Spectrum of activity The drug inhibits replication of varicella zoster virus (VZV) – which causes herpes zoster – and herpes simplex virus type 1 (HSV-1), but not HSV-2 which typically causes genital herpes. In vitro, inhibitory concentrations against VZV are 200- to 1000-fold lower than those of aciclovir and penciclovir, theoretically indicating a much higher potency of<unk> . Clinically relevant VZV strains are particularly sensitive. Mechanism of action<unk>  is an analogue of the nucleoside thymidine. The active compound is<unk>  5'-triphosphate, which is formed in subsequent phosphorylations by viral (but not human) thymidine kinase and presumably by nucleoside-diphosphate kinase.<unk>  5'-triphosphate works because it is incorporated into the viral DNA, but then blocks the action of DNA polymerases, thus inhibiting viral replication. Pharmacokinetics<unk>  is well and rapidly absorbed from the gut and undergoes first-pass metabolism in the liver, where the enzyme thymidine phosphorylase quickly splits off the sugar component, leading to a bioavailability of 30%. The resulting metabolite is bromovinyluracil (BVU), which does not have antiviral activity. BVU is also the only metabolite that can be detected in the blood plasma. Highest blood plasma concentrations are reached after one hour.<unk>  is almost completely (>95%) bound to plasma proteins. Terminal half-life is 16 hours; 65% of the substance are found in the urine and 20% in the faeces, mainly in form of an acetic acid derivative (which is not detectable in the plasma), but also other water-soluble metabolites, which are urea derivatives. Less than 1% is excreted in form of the original compound. File:Brivudine triphosphate.Brivudine 5'-triphosphate, the active metabolite File:Bromovinyluracil skeletal.Bromovinyluracil (BVU), the main inactive metabolite File:Uracil acetic acid.The acetic acid derivative predominantly found in urine
Brivudine
Fostemsavir
Censavudine
Saquinavir
Maribavir
Coronavir
Tipranavir
Stavudine