| Literature DB >> 33686850 |
Steven J Smith1, Xue Zhi Zhao2, Dario Oliveira Passos3, Valerie E Pye4, Peter Cherepanov4,5, Dmitry Lyumkis3,6, Terrence R Burke2, Stephen H Hughes1.
Abstract
Integrase strand transfer inhibitors (INSTIs) block the integration step of the retroviral lifecycle and are first-line drugs used for the treatment of HIV-1/AIDS. INSTIs have a polycyclic core with heteroatom triads, chelate the metal ions at the active site, and have a halobenzyl group that interacts with viral DNA attached to the core by a flexible linker. The most broadly effective INSTIs inhibit both wild-type (WT) integrase (IN) and a variety of well-known mutants. However, because there are mutations that reduce the potency of all of the available INSTIs, new and better compounds are needed. Models based on recent structures of HIV-1 and red-capped mangabey SIV INs suggest modifications in the INSTI structures that could enhance interactions with the 3'-terminal adenosine of the viral DNA, which could improve performance against INSTI resistant mutants. We designed and tested a series of INSTIs having modifications to their naphthyridine scaffold. One of the new compounds retained good potency against an expanded panel of HIV-1 IN mutants that we tested. Our results suggest the possibility of designing inhibitors that combine the best features of the existing compounds, which could provide additional efficacy against known HIV-1 IN mutants.Entities:
Keywords: inhibition; integrase; mutant; potency; strand transfer; susceptibility
Year: 2021 PMID: 33686850 DOI: 10.1021/acsinfecdis.0c00819
Source DB: PubMed Journal: ACS Infect Dis ISSN: 2373-8227 Impact factor: 5.084