Anti-HIV effects<unk>  falls in the NNRTI class of antiretrovirals. Both nucleoside and non-nucleoside RTIs inhibit the same target, the reverse transcriptase enzyme, an essential viral enzyme which transcribes viral RNA into DNA. Unlike nucleoside RTIs, which bind at the enzyme's active site, NNRTIs act allosterically by binding to a distinct site away from the active site known as the NNRTI pocket.<unk>  is not effective against HIV-2, as the pocket of the HIV-2 reverse transcriptase has a different structure, which confers intrinsic resistance to the NNRTI class. As most NNRTIs bind within the same pocket, viral strains which are resistant to<unk>  are usually also resistant to the other NNRTIs, nevirapine and delavirdine. The most common mutation observed after<unk>  treatment is K103N, which is also observed with other NNRTIs. Nucleoside reverse-transcriptase inhibitors (NRTIs) and<unk>  have different binding targets, so cross-resistance is unlikely; the same is true with regard to<unk>  and protease inhibitors. Neuropsychiatric effects As of 2016 the mechanism of<unk> ' neuropsychiatric adverse effects was not clear.<unk>  appears to have neurotoxicity, possibly by interfering with mitochondrial function, which may in turn possibly be caused by inhibiting creatine kinase but also possibly by disrupting mitochondrial membranes or by interfering with nitric oxide signalling. Some neuropsychiatric adverse effects may be mediated through cannabinoid receptors, or through activity at the 5-HT2A receptor, but<unk>  interacts with many CNS receptors, so this is not clear. The neuropsychiatric adverse effects are dose-dependent.
Efavirenz
Saquinavir
Zidovudine
Lamivudine
Entecavir
Amprenavir
Fosamprenavir
Telbivudine