Obefazimod effectively suppresses HIV-1 production in cells infected with PBMC and macrophages. It exhibits robust inhibitory action against all tested HIV-1 subtypes, including B, C, and recombinant forms. Obefazimod also strongly prevents the replication of viral strains that possess mutations granting resistance to various therapeutic drugs in vitro. Unlike the antiviral medication 3TC, which shows limited activity against K65R and M184V mutant strains, Obefazimod successfully inhibits both. In an effort to extend the understanding of Obefazimod's impact on HIV-1 replication in other primary cells, treatments range from 0.01 μM to 30 μM of Obefazimod, with monitoring of p24 antigen levels in culture supernatants across a span of 12 days. Obefazimod demonstrates a dose-responsive blockade of virus replication, with an IC50 value between 0.1 μM and 1 μM[1].
Obefazimod 动物研究
Animal study
Humanized mice, which are reconstituted with human lymphoid cells, offer a fast, dependable, and consistent system for in vivo testing of Obefazimod's effectiveness. Initially, SCID mice are reconstituted with PBMCs and infected with the HIV-1 JR-CSF strain. These mice receive 20 mg/kg of Obefazimod orally twice daily for 15 days. Viral RNA measurements indicate that this oral Obefazimod regimen significantly lowers the viral load over the treatment period. Furthermore, FACS analysis of blood samples reveals that Obefazimod treatment hinders the loss of CD4+ cells post-infection in the reconstituted mice, thus normalizing the CD8+/CD4+ ratio to that seen in uninfected mice[1].
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