| Indication | For the treatment and management of herpes zoster (shingles), genital herpes, and chickenpox |
| Pharmacodynamics | Aciclovir (INN) or acyclovir (USAN, former BAN) is a synthetic deoxyguanosine analog and it is the prototype antiviral agent that is activated by viral thymidine kinase. The selective activity of aciclovir is due to its affinity for the thymidine kinase enzyme encoded by HSV and VZV. |
| Mechanism of action | Viral (HSV-1, HSV-2 and VZV) thymidine kinase converts aciclovir to the aciclovir monophosphate, which is then converted to the diphosphate by cellular guanylate kinase, and finally to the triphosphate by phosphoglycerate kinase, phosphoenolpyruvate carboxykinase, and pyruvate kinase. Aciclovir triphosphate competitively inhibits viral DNA polymerase and competes with the natural deoxyguanosine triphosphate, for incorporation into viral DNA. Once incorporated, aciclovir triphosphate inhibits DNA synthesis by acting as a chain terminator. |
| Absorption | Oral: bioavailability 10 to 20% |
| Volume of distribution | Not Available |
| Protein binding | 9%-33% |
| Metabolism | Hepatic, the only major urinary metabolite that has been detected is 9-carboxymethoxymethylguanine. |
| Route of elimination | Acyclovir is cleared renally. |
| Half life | 2.5-3.3 hours |
| Clearance | Not Available |
| Toxicity | Aciclovir may cause nephrotoxicity (crystallization of aciclovir within renal tubules, elevation of serum creatinine, transient), and neurotoxicity (coma, hallucinations, lethargy, seizures, tremors). Nephrotoxicity and neurotoxicity usually resolve after cessation of aciclovir therapy. However, there is no well-defined relationship between aciclovir concentrations in the blood and these adverse effects. |
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