| Literature DB >> 26637161 |
Cody J Peer1, Andrew K L Goey1, Tristan M Sissung1, Sheryl Erlich1, Min-Jung Lee2, Yusuke Tomita2, Jane B Trepel2, Richard Piekarz3, Sanjeeve Balasubramaniam2, Susan E Bates2, William D Figg1,4.
Abstract
Belinostat is a second-generation zinc-binding histone deacetylase inhibitor that is approved for peripheral T-cell lymphoma and is currently being studied in small cell lung cancer and other advanced carcinomas as a 48-hour continuous intravenous infusion. Belinostat is predominantly metabolized by UGT1A1, which is polymorphic. Preliminary analyses revealed a difference in belinostat clearance based on UGT1A1 genotype. A 2-compartment population pharmacokinetic (PK) model was developed and validated that incorporated the UGT1A1 genotype, albumin, and creatinine clearance on the clearance parameter; body weight was a significant covariate on volume. Simulated doses of 600 and 400 mg/m(2) /24 h given to patients considered extensive or impaired metabolizers, respectively, provided equivalent AUCs. This model and subsequent simulations supported additional PK/toxicity and pharmacogenomics/toxicity analyses to suggest a UGT1A1 genotype-based dose adjustment to normalize belinostat exposure and allow for more tolerable therapy. In addition, global protein lysine acetylation was modeled with PK and demonstrated a reversible belinostat exposure/response relationship, consistent with previous reports.Entities:
Keywords: clinical pharmacology; oncology; pharmacogenetics; pharmacokinetics; pharmacometrics; population
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Year: 2015 PMID: 26637161 PMCID: PMC6357964 DOI: 10.1002/jcph.627
Source DB: PubMed Journal: J Clin Pharmacol ISSN: 0091-2700 Impact factor: 3.126