Famvir (famciclovir) coated tablets 500 mg. №14

Description

Famvir 500 mg Composition
active substance: famciclovir;

1 tablet of 500 mg contains 500 mg of famciclovir;

excipients: hydroxypropyl cellulose, lactose, sodium starch, magnesium stearate, hypromellose, titanium dioxide (E 171), polyethylene glycol 4000, polyethylene glycol 6000 (500 mg tablets do not contain anhydrous lactose).

Famvir 500 mg Dosage form
Film-coated tablets.

Basic physical and chemical properties: tablets 500 mg – white, oval, biconvex film-coated tablets with beveled edges, embossed “FV 500” on one side and smooth on the other side.

Famvir 500 mg Pharmacotherapeutic group
Direct-acting antiviral agents. Nucleosides and nucleotides. Famciclovir. ATX code J05A B09.

Pharmacodynamics
Famciclovir is rapidly converted in vivo to penciclovir, which demonstrates in vitro antiviral activity against herpes simplex viruses (types 1 and 2), varicella-zoster virus, Epstein-Barr virus and cytomegalovirus.

The antiviral effect of orally administered famciclovir has been observed in various animal models. In cells infected with a virus, penciclovir is rapidly and efficiently converted to triphosphate (this process occurs indirectly through a virus-induced thymidine kinase). This triphosphate is present in infected cells for more than 12 hours and inhibits viral DNA replication. Penciclovir triphosphate has a half-life of 10 hours in HSV-1 cells, 20 hours in HSV-2 cells, and 7 hours in VZV-infected cells grown in culture.

In uninfected cells exposed to penciclovir, the concentration of penciclovir triphosphate is barely detectable. Therefore, the likelihood of its toxic effect on mammalian cells is too low and it is unlikely that uninfected cells will be damaged at therapeutic concentrations of penciclovir.

As with acyclovir, resistance to penciclovir is associated mainly with mutations in the TK gene, which leads to a deficiency or altered substrate specificity of this enzyme, and to a much lesser extent with mutations in the DNA polymerase gene. Most clinical isolates of HSV and VZV resistant to acyclovir are also resistant to penciclovir, but cross-resistance is not universal.

The most common form of acyclovir resistance among herpes simplex virus strains is a deficiency in the synthesis of the enzyme thymidine kinase (TC). In such TC-deficient strains, cross-resistance to both penciclovir and acyclovir is observed. However, the activity of penciclovir has been shown in relatively recently isolated acyclovir-resistant strains of herpes simplex virus with damaged DNA polymerase.

Indications
Infections caused by Varicella Zoster viruses (VZV) – shingles;

herpes zoster, including herpes zoster with localization in immunocompetent adult patients;
shingles in immunocompromised adults.
Infections caused by Herpes Simplex viruses (HSV) – genital herpes;

treatment of the first manifestations and relapses of infectious genital herpes in immunocompetent adult patients;
treatment of recurrent genital herpes in immunocompromised adult patients;
suppression of recurrent genital herpes in immunocompetent adult patients and in immunocompromised adult patients.

Contraindications
Hypersensitivity to famciclovir or other components of the drug, as well as sensitivity to penciclovir.