强CYP3A抑制和诱导对口服蛋白酶体抑制剂Ixazomib药代动力学的影响:晚期实体瘤或淋巴瘤患者的药物相互作用研究结果和基于生理的药代动力学分析。

IF 2.4 4区 医学 Q3 PHARMACOLOGY & PHARMACY
Journal of clinical pharmacology Pub Date : 2018-02-01 Epub Date: 2017-08-11 DOI:10.1002/jcph.988
Neeraj Gupta, Michael J Hanley, Karthik Venkatakrishnan, Alberto Bessudo, Drew W Rasco, Sunil Sharma, Bert H O'Neil, Bingxia Wang, Guohui Liu, Alice Ke, Chirag Patel, Karen Rowland Yeo, Cindy Xia, Xiaoquan Zhang, Dixie-Lee Esseltine, John Nemunaitis
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引用次数: 34

摘要

在临床相关的伊唑唑米浓度下,体外研究表明,没有特定的细胞色素P450 (CYP)酶主要参与伊唑唑米的代谢。然而,在高于临床浓度时,伊唑唑米被多种CYP亚型代谢,CYP3A的估计相对贡献最高,为42%。这项多组1期研究(Clinicaltrials.gov标识号:NCT01454076)探讨了强CYP3A抑制剂酮康唑和克拉霉素以及强CYP3A诱诱剂利福平对伊沙唑米药代动力学的影响。88名患者参与了3项药物-药物相互作用研究;ixazomib的毒性与先前的研究一致。酮康唑和克拉霉素对伊唑唑米的药代动力学无明显影响。在给药后0 ~ 264 h,酮康唑组与未给药组血浆浓度-时间曲线下的几何最小二乘平均面积(90%CI)分别为1.09(0.91 ~ 1.31)和1.11(0.86 ~ 1.43)。伊唑唑米与利福平联合给药后血浆暴露量减少。在利福平存在的情况下,Ixazomib在血浆浓度-时间曲线下的面积从时间0到最后可量化浓度时间减少了74%(几何最小二乘平均比为0.26 [90%CI 0.18-0.37]),最大观察血浆浓度减少了54%(几何最小二乘平均比为0.46 [90%CI 0.29-0.73])。临床药物-药物相互作用研究结果与基于生理学的药代动力学模型很好地吻合,该模型考虑了CYP3A对伊沙唑米总体清除率的微小贡献,并定量考虑了利福平诱导CYP3A和肠p糖蛋白的强度。基于这些研究结果,依沙唑米的处方信息建议患者应避免与依沙唑米同时使用强效CYP3A诱导剂。
本文章由计算机程序翻译,如有差异,请以英文原文为准。

Effects of Strong CYP3A Inhibition and Induction on the Pharmacokinetics of Ixazomib, an Oral Proteasome Inhibitor: Results of Drug-Drug Interaction Studies in Patients With Advanced Solid Tumors or Lymphoma and a Physiologically Based Pharmacokinetic Analysis.

Effects of Strong CYP3A Inhibition and Induction on the Pharmacokinetics of Ixazomib, an Oral Proteasome Inhibitor: Results of Drug-Drug Interaction Studies in Patients With Advanced Solid Tumors or Lymphoma and a Physiologically Based Pharmacokinetic Analysis.

Effects of Strong CYP3A Inhibition and Induction on the Pharmacokinetics of Ixazomib, an Oral Proteasome Inhibitor: Results of Drug-Drug Interaction Studies in Patients With Advanced Solid Tumors or Lymphoma and a Physiologically Based Pharmacokinetic Analysis.

Effects of Strong CYP3A Inhibition and Induction on the Pharmacokinetics of Ixazomib, an Oral Proteasome Inhibitor: Results of Drug-Drug Interaction Studies in Patients With Advanced Solid Tumors or Lymphoma and a Physiologically Based Pharmacokinetic Analysis.

At clinically relevant ixazomib concentrations, in vitro studies demonstrated that no specific cytochrome P450 (CYP) enzyme predominantly contributes to ixazomib metabolism. However, at higher than clinical concentrations, ixazomib was metabolized by multiple CYP isoforms, with the estimated relative contribution being highest for CYP3A at 42%. This multiarm phase 1 study (Clinicaltrials.gov identifier: NCT01454076) investigated the effect of the strong CYP3A inhibitors ketoconazole and clarithromycin and the strong CYP3A inducer rifampin on the pharmacokinetics of ixazomib. Eighty-eight patients were enrolled across the 3 drug-drug interaction studies; the ixazomib toxicity profile was consistent with previous studies. Ketoconazole and clarithromycin had no clinically meaningful effects on the pharmacokinetics of ixazomib. The geometric least-squares mean area under the plasma concentration-time curve from 0 to 264 hours postdose ratio (90%CI) with vs without ketoconazole coadministration was 1.09 (0.91-1.31) and was 1.11 (0.86-1.43) with vs without clarithromycin coadministration. Reduced plasma exposures of ixazomib were observed following coadministration with rifampin. Ixazomib area under the plasma concentration-time curve from time 0 to the time of the last quantifiable concentration was reduced by 74% (geometric least-squares mean ratio of 0.26 [90%CI 0.18-0.37]), and maximum observed plasma concentration was reduced by 54% (geometric least-squares mean ratio of 0.46 [90%CI 0.29-0.73]) in the presence of rifampin. The clinical drug-drug interaction study results were reconciled well by a physiologically based pharmacokinetic model that incorporated a minor contribution of CYP3A to overall ixazomib clearance and quantitatively considered the strength of induction of CYP3A and intestinal P-glycoprotein by rifampin. On the basis of these study results, the ixazomib prescribing information recommends that patients should avoid concomitant administration of strong CYP3A inducers with ixazomib.

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来源期刊
CiteScore
5.10
自引率
3.40%
发文量
176
审稿时长
2 months
期刊介绍: The Journal of Clinical Pharmacology (JCP) is a Human Pharmacology journal designed to provide physicians, pharmacists, research scientists, regulatory scientists, drug developers and academic colleagues a forum to present research in all aspects of Clinical Pharmacology. This includes original research in pharmacokinetics, pharmacogenetics/pharmacogenomics, pharmacometrics, physiologic based pharmacokinetic modeling, drug interactions, therapeutic drug monitoring, regulatory sciences (including unique methods of data analysis), special population studies, drug development, pharmacovigilance, womens’ health, pediatric pharmacology, and pharmacodynamics. Additionally, JCP publishes review articles, commentaries and educational manuscripts. The Journal also serves as an instrument to disseminate Public Policy statements from the American College of Clinical Pharmacology.
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