Chen Xinhui, Seifert Sharon M, Castillo-Mancilla Jose R, Bushman Lane R, Zheng Jia-Hua, Kiser Jennifer J, MaWhinney Samantha, Anderson Peter L
University of Colorado, Skaggs School of Pharmacy and Pharmaceutical Sciences, Aurora, CO, United States of America.
University of Colorado, School of Medicine, Division of Infectious Diseases, Aurora, CO, United States of America.
PLoS One. 2016 Nov 10;11(11):e0165505. doi: 10.1371/journal.pone.0165505. eCollection 2016.
The coformulation of the nucleos(t)ide analogs (NA) tenofovir (TFV) disoproxil fumarate (TDF) and emtricitabine (FTC) is approved for HIV-infection treatment and prevention. Plasma TFV and FTC undergo complicated hybrid processes to form, accumulate, and retain as their active intracellular anabolites: TFV-diphosphate (TFV-DP) and FTC-triphosphate (FTC-TP). Such complexities manifest in nonlinear intracellular pharmacokinetics (PK). In target cells, TFV-DP/FTC-TP compete with endogenous deoxynucleoside triphosphates (dNTP) at the active site of HIV reverse transcriptase, underscoring the importance of analog:dNTP ratios for antiviral efficacy. However, NA such as TFV and FTC have the potential to disturb the dNTP pool, which could augment or reduce their efficacies. We conducted a pharmacokinetics-pharmacodynamics (PKPD) study among forty subjects receiving daily TDF/FTC (300 mg/200 mg) from the first-dose to pharmacological intracellular steady-state (30 days). TFV/FTC in plasma, TFV-DP/FTC-TP and dNTPs in peripheral blood mononuclear cells (PBMC) were quantified using validated LC/MS/MS methodologies. Concentration-time data were analyzed using nonlinear mixed effects modeling (NONMEM). Formations and the accumulation of intracellular TFV-DP/FTC-TP was driven by plasma TFV/FTC, which was described by a hybrid of first-order formation and saturation. An indirect response link model described the interplay between TFV-DP/FTC-TP and the dNTP pool change. The EC50 (interindividual variability, (%CV)) of TFV-DP and FTC-TP on the inhibition of deoxyadenosine triphosphate (dATP) and deoxycytidine triphosphate (dCTP) production were 1020 fmol/106 cells (130%) and 44.4 pmol/106 cells (82.5%), resulting in (90% prediction interval) 11% (0.45%, 53%) and 14% (2.6%, 35%) reductions. Model simulations of analog:dNTP molar ratios using IPERGAY dosing suggested that FTC significantly contributes to the protective effect of preexposure prophylaxis (PrEP). Simulation-based intracellular operational multiple dosing half-lives of TFV-DP and FTC-TP were 6.7 days and 33 hours. This model described the formation of intracellular TFV-DP/FTC-TP and the interaction with dNTPs, and can be used to simulate analog:dNTP time course for various dosing strategies.
核苷(酸)类似物替诺福韦(TFV)富马酸替诺福韦二吡呋酯(TDF)和恩曲他滨(FTC)的复方制剂已被批准用于治疗和预防HIV感染。血浆中的TFV和FTC会经历复杂的混合过程,形成、积累并保留为其活性细胞内代谢物:替诺福韦二磷酸酯(TFV-DP)和恩曲他滨三磷酸酯(FTC-TP)。这些复杂性表现为非线性细胞内药代动力学(PK)。在靶细胞中,TFV-DP/FTC-TP在HIV逆转录酶的活性位点与内源性脱氧核苷三磷酸(dNTP)竞争,突出了类似物与dNTP的比例对抗病毒疗效的重要性。然而,像TFV和FTC这样的核苷(酸)类似物有可能干扰dNTP池,这可能会增强或降低它们的疗效。我们对40名从首剂至药理学细胞内稳态(30天)每日接受TDF/FTC(300毫克/200毫克)的受试者进行了一项药代动力学-药效学(PKPD)研究。使用经过验证的液相色谱-串联质谱(LC/MS/MS)方法对血浆中的TFV/FTC、外周血单核细胞(PBMC)中的TFV-DP/FTC-TP和dNTP进行定量。使用非线性混合效应模型(NONMEM)分析浓度-时间数据。细胞内TFV-DP/FTC-TP的形成和积累由血浆TFV/FTC驱动,这由一级形成和饱和的混合模型描述。一个间接反应链接模型描述了TFV-DP/FTC-TP与dNTP池变化之间的相互作用。TFV-DP和FTC-TP对脱氧腺苷三磷酸(dATP)和脱氧胞苷三磷酸(dCTP)产生抑制作用的半数有效浓度(个体间变异性,(%CV))分别为1020飞摩尔/10^6个细胞(130%)和44.4皮摩尔/10^6个细胞(82.5%),导致(90%预测区间)分别降低11%(0.45%,53%)和14%(2.6%,35%)。使用IPERGAY给药方案对类似物与dNTP摩尔比进行的模型模拟表明,FTC对暴露前预防(PrEP)的保护作用有显著贡献。基于模拟的TFV-DP和FTC-TP的细胞内多次给药半衰期分别为6.7天和33小时。该模型描述了细胞内TFV-DP/FTC-TP的形成以及与dNTP的相互作用,可用于模拟各种给药策略下类似物与dNTP的时间进程。