Landry Ishani, Zhu Li, Abu Tarif Malaz, Hruska Matthew, Sadler Brian M, Pitsiu Maria, Joshi Samit, Hanna George J, Lataillade Max, Boulton David W, Bertz Richard J
Bristol-Myers Squibb, Research and Development, Princeton, New Jersey, USA.
ICON plc, Cary, North Carolina, USA.
Antimicrob Agents Chemother. 2016 Apr 22;60(5):2782-9. doi: 10.1128/AAC.02503-15. Print 2016 May.
BMS-663068 is an oral prodrug of the HIV-1 attachment inhibitor BMS-626529, which prevents viral attachment to host CD4(+) T cells by binding to HIV-1 gp120. To guide dose selection for the phase 3 program, pharmacokinetic/pharmacodynamic modeling was performed using data from two phase 2 studies with HIV-1-infected subjects (n = 244). BMS-626529 population pharmacokinetics were described by a two-compartment model with first-order elimination from the central compartment, zero-order release of prodrug from the extended-release formulation into a hypothetical absorption compartment, and first-order absorption into the central compartment. The covariates of BMS-663068 formulation type, lean body mass, baseline CD8(+) T-cell percentage, and ritonavir coadministration were found to be significant contributors to intersubject variability. Exposure-response analyses showed a relationship between the loge-transformed concentration at the end of a dosing interval (Ctau) normalized for the protein binding-adjusted BMS-626529 half-maximal (50%) inhibitory concentration (PBAIC50) and the change in the HIV-1 RNA level from the baseline level after 7 days of BMS-663068 monotherapy. The probability of achieving a decline in HIV-1 RNA level of >0.5 or >1.0 log10 copies/ml as a function of the loge-transformed PBAIC50-adjusted Ctau after 7 days of monotherapy was 99 to 100% and 57 to 73%, respectively, for proposed BMS-663068 doses of 400 mg twice daily (BID), 600 mg BID (not studied in the phase 2b study), 800 mg BID, 600 mg once daily (QD), and 1,200 mg QD. On the basis of a slight advantage in efficacy of BID dosing over QD dosing, similar responses for the 600- and 800-mg BID doses, and prior clinical observations, BMS-663068 at 600 mg BID was predicted to have the optimal benefit-risk profile and selected for further clinical investigation. (The phase 2a proof-of-concept study AI438006 and the phase 2b study AI438011 are registered at ClinicalTrials.gov under numbers NCT01009814 and NCT01384734, respectively.).
BMS-663068是HIV-1附着抑制剂BMS-626529的口服前体药物,它通过与HIV-1 gp120结合来阻止病毒附着于宿主CD4(+) T细胞。为指导3期临床试验的剂量选择,利用两项针对HIV-1感染受试者的2期研究(n = 244)的数据进行了药代动力学/药效学建模。BMS-626529的群体药代动力学由一个二室模型描述,中央室以一级速率消除,前体药物从缓释制剂以零级速率释放到一个假设的吸收室,然后以一级速率吸收进入中央室。发现BMS-663068的制剂类型、瘦体重、基线CD8(+) T细胞百分比和利托那韦合用等协变量是受试者间变异性的重要影响因素。暴露-反应分析显示,在BMS-663068单药治疗7天后,经蛋白结合调整的BMS-626529半数最大(50%)抑制浓度(PBAIC50)归一化后的给药间隔末期对数转换浓度(Ctau)与HIV-1 RNA水平相对于基线水平的变化之间存在关系。对于提议的BMS-663068剂量,即每日两次400 mg(BID)、每日两次600 mg(2b期研究未研究此剂量)、每日两次800 mg、每日一次600 mg(QD)和每日一次1200 mg,单药治疗7天后,HIV-1 RNA水平下降>0.5或>1.0 log10拷贝/ml的概率分别为99%至100%和57%至73%。基于每日两次给药在疗效上略优于每日一次给药、600 mg和800 mg每日两次剂量的反应相似以及既往临床观察结果,预计每日两次600 mg的BMS-663068具有最佳的效益风险比,并被选择进行进一步的临床研究。(2a期概念验证研究AI438006和2b期研究AI438011分别在ClinicalTrials.gov上注册,注册号为NCT01009814和NCT01384734。)