Acetazolamide | Acetylcholine | Acyclovir | Adalimumab | Amikacin | Amphotericin B | Ampicillin | Apraclonidine| Atropine | Azathioprine | Azelastine | Betaxolol | Bevacizumab| Biologicals | Brimonidine | Brinzolamide  | Bupivacaine | Capsofungin  | Cefazolin | Cidofovir | Ciprofloxacin | Clotrimazole | Corticosteroids | Cyclopentolate | Cyclosporine A | Cyclophosphamide | Daclizumab | Dorzolamide | EDTA | Epinephrine | Etanercept| Erythromycin | Famciclovir | Foscarnet | Fluconazole | Fluorescein Sodium | Fluorometholone | 5-Fluorouracil | Flurbiprofen   | Ganciclovir | Gatifloxacin | Gentamicin | Glycerin | Homatropine | Hydroxypropyl | Idoxurudine | Indocyanine Green | Infliximab | Interferon alpha | Itraconazole | Ketoconazole | Ketorolac | Latanoprost | Leflunomide | Lidocaine | Loteprednol | Mannitol  | Methotrexate | Methylene Blue | Mitomycin | Moxifloxacin | Mycophenolate Mofetil | Naphazoline | Natamycin | Nedocromil Sodium | Neomycin Sulfate | Ofloxacin | Olopatadine | Pegaptanib | Pilocarpine | Timolol | Valacyclovir | Valganciclovir | Vidarabine | Voriconazole


Acyclovir is a synthetic purine nucleoside analog derived from guanine.

Mode of action

Acyclovir interferes with DNA synthesis, thus inhibiting virus replication. The antiviral activity of acyclovir is dependent primarily on the intracellular conversion of acyclovir to acyclovir triphosphate. Acyclovir requires three phosphorylation steps for activation to acyclovir triphosphate. It is converted first to the monophosphate derivative by the virus-specified thymidine kinase and then to the di- and triphosphate compounds by host cell enzymes. Because it requires the viral kinase for initial phosphorylation, acyclovir is selectively activated only in infected cells.


Administration of acyclovir can be by an intravenous, oral, or topical route. The bioavailability of oral acyclovir is 15-20% and is unaffected by food. Topical formulations produce high concentrations in herpetic lesions. Acyclovir is cleared primarily by glomerular filtration and tubular secretion. Acyclovir accumulates in patients with renal failure. The half-life is approximately 3 hours in patients with normal renal function. Acyclovir diffuses readily into most tissues and body fluids. Cerebrospinal fluid concentrations are 50% of serum values.


Anti-viral profile

Herpes simplex virus (HSV) Types 1 and 2, varicella-zoster virus (VZV), and some Epstein-Barr virus mediated infections are sensitive to acyclovir. Acyclovir is the treatment of choice in HSV encephalitis.

Adverse effects

Acyclovir is generally well tolerated. Local irritation may occur from topical application; headache, diarrhoea, nausea, and vomiting may result after oral administration. Major side effect of acyclovir is on renal function. This is due to crystallization and deposition of the drug in the kidneys of patients who are dehydrated or have preexisting renal insufficiency. Renal dysfunction can be avoided by infusing acyclovir slowly over 1 hour and administering 1 liter of fluid with each gram of the drug. Oral acyclovir has rarely been associated with renal dysfunction. Nausea, vomiting, and abdominal pain can occur and probably represent a direct toxic effect on the gastrointestinal tract.


Resistant viral strains to acyclovir due to altered or deficient thymidine kinase and DNA polymerases have been found and are most commonly isolated from immunocompromised patients. These strains are cross-resistant to valacyclovir, famciclovir, and ganciclovir also because of their similar mechanism of action. Drugs like foscarnet, cidofovir, and trifluridine do not require activation by viral thymidine kinase and thus can be used against the most prevalent acyclovir-resistant strains.

Cytomegalovirus (CMV) is resistant to acyclovir, because it lacks a specific viral thymidine kinase

Statutory Warning

Materials / Informations provided here are for educational purpose only ; and not to be used for medical advice, diagnosis or treatment