{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,10,9]],"date-time":"2026-10-09T11:42:09Z","timestamp":1791546129314,"version":"4.3.4"},"reference-count":70,"publisher":"American Society for Microbiology","issue":"7","license":[{"start":{"date-parts":[[2016,6,20]],"date-time":"2016-06-20T00:00:00Z","timestamp":1466380800000},"content-version":"vor","delay-in-days":0,"URL":"http:\/\/creativecommons.org\/licenses\/by\/4.0\/"},{"start":{"date-parts":[[2016,7,1]],"date-time":"2016-07-01T00:00:00Z","timestamp":1467331200000},"content-version":"tdm","delay-in-days":0,"URL":"https:\/\/journals.asm.org\/non-commercial-tdm-license"}],"content-domain":{"domain":["journals.asm.org"],"crossmark-restriction":true},"short-container-title":["Antimicrob Agents Chemother"],"published-print":{"date-parts":[[2016,7]]},"abstract":"<jats:title>ABSTRACT<\/jats:title>\n          <jats:p>\n            BMS-955176 is a second-generation human immunodeficiency virus type 1 (HIV-1) maturation inhibitor (MI). A first-generation MI, bevirimat, showed clinical efficacy in early-phase studies, but \u223c50% of subjects had viruses with reduced susceptibility associated with naturally occurring polymorphisms in Gag near the site of MI action. MI potency was optimized using a panel of engineered reporter viruses containing site-directed polymorphic changes in Gag that reduce susceptibility to bevirimat (including V362I, V370A\/M\/\u0394, and T371A\/\u0394), leading incrementally to the identification of BMS-955176. BMS-955176 exhibits potent activity (50% effective concentration [EC\n            <jats:sub>50<\/jats:sub>\n            ], 3.9 \u00b1 3.4 nM [mean \u00b1 standard deviation]) toward a library (\n            <jats:italic>n<\/jats:italic>\n            = 87) of\n            <jats:italic>gag\/pr<\/jats:italic>\n            recombinant viruses representing 96.5% of subtype B polymorphic Gag diversity near the CA\/SP1 cleavage site. BMS-955176 exhibited a median EC\n            <jats:sub>50<\/jats:sub>\n            of 21 nM toward a library of subtype B clinical isolates assayed in peripheral blood mononuclear cells (PBMCs). Potent activity was maintained against a panel of reverse transcriptase, protease, and integrase inhibitor-resistant viruses, with EC\n            <jats:sub>50<\/jats:sub>\n            s similar to those for the wild-type virus. A 5.4-fold reduction in EC\n            <jats:sub>50<\/jats:sub>\n            occurred in the presence of 40% human serum plus 27 mg\/ml of human serum albumin (HSA), which corresponded well to an\n            <jats:italic>in vitro<\/jats:italic>\n            measurement of 86% human serum binding. Time-of-addition and pseudotype reporter virus studies confirm a mechanism of action for the compound that occurs late in the virus replication cycle. BMS-955176 inhibits HIV-1 protease cleavage at the CA\/SP1 junction within Gag in virus-like particles (VLPs) and in HIV-1-infected cells, and it binds reversibly and with high affinity to assembled Gag in purified HIV-1 VLPs. Finally,\n            <jats:italic>in vitro<\/jats:italic>\n            combination studies showed no antagonistic interactions with representative antiretrovirals (ARVs) of other mechanistic classes. In conclusion, BMS-955176 is a second-generation MI with potent\n            <jats:italic>in vitro<\/jats:italic>\n            anti-HIV-1 activity and a greatly improved preclinical profile compared to that of bevirimat.\n          <\/jats:p>","DOI":"10.1128\/aac.02560-15","type":"journal-article","created":{"date-parts":[[2016,4,19]],"date-time":"2016-04-19T03:28:50Z","timestamp":1461036530000},"page":"3956-3969","update-policy":"https:\/\/doi.org\/10.1128\/asmj-crossmark-policy-page","source":"Crossref","is-referenced-by-count":68,"title":["Identification and Characterization of BMS-955176, a Second-Generation HIV-1 Maturation Inhibitor with Improved Potency, Antiviral Spectrum, and Gag Polymorphic Coverage"],"prefix":"10.1128","volume":"60","author":[{"given":"Beata","family":"Nowicka-Sans","sequence":"first","affiliation":[{"name":"Bristol-Myers Squibb, Research and Development, Department of Virology, Wallingford, Connecticut, 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