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Home / Drugs / Starting with T / Tenofovir

Tenofovir, marketed by Gilead Sciences under the trade name Viread®, belongs to a class of antiretroviral drugs known as nucleotide analogue reverse transcriptase inhibitors (nRTIs), which block reverse transcriptase, an enzyme crucial to viral production in HIV-infected people. [Wikipedia]
CategoriesAnti-HIV Agents
Nucleoside and Nucleotide Reverse Transcriptase Inhibitors
Reverse Transcriptase Inhibitors
ManufacturersGilead sciences inc
Gilead Sciences, Inc.
PackagersA-S Medication Solutions LLC
Bristol-Myers Squibb Co.
Cardinal Health
Dept Health Central Pharmacy
Gilead Sciences Inc.
Kaiser Foundation Hospital
Lake Erie Medical and Surgical Supply
Nycomed Inc.
Patheon Inc.
Physicians Total Care Inc.
Quality Care
Remedy Repack
Tenofovir disoproxil
Tenofovir disoproxil fumarate


For use, in combination with other antiretroviral agents, for the treatment of HIV-1 infection.


Tenofovir belongs to a class of antiretroviral drugs known as nucleotide analogue reverse transcriptase inhibitors (NtRTIs), which block reverse transcriptase, an enzyme crucial to viral production in HIV-infected people. Tenofovir is currently in late-stage clinical trials for the treatment of hepatitis B. Tenofovir disoproxil fumarate is an acyclic nucleoside phosphonate diester analog of adenosine monophosphate. Tenofovir requires initial diester hydrolysis for conversion to tenofovir and subsequent phosphorylations by cellular enzymes to form tenofovir diphosphate. Tenofovir diphosphate is a weak inhibitor of mammalian DNA polymerases α, β, and mitochondrial DNA polymerase γ.

mechanism of action

Tenofovir inhibits the activity of HIV reverse transcriptase by competing with the natural substrate deoxyadenosine 5’-triphosphate and, after incorporation into DNA, by DNA chain termination. Specifically, the drugs are analogues of the naturally occurring deoxynucleotides needed to synthesize the viral DNA and they compete with the natural deoxynucleotides for incorporation into the growing viral DNA chain. However, unlike the natural deoxynucleotides substrates, NRTIs and NtRTIs (nucleoside/tide reverse transcriptase inhibitors) lack a 3'-hydroxyl group on the deoxyribose moiety. As a result, following incorporation of an NRTI or an NtRTI, the next incoming deoxynucleotide cannot form the next 5'-3' phosphodiester bond needed to extend the DNA chain. Thus, when an NRTI or NtRTI is incorporated, viral DNA synthesis is halted, a process known as chain termination. All NRTIs and NtRTIs are classified as competitive substrate inhibitors.


Limited clinical experience at doses higher than the therapeutic dose of tenofovir 300 mg is available. In Study 901 tenofovir disoproxil fumarate 600 mg was administered to 8 patients orally for 28 days. No severe adverse reactions were reported. The effects of higher doses are not known.


Neither tenofovir disoproxil nor tenofovir are substrates of CYP450 enzymes.


The oral bioavailability in fasted patients is approximately 25%. Administration of food (high fat meal containing 40 to 50% fat) increases the oral bioavailability, with an increase in the AUC of approximately 40%.

half life

Approximately 17 hours.

drug interactions

Atazanavir: Concomitant therapy may result in decreased serum levels of Atazanavir and increased levels of Tenofovir. Concomitant therapy should only be used with the inclusion of Ritonavir.

Didanosine: Tenofovir may decrease the therapeutic effects and increase the adverse effects of Didanosine. Monitor for changes in virologic response and Didanosine toxicity during concomitant therapy.

Valganciclovir: The excretion rates of Valganciclovir and/or Tenofovir may decrease as both drugs are eliminated by active tubular secretion. Monitor for increased serum concentrations and toxicity of both agents.