Department of Pharmacy, Radboud Institute for Health Sciences & Radboudumc Center for Infectious Diseases, Radboud University Medical Center, Nijmegen, The Netherlands.
Department of Pharmacology and Toxicology, Radboud Institute for Molecular Life Sciences, Radboud University Medical Center, Nijmegen, The Netherlands.
J Clin Pharmacol. 2022 Mar;62(3):385-396. doi: 10.1002/jcph.1972. Epub 2021 Oct 25.
Moxifloxacin has an important role in the treatment of tuberculosis (TB). Unfortunately, coadministration with the cornerstone TB drug rifampicin results in suboptimal plasma exposure. We aimed to gain insight into the moxifloxacin pharmacokinetics and the interaction with rifampicin. Moreover, we provided a mechanistic framework to understand moxifloxacin pharmacokinetics. We developed a physiologically based pharmacokinetic model in Simcyp version 19, with available and newly generated in vitro and in vivo data, to estimate pharmacokinetic parameters of moxifloxacin alone and when administered with rifampicin. By combining these strategies, we illustrate that the role of P-glycoprotein in moxifloxacin transport is limited and implicate MRP2 as transporter of moxifloxacin-glucuronide followed by rapid hydrolysis in the gut. Simulations of multiple dose area under the plasma concentration-time curve (AUC) of moxifloxacin (400 mg once daily) with and without rifampicin (600 mg once daily) were in accordance with clinically observed data (predicted/observed [P/O] ratio of 0.87 and 0.80, respectively). Importantly, increasing the moxifloxacin dose to 600 mg restored the plasma exposure both in actual patients with TB as well as in our simulations. Furthermore, we extrapolated the single dose model to pediatric populations (P/O AUC ratios, 1.04-1.52) and the multiple dose model to children with TB (P/O AUC ratio, 1.51). In conclusion, our combined approach resulted in new insights into moxifloxacin pharmacokinetics and accurate simulations of moxifloxacin exposure with and without rifampicin. Finally, various knowledge gaps were identified, which may be considered as avenues for further physiologically based pharmacokinetic refinement.
莫西沙星在结核病(TB)治疗中具有重要作用。不幸的是,与基石抗结核药物利福平联合使用会导致其血浆暴露不理想。我们旨在深入了解莫西沙星的药代动力学及其与利福平的相互作用。此外,我们提供了一个机制框架来理解莫西沙星的药代动力学。我们在 Simcyp 版本 19 中开发了一个基于生理学的药代动力学模型,结合了可用的和新生成的体外和体内数据,以单独估计莫西沙星和与利福平联合使用时的药代动力学参数。通过结合这些策略,我们表明 P-糖蛋白在莫西沙星转运中的作用有限,并暗示 MRP2 是莫西沙星-葡萄糖醛酸的转运体,随后在肠道中快速水解。模拟莫西沙星(400mg 每天一次)多次给药后血浆浓度-时间曲线下面积(AUC),并与利福平(600mg 每天一次)联合或不联合,与临床观察到的数据一致(预测/观察 [P/O] 比值分别为 0.87 和 0.80)。重要的是,将莫西沙星剂量增加到 600mg 可恢复实际结核病患者和我们模拟中的血浆暴露。此外,我们将单次剂量模型外推至儿科人群(P/O AUC 比值,1.04-1.52)和结核病儿童的多次剂量模型(P/O AUC 比值,1.51)。总之,我们的综合方法为莫西沙星药代动力学提供了新的见解,并准确模拟了莫西沙星与利福平联合或不联合使用时的暴露情况。最后,确定了各种知识空白,这些空白可能被视为进一步基于生理学的药代动力学细化的途径。