Understanding the interactions of drugs and xenobiotics with the liver has been a major focus of research at the University of Kansas for more than 20 years. Through a close partnership between the School of Medicine and the School of Pharmacy, KU has developed one of the premier University-based drug development centers in the United States. Liver Center investigators from both KUMC in Kansas City and KU in Lawrence collaborate on projects involving hepatic drug metabolism, liver toxicology and hepatoprotection, bile acid and organic ion transport, nuclear receptor control of hepatic function, and liver metabolomics.
David Buckley, PhD (XenoTech, LLC)
Bryan Copple, PhD
Regulation of Inflammation in the Liver by Early Growth Response Factor-1Grace Guo, PhD
Endobiotic and xenobiotic nuclear receptors in human healthBruno Hagenbuch, PhD
Organic Anion Transport, Bile Acid Transport, Transport Physiology, Hepatic Drug ClearanceCurtis Klaassen, PhD
Toxicology, biliary drug excretion, transgenic animals, gene expression, drug development to prevent and treat liver diseaseXiaochao Ma, PhD
Metabolism, Metabolomics, Metabolism-mediated toxicity
Andrew Parkinson, PhD (XenoTech, LLC)
Hepatic drug metabolism and toxicity, with a special emphasis on cytochrome P450 and human-based in vitro systems
Gregory Reed, PhD
Xenobiotic metabolism, drug disposition in humans, drug-drug and drug-diet interactions, pharmacokinetics, inter- and intra-individual variability in pharmacokineticsYu-Jui Yvonne Wan, PhD
Retinoic acid and its receptors, xenobiotic metabolism, alcoholic liver disease, liver cancer, and liver regenerationScott Weir, PharmD, PhD
Clinical pharmacology and developing innovative approaches to advance promising drug candidates from discovery through early drug development
Bao-Ting Zhu, PhD
Focuses on characterizing the diverse biological actions of naturally-occurring compounds in multiple human tissues in order to develop new therapeutic strategies for a variety of human diseases
Xiao-bo, Zhong, PhD
Influence on drug metabolism by genetic polymorphisms and epigenetic alterations in cytochrome P450, cytochrome P450 oxidoreductase (POR), glucuronosyltransferase (UGT), and nuclear receptor genes.

