Jayachandran Devaraj, Laínez-Aguirre José, Rundell Ann, Vik Terry, Hannemann Robert, Reklaitis Gintaras, Ramkrishna Doraiswami
School of Chemical Engineering, Purdue University, 480 Stadium Mall Way, West Lafayette, IN, 47907, United States of America.
Weldon School of Biomedical Engineering, Purdue University, 206 South Martin Jischke Drive, West Lafayette, IN, 47907, United States of America.
PLoS One. 2015 Jul 30;10(7):e0133244. doi: 10.1371/journal.pone.0133244. eCollection 2015.
6-Mercaptopurine (6-MP) is one of the key drugs in the treatment of many pediatric cancers, auto immune diseases and inflammatory bowel disease. 6-MP is a prodrug, converted to an active metabolite 6-thioguanine nucleotide (6-TGN) through enzymatic reaction involving thiopurine methyltransferase (TPMT). Pharmacogenomic variation observed in the TPMT enzyme produces a significant variation in drug response among the patient population. Despite 6-MP's widespread use and observed variation in treatment response, efforts at quantitative optimization of dose regimens for individual patients are limited. In addition, research efforts devoted on pharmacogenomics to predict clinical responses are proving far from ideal. In this work, we present a Bayesian population modeling approach to develop a pharmacological model for 6-MP metabolism in humans. In the face of scarcity of data in clinical settings, a global sensitivity analysis based model reduction approach is used to minimize the parameter space. For accurate estimation of sensitive parameters, robust optimal experimental design based on D-optimality criteria was exploited. With the patient-specific model, a model predictive control algorithm is used to optimize the dose scheduling with the objective of maintaining the 6-TGN concentration within its therapeutic window. More importantly, for the first time, we show how the incorporation of information from different levels of biological chain-of response (i.e. gene expression-enzyme phenotype-drug phenotype) plays a critical role in determining the uncertainty in predicting therapeutic target. The model and the control approach can be utilized in the clinical setting to individualize 6-MP dosing based on the patient's ability to metabolize the drug instead of the traditional standard-dose-for-all approach.
6-巯基嘌呤(6-MP)是治疗多种儿科癌症、自身免疫性疾病和炎症性肠病的关键药物之一。6-MP是一种前体药物,通过涉及硫嘌呤甲基转移酶(TPMT)的酶促反应转化为活性代谢物6-硫鸟嘌呤核苷酸(6-TGN)。在TPMT酶中观察到的药物基因组变异在患者群体中产生了显著的药物反应差异。尽管6-MP广泛使用且观察到治疗反应存在差异,但针对个体患者剂量方案进行定量优化的努力有限。此外,致力于药物基因组学以预测临床反应的研究远非理想。在这项工作中,我们提出了一种贝叶斯群体建模方法来开发人类6-MP代谢的药理学模型。面对临床环境中数据的稀缺性,使用基于全局敏感性分析的模型简化方法来最小化参数空间。为了准确估计敏感参数,利用了基于D-最优性准则的稳健最优实验设计。利用患者特异性模型,使用模型预测控制算法来优化剂量调度,目标是将6-TGN浓度维持在其治疗窗口内。更重要的是,我们首次展示了整合来自不同生物反应链水平(即基因表达-酶表型-药物表型)的信息如何在确定预测治疗靶点的不确定性方面发挥关键作用。该模型和控制方法可在临床环境中用于根据患者代谢药物的能力对6-MP给药进行个体化,而不是采用传统的一刀切标准剂量方法。