Medication Valtrex (Valacyclovir)

• Generic name: Valacyclovir hydrochloride
• Brand/Trade names: Valtrex
• Dosage forms and strength: 500 mg, 1000 mg oral caplets
• Pharmacologic category: guanosine nucleoside antiviral agent
• FDA approved: December 15, 1995
• Habit forming? No
• Pregnancy risk factor: B
• Patent Expiration Date: June 2009

Valacyclovir hydrochloride (Valtrex) is indicated for the treatment of herpes zoster (shingles); initial and recurrent episodes of genital herpes; suppression of recurrent genital herpes; cold sores. It is also DFA approved for the reduction of transmission of genital herpes.

This medication does not cure a herpes infection but may relieve the symptoms of viral infection and shorten the duration of an outbreak.

The most common side effects are headache, nausea and abdominal pain [1].

• Absorption and Bioavailability: After oral administration, valacyclovir is rapidly absorbed from the GI tract and nearly completely converted to acyclovir and L-valine. Bioavailability is about 50-60%. Acyclovir bioavailability from the administration of Valtrex is not altered by administration with food.
• Metabolism: Valacyclovir is converted to acyclovir and L-valine by first-pass intestinal and/or hepatic metabolism. Neither valacyclovir nor acyclovir is metabolized by cytochrome P450 enzymes.
• Elimination half-life: Elimination half-life of acyclovir is about 2.5-3.3 hours.
• Excretion: About 46% is recovered in urine. About 47% is recovered in feces.

• convenient dosing regimen
• suppresses asymptomatic viral shedding
• excellent safety profile
• high efficacy
• very low risk of drug interactions

• does not cure the viral infection
• risk of renal and nervous system problems

• Prophylaxis for herpes simplex virus [2]
• Posttransplantation cytomegalovirus (CMV) infection [3]
• Reduction of schizophrenia symptoms in cytomegalovirus-seropositive individuals [4]
• Suppressive therapy of recurrent genital herpes in pregnant women [5]
• Herpes zoster ophthalmicus [6]

Valacyclovir prevents the growth and multiplication of the herpes virus.

Valacyclovir is selectively phosphorylated only within virus-infected cells by viral thymidine kinase (TK). Further phosphorylation by cellular enzymes leads to the production of acyclovir triphosphate, which compete with the natural nucleotide, dGTP, resulting in the selective inhibition of viral DNA polymerase. Incorporation of the analogue triphosphate into the growing DNA chain prevents continued extension of the DNA chain.

• 1. U.S. Food and Drug Administration. Valtrex (Valacyclovir) U.S. Prescribing Information. Available at (PDF format): Prescribing Information
• 2. Beeson WH, Rachel JD. Valacyclovir prophylaxis for herpes simplex virus infection or infection recurrence following laser skin resurfacing. Dermatol Surg. 2002 Apr;28(4):331-6.
• 3. Fiddian P, Sabin CA, Griffiths PD. Valacyclovir provides optimum acyclovir exposure for prevention of cytomegalovirus and related outcomes after organ transplantation. J Infect Dis. 2002 Oct 15;186 Suppl 1:S110-5.
• 4. Dickerson FB, Boronow JJ, Stallings CR, Origoni AE, Yolken RH. Reduction of symptoms by valacyclovir in cytomegalovirus-seropositive individuals with schizophrenia. Am J Psychiatry. 2003 Dec;160(12):2234-6.
• 5. Andrews WW, Kimberlin DF, Whitley R, Cliver S, Ramsey PS, Deeter R. Valacyclovir therapy to reduce recurrent genital herpes in pregnant women. Am J Obstet Gynecol. 2006 Mar;194(3):774-81.
• 6. Colin J, Prisant O, Cochener B, Lescale O, Rolland B, Hoang-Xuan T. Comparison of the efficacy and safety of valaciclovir and acyclovir for the treatment of herpes zoster ophthalmicus. Ophthalmology. 2000 Aug;107(8):1507-11. PubMed

Last modified: April, 2010