In silico analysis of interactions of flucloxacillin and its metabolites with HLA-B*57:01
Author:
Affiliation:
1. Department of Basic and Molecular Medicine, Tokai University School of Medicine
2. Institute of Advanced Biosciences, Tokai University
Publisher
Chem-Bio Informatics Society
Subject
Biochemistry
Link
https://www.jstage.jst.go.jp/article/cbij/19/0/19_1/_pdf
Reference10 articles.
1. [1] Wing, K.; Bhaskaran, K.; Pealing, L.; Root, A.; Smeeth, L.; et al. Quantification of the risk of liver injury associated with flucloxacillin: a UK population-based cohort study. J. Antimicrob. Chemother., 2017, 72, 2636–2646.
2. [2] Stevens, J. L.; Baker, T. K. The future of drug safety testing: expanding the view and narrowing the focus. Drug Discov.Today. , 2009, 14,162–167.
3. [3] Daly A. K.; Donaldson, P. T.; Bhatnagar, P.; Shen, Y.; Pe’er, I.; et al. HLA-B*5701 genotype is a major determinant of drug-induced liver injury due to flucloxacillin. Nat. Genet., 2009, 41, 816–819.
4. [4] Illing, P. T.; Vivian, J. P.; Dudek, N. L.; Kostenko, L.; Chen, Z. et al. Immune self-reactivity triggered by drug-modified HLA-peptide repertoire. Nature, 2012, 486, 554–558.
5. [5] Keun, H. C.; Athersuch, T. J.; Beckonert, O.; Wang, Y.; Saric, J.; et al. Heteronuclear 19F-1H statistical total correlation spectroscopy as a tool in drug metabolism: study of flucloxacillin biotransformation. Anal. Chem., 2008, 80, 1073–1079.
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