Comprehensive, up-to-date information on HIV/AIDS treatment, prevention, and policy from the University of California San Francisco

The first name listed is the generic name, which, in the United States, is determined prior to licensing by the U.S. Adopted Name Council subject to the approval of the World Health Organization. The generic name remains in the public domain and is used by other companies producing the drug after the patent expires, or in countries where international trade agreements permit production of the drug outside U.S. patent protection.

The second name listed is the brand (proprietary or trademark) name, which is developed by the manufacturer as a marketing consideration, subject to the approval of the Food and Drug Administration (FDA). The brand name remains the property of the manufacturer. Proprietary names widely used outside the United States are also included.

When commonly used, the chemical name, abbreviations based on it, or the manufacturer's designation used in pre-marketing trials of the drug, may be listed following the brand name.

The class of each drug appears after the name of the drug. There are currently 6 major classes of antiretroviral drugs: nucleoside analogue reverse transcriptase inhibitor (NRTI), nonnucleoside reverse transcriptase inhibitor (NNRTI), protease inhibitor (PI), fusion inhibitor, chemokine coreceptor antagonist (consisting of 2 subclasses: CCR5 antagonist and CXCR4 antagonist), and integrase inhibitor.

NRTIs function by inhibiting the synthesis of DNA by reverse transcriptase, the viral enzyme that copies viral RNA into DNA in newly infected cells. Nucleoside analogues bear a structural resemblance to the natural building blocks of DNA: the nucleosides adenosine and guanosine, thymidine and cytidine. Nucleoside analogues are triphosphorylated within the cell, and some undergo further modifications (didanosine, for example, is converted into its active moiety, 2',3'-dideoxyadenosine-5'-triphosphate). Nucleotide analogues resemble monophosphorylated nucleosides, and therefore require only 2 additional phosphorylations to become active inhibitors of DNA synthesis. Reverse transcriptase fails to distinguish the phosphorylated NRTIs from their natural counterparts, and attempts to use the drugs in the synthesis of viral DNA. When an NRTI is incorporated into a strand of DNA being synthesized, the addition of further nucleotides is prevented, and a full-length copy of the viral DNA is not produced.

NNRTIs also inhibit the synthesis of viral DNA, but rather than act as false nucleotides, the NNRTIs bind to reverse transcriptase in a way that inhibits the enzyme's activity.

PIs bind to the active site of the viral protease enzyme, preventing the processing of viral proteins into functional conformations. Viral particles are still produced when the protease is inhibited, but these particles are not effective at infecting new cells.

Fusion inhibitors prevent HIV from entering target cells. Drugs of this class bind to the HIV envelope protein gp41, which is involved in viral entry. By blocking the interactions between regions of the gp41 molecule, fusion inhibitors interfere with the conformational change (folding) of the envelope molecule required for fusion with the target cell membrane.

Chemokine coreceptor antagonists also prevent the entry of HIV into target cells. They bind to coreceptors (either CCR5 or CXCR4) on the surface of CD4 cells. By doing so, they block a required step in viral entry. In contrast to drugs from other classes, which act on viral enzymes, coreceptor antagonists bind human proteins.

Integrase inhibitors bind a viral enzyme known as integrase and interfere with the incorporation of reverse-transcribed HIV DNA into the chromosomes of host cells.