REVIEW 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. REFERENCES
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SCHOOFS, MARK (MAY 13, 2011). Researchers Manipulate Drug's Chemistry in Bid to Lower Treatment Cost. Wall Street Journal.
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Viread Prescribing Guidelines (PDF). U.S. Food and Drug Administration. March 2006. Archived from the original on 2007-09-30. Retrieved 2007-02-12.
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Delahunty T, Bushman L, Robbins B, Fletcher CV (2009). The simultaneous assay of tenofovir and emtricitabine in plasma using LC/MS/MS and isotopically labeled internal standards. J. Chrom. B 877 (20-21): 1907-1914. doi:10.1016/j.jchromb.2009.05.029.
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