Bictegravir is a component of the fixed-dose combination product bictegravir/emtricitabine/tenofovir alafenamide (BIKTARVY®), which received marketing approval for the treatment of human immunodeficiency virus (HIV) infection by the U.S. Food and Drug Administration in February 2018. Bictegravir inhibits the strand transfer activity of HIV-1 integrase, an HIV-1 encoded enzyme that is required for viral replication. Inhibition of integrase prevents the integration of linear HIV-1 DNA into host genomic DNA, blocking the formation of the HIV-1 provirus and propagation of the virus.

Rilpivirine is a non-nucleoside reverse transcriptase inhibitor (NNRTI) which is used for the treatment of HIV-1 infections in treatment-naive patients. It is active against wild-type and NNRTI-resistant HIV-1. Rilpivirine is a diarylpyrimidinethat inhibits HIV-1 replication by non-competitive inhibition of HIV-1 reverse transcriptase (RT). Rilpivirine does not inhibit the human cellular DNA polymerases α, β and γ.

Lamivudine is a reverse transcriptase inhibitor used alone or in combination with other classes of anti-human immunodeficiency virus (HIV) drugs in the treatment of HIV infection. This molecule has two stereo-centers, thus giving rise to four stereoisomers: (+/-)-cis-lamivudine and (+/-)-trans-lamivudine. The latter is considered to be impurity of the pharmaceutically active isomer, (-)-cis-lamivudine.

Emtricitabine (minus enantiomer) is a synthetic nucleoside analog of cytosine with activity against HIV-1. It’s more active and significantly less toxic than the (+) enantiomer.

Emtricitabine was discovered by Emory researchers Dr. Dennis C. Liotta, Dr. Raymond F. Schinazi and Dr. Woo-Baeg Choi and licensed to Triangle Pharmaceuticals by Emory University in 1996. Triangle was acquired by Gilead in 2003. Emtricitabine, marketed by Gilead as Emtriva, was first approved by the U.S. Food and Drug Administration in July 2003 for the treatment of HIV infection in combination with other antiretroviral agents. Emtricitabine, a synthetic nucleoside analog of cytidine, is phosphorylated by cellular enzymes to form emtricitabine 5'-triphosphate. Emtricitabine 5'-triphosphate inhibits the activity of the HIV-1 reverse transcriptase by competing with the natural substrate deoxycytidine 5'-triphosphate and by being incorporated into nascent viral DNA which results in chain termination.

Emtricitabine was discovered by Emory researchers Dr. Dennis C. Liotta, Dr. Raymond F. Schinazi and Dr. Woo-Baeg Choi and licensed to Triangle Pharmaceuticals by Emory University in 1996. Triangle was acquired by Gilead in 2003. Emtricitabine, marketed by Gilead as Emtriva, was first approved by the U.S. Food and Drug Administration in July 2003 for the treatment of HIV infection in combination with other antiretroviral agents. Emtricitabine, a synthetic nucleoside analog of cytidine, is phosphorylated by cellular enzymes to form emtricitabine 5'-triphosphate. Emtricitabine 5'-triphosphate inhibits the activity of the HIV-1 reverse transcriptase by competing with the natural substrate deoxycytidine 5'-triphosphate and by being incorporated into nascent viral DNA which results in chain termination.

(R)-9-(2-Phosphonylmethoxypropyl)adenine (PMPA known as tenofovir) is an antiviral drug. Diphosphate of PMPA acts as a selective inhibitor of the HIV-1 reverse transcriptase. Tenofovir disoproxil was approved for clinical use for the treatment of HIV infection (AIDS) and chronic HBV infection.