV infections in animal models.

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Eighty-nine patients with chronic HBV infection were randomly divided into three groups. Thirty-two patients were treated with famciclovir, 29 patients and 28 patients with chronic HBV infection were treated with interferon (IFN) alpha and lamivudine, respectively, as Glucotrol Drug Interactions the control.

famvir 250mg dosing 2016-01-18

Chronic hepatitis B virus (HBV) infection imposes an enormous public health burden. In patients with chronic hepatitis and high levels of viral replication, inhibitors of the virus polymerase can reduce serum titre and favourably affect the inflammatory process in Sildenafil Cenforce 150 Mg Tabletten the liver. Lamivudine, a reverse transcriptase inhibitor, is the first nucleoside analogue to be licensed for treatment of chronic HBV infection. Treatment effects a rapid and profound decrease of serum virus titre, with attendant clinical benefit. Unfortunately drug-resistant species may emerge after 6 months of suppressive therapy. Lamivudine-resistant species have specific amino acid substitutions in the HBV-encoded polymerase. Emergence of these species is frequently associated with loss of clinical benefit. Published data suggest that lamivudine-resistant species exhibit cross-resistance to famciclovir, thereby limiting the potential use of famciclovir with lamivudine as combination therapy. Adefovir is under clinical evaluation for treatment of wild-type and lamivudine-resistant HBV. Preliminary data suggest that adefovir achieves potent inhibition of both species. Studies of drug resistance have followed hot-on-the-heels of the development of potent antiviral therapy for chronic HBV.

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Prolonged administration of nucleoside analogues for chronic hepatitis B may result in the emergence of hepatitis B viral polymerase mutants. 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. The antiviral response was independent of viral genotypes, and nonresponse to famciclovir was associated with a complex variability of the RT domain Indocin 50 Mg Gout . No mutation in the YMDD motif was observed, whereas an L528M mutation was clearly selected by famciclovir treatment in 2 patients, as well as 14 novel mutations in 7 patients. Clone sequence analysis of the RT domains of patients undergoing retreatment with famciclovir and/or lamivudine showed the selection of a preexisting drug-resistant mutant in one case and indicated that sequential antiviral therapy may allow the rapid selection of resistant strains.

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To review the clinically significant antiinfectives approved by the Food and Drug Administration (FDA) since Zoloft And Alcohol Use 1996, with an emphasis on agents used for treatment, prevention, or suppression of infection in immunocompromised individuals.

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Ten eyes of 10 patients ranging in age from 26 to 82 were included. All patients had normal renal and hepatic function as determined by history and laboratory values. Mean serum penciclovir concentration +/- standard deviation was 4.45 +/- 1.31 microg/ml (range, 2.51 to 6.34 microg/ml). Mean vitreous penciclovir concentration was 1.21 +/- 0 Lasuna Dosage .38 microg/ml (range, 0.39 to 1.88 microg/ml). Mean vitreous-to-serum concentration ratio of penciclovir was 0.28 +/- 0.09 (range, 0.16 to 0.41).

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The median age at onset was 5 years. Mean follow-up was 3.6 years. Eighteen eyes had HBC only; 4 patients in this group had bilateral disease. Of 39 eyes with keratitis, 74% had stromal disease. Thirty percent of HSK cases were misdiagnosed before presentation. Seventy-nine percent of patients Naprosyn 500 Mg Tablet Uses with keratitis had corneal scarring and 26% had vision of 20/40 or worse at the last visit. Eighty percent of patients had recurrent disease. Six of 16 patients (37%) receiving long-term oral acyclovir had recurrent HSV, at least one case of which followed a growth spurt that caused the baseline dosage of acyclovir to become subtherapeutic.

famvir dosing 2016-02-03

After several nucleoside analogues have been tested against chronic hepatitis B virus (HBV) infection with minimal success, lamivudine seems to be a highly effective new therapeutic option. This review focuses on nucleoside metabolism and on the molecular action of lamivudine as well as Buspar Medication Buspar Xanax on results of clinical studies for several indications. We report on results of trials on the use of lamivudine for chronic HBV infection, chronic HBV under immunosuppression and prophylaxis or treatment of HBV reinfection before or after orthotopic liver transplantation. Aspects of combination therapy of different nucleoside analogues as well as on combination of lamivudine with interferon are also highlighted. Although lamivudine seems to be highly effective in most patients at the start of therapy, development of resistance by mutations in the viral polymerase is a significant clinical problem. The mode of resistance development is compared with the situation in HIV infection. Possible cross-resistance with other nucleoside analogues and the perspectives of lamivudine therapy are also considered.

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In this systematic review we present information relating Depakote 1000 Mg Per Day to the effectiveness and safety of the following interventions: aciclovir, famciclovir, and valaciclovir.

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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' Artane Generic s most debilitating complication, postherpetic neuralgia.