Abacavir is a nucleoside reverse transcriptase inhibitor used for treatment of HIV infection (either alone or in combination with other antiviral drugs). It was shown that abacavir exerts its antiviral activity through its active metabolite, carbovir triphosphate. Carbovir triphosphate is a guanine analogue and a potent and selective inhibitor of viral reverse transcriptases. Upon administration, abacavir is first converted to abacavir monophosphate by ADK, then the monophosphate is deaminated to carbovir monophosphate, which is then anabolized by cellular kinases to carbovir diphosphate and then finally to carbovir triphosphate. Abacavir causes hypersensitivity reaction in patients with HLA-B*57:01 allele.

Zidovudine is a nucleoside reverse transcriptase inhibitor (NRTI) with activity against Human Immunodeficiency Virus Type 1 (HIV-1). Zidovudine is phosphorylated to active metabolites that compete for incorporation into viral DNA. They inhibit the HIV reverse transcriptase enzyme competitively and act as a chain terminator of DNA synthesis. The lack of a 3'-OH group in the incorporated nucleoside analogue prevents the formation of the 5' to 3' phosphodiester linkage essential for DNA chain elongation, and therefore, the viral DNA growth is terminated. Zidovudine, a structural analog of thymidine, is a prodrug that must be phosphorylated to its active 5′-triphosphate metabolite, zidovudine triphosphate (ZDV-TP). It inhibits the activity of HIV-1 reverse transcriptase (RT) via DNA chain termination after incorporation of the nucleotide analogue. It competes with the natural substrate dGTP and incorporates itself into viral DNA. It is also a weak inhibitor of cellular DNA polymerase α and γ. Zidovudine is used in combination with other antiretroviral agents for the treatment of human immunovirus (HIV) infections. Zidovudine is marketed as Retrovir.