Please note: Any medical or genetic information present in this entry is not intended as a diagnosis of your problem, but rather is provided as a helpful guide for research, educational and informational purposes only. It is not in any way intended to be used as a substitute for professional medical advice, diagnosis, treatment or care. Information is not necessarily complete. Please see your doctor for diagnosis and treatment.

Please note: DNAtraffic database is the project under construction and information on this page is not finished yet.

Aciclovir


ACCESSION NB: DB00787 (APRD00567, EXPT00406)


TYPE: small molecule


GROUP: approved


DESCRIPTION:
A guanosine analog that acts as an antimetabolite. Viruses are especially susceptible. Used especially against herpes. [PubChem]

VOLUME OF DISTRIBUTION: Not Available

CATEGORIES:
Antiviral Agents Nucleosides and Nucleotides

ABSORPTION: Oral: bioavailability 10 to 20%

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.

PROTEIN BINDING:
9%-33%

METABOLISM:
Hepatic, the only major urinary metabolite that has been detected is 9-carboxymethoxymethylguanine.

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.

AFECTED ORGANISMS:
Human Herpes Virus