Nowicka-Sans Beata, Protack Tricia, Lin Zeyu, Li Zhufang, Zhang Sharon, Sun Yongnian, Samanta Himadri, Terry Brian, Liu Zheng, Chen Yan, Sin Ny, Sit Sing-Yuen, Swidorski Jacob J, Chen Jie, Venables Brian L, Healy Matthew, Meanwell Nicholas A, Cockett Mark, Hanumegowda Umesh, Regueiro-Ren Alicia, Krystal Mark, Dicker Ira B
Bristol-Myers Squibb, Research and Development, Department of Virology, Wallingford, Connecticut, USA.
Bristol-Myers Squibb, Research and Development, Department of Discovery Chemistry, Wallingford, Connecticut, USA.
Antimicrob Agents Chemother. 2016 Jun 20;60(7):3956-69. doi: 10.1128/AAC.02560-15. Print 2016 Jul.
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 ∼50% 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/Δ, and T371A/Δ), leading incrementally to the identification of BMS-955176. BMS-955176 exhibits potent activity (50% effective concentration [EC50], 3.9 ± 3.4 nM [mean ± standard deviation]) toward a library (n = 87) of gag/pr recombinant viruses representing 96.5% of subtype B polymorphic Gag diversity near the CA/SP1 cleavage site. BMS-955176 exhibited a median EC50 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 EC50s similar to those for the wild-type virus. A 5.4-fold reduction in EC50 occurred in the presence of 40% human serum plus 27 mg/ml of human serum albumin (HSA), which corresponded well to an in vitro 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, in vitro 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 in vitro anti-HIV-1 activity and a greatly improved preclinical profile compared to that of bevirimat.
BMS-955176是第二代1型人类免疫缺陷病毒(HIV-1)成熟抑制剂(MI)。第一代MI贝维拉马在早期研究中显示出临床疗效,但约50%的受试者体内的病毒对MI作用位点附近Gag中自然发生的多态性具有降低的敏感性。使用一组经过基因工程改造的报告病毒优化MI效力,这些病毒在Gag中含有定点多态性变化,可降低对贝维拉马的敏感性(包括V362I、V370A/M/Δ和T371A/Δ),逐步鉴定出了BMS-955176。BMS-955176对一个代表CA/SP1切割位点附近96.5% B亚型多态性Gag多样性的gag/pr重组病毒库(n = 87)表现出强效活性(50%有效浓度[EC50],3.9±3.4 nM[平均值±标准差])。BMS-955176对外周血单核细胞(PBMC)中检测的B亚型临床分离株库的EC50中位数为21 nM。对一组逆转录酶、蛋白酶和整合酶抑制剂耐药病毒保持了强效活性,其EC50与野生型病毒相似。在40%人血清加27 mg/ml人血清白蛋白(HSA)存在的情况下,EC50降低了5.4倍,这与86%人血清结合的体外测量结果非常吻合。加样时间和假型报告病毒研究证实了该化合物在病毒复制周期后期发生作用的机制。BMS-955176在病毒样颗粒(VLP)和HIV-1感染细胞中抑制Gag内CA/SP1连接处的HIV-1蛋白酶切割,并且它以可逆且高亲和力的方式结合纯化的HIV-1 VLP中组装好的Gag。最后,体外联合研究表明,它与其他作用机制类别的代表性抗逆转录病毒药物(ARV)没有拮抗相互作用。总之,与贝维拉马相比,BMS-955176是一种具有强效体外抗HIV-1活性且临床前特征有极大改善的第二代MI。