ACYCLOVIR

INTRODUCTION: Acyclovir is an acyclic guanosine derivative with clinical activity against HSV-1, HSV-2, and VZV, but it is approximately 10 times more potent against HSV-1 and HSV-2 than against VZV. In vitro activity against Epstein-Barr virus (EBV), cytomegalovirus (CMV), and human herpes virus-6 (HHV-6) is present but weaker.

PHARMACOKINETICS: Acyclovir requires three phosphorylation steps for activation. It is converted first to the monophosphate derivative by the virus pecified thymidine kinase and then to the di- and triphosphate compounds by host cell enzymes. Enzymes

Because it requires the viral kinase for initial phosphorylation, acyclovir is selectively activated and the active metabolite accumulates only in infected cells. Acyclovir triphosphate inhibits viral DNA synthesis by two mechanisms: competition with deoxyGTP for the viral DNA polymerase, resulting in binding to the DNA template as an irreversible complex; and chain termination following incorporation into the viral DNA. DNA the genetic material

The bioavailability of oral acyclovir is low (15–20%) and is unaffected by food. An intravenous formulation is available. Topical formulations produce high concentrations in herpetic lesions, but systemic concentrations are undetectable by this route. Acyclovir is cleared primarily by glomerular filtration and tubular secretion. The half-life is 2.5–3 hours in patients with normal renal function and 20 hours in patients with anuria.

RELATED;

1.  NEVIRAPINE  2.  ZIDOVUDINE

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