Brendan D. Stamper, PhD

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Office Location: 
Creighton Hall 466


Block Coordinator

PHRM 560 | Biochemistry I

PHRM 580 | Gastrointestinal & Nutrition


PHRM 586 | Infectious Diseases

AUD 513 | Pharmacology & Ototoxicity


2010-2012 | Postdoctoral Fellow, Seattle Children’s Research Institute, Seattle, WA

2010 | Doctor of Philosophy, Medicinal Chemistry, University of Washington, Seattle, WA

2002 | Bachelor of Science, Chemistry, Santa Clara University, CA

2002 | Bachelor of Sciences, Combined Sciences, Santa Clara University, CA

Areas of Research & Specialization

My research is focused on projects that utilize comparative genomic, transcriptomic, and proteomic approaches to identify key pathways critical to propagating toxicologic and pathologic outcomes. The adaptability of ‘omic allows my lab to investigate pathologic mechanisms across a wide array of disease states, both inborn and drug-induced. Projects currently underway include mechanistic studies looking at acetaminophen-induced hepatotoxicity, hepatotoxicity associated with various natural products.

Acetaminophen project: This project is an ongoing toxicogenomic study investigating the differential toxicity associated with acetaminophen and its regioisomer, 3-hydroxyacetanilide.  Acetaminophen is a widely available analgesic and antipyretic, and while considered to be relatively safe at recommended doses, over 50,000 emergency room visits occur annually in the United States due to overdose.  At therapeutic levels, the majority of an acetaminophen dose is metabolized to relatively non-toxic products via sulfation and glucuronidation reactions.  A smaller percentage of the dose is metabolized to the reactive intermediate, N-acetyl-p-quinoneimine (NAPQI), which is conjugated to glutathione and safely cleared.  In overdose situations, NAPQI concentrations rise, resulting in glutathione depletion, protein adduct formation, oxidative stress, and eventually liver injury.  Using 3-hydroxyacetanilide as a comparative tool, gene expression profiling studies have been able to identify key biologic targets and pathways associated with the toxic response following acetaminophen overdose.  Efforts are currently underway to understand of the role these targets play in signal transduction in hopes of gaining clearer insight into the cellular mechanisms that mediate drug-induced liver injury.

In other words: Acetaminophen and AMAP are structurally similar, yet only acetaminophen is toxic at high doses.  While acetaminophen and AMAP trigger many of the same effects in cells, some cellular outcomes are different. It’s within these differences that we hope to clarify precisely why high-dose acetaminophen can lead to liver toxicity.


Stamper BD, Garcia M, Nguyen DQ, Beyer RP, Bammler TK, Farin FM, Kavanagh TJ, Nelson SD.p53 contributes to differentiating gene expression following exposure to acetaminophen and its less hepatotoxic regioisomer both in vitro and in vivo. Gene Regul Syst Bio 2015 9:1-14.

Park SS, Beyer RP, Smyth MD, Clarke CM, Timms AE, Bammler TK, Stamper BD, Gustafson J, Cunningham ML. Osteoblast differentiation profiles define sex specific gene expression patterns in craniosynostosis. Bone 2015 76:169-176.

Stamper BD. Transcriptional profiling of reactive metabolites for elucidating toxicological mechanisms:  a case study of quioneimine-forming agents. Drug Metab Rev 2015 47(1):1-11.

Mohar I, Stamper BD, Rademacher PM, White CC, Nelson SD, Kavanagh TJ. Acetaminophen-induced liver damage in mice is associated with gender-specific adduction of peroxiredoxin-6. Redox Biol 2014, 2:377-387.

Stamper BD. The utilization of online gene expression data repositories to generate testable hypotheses in the laboratory. Transcriptomics 2013, 1:e104.

Stamper BD, Mecham B, Park SS, Wilkerson HW, Farin FM, Beyer RP, Bammler TK, Mangravite LM, Cunningham ML. Transcriptome correlation analysis identifies two unique craniosynostosis subtypes associated with IRS1 activation. Physiol Genomics 2012, 44(23):1154-63.

Stamper, B.D., Park, S.S., Beyer, R.P., Bammler, T.K., Cunningham, M.L. Unique sex-based approach identifies transcriptomic biomarkers associated with non-syndromic craniosynostosis.Gene Regul Syst Bio. 2012; 6:81-92.

Harrelson, J.P., Stamper, B.D., Chapman, J.D., Goodlett, D.R., Nelson, S.D. Covalent Modification and Time-Dependent Inhibition of Human CYP2E1 by the Meta Isomer of Acetaminophen. Drug Metab Dispos 2012, 40(8):1460-5.

Rieder, M.J., Green, G.E., Park, S.S., Stamper, B.D., Gordon, C.T., Johnson, J.M., Cunniff, C.M., Smith, J.D., Emery, S.B., Lyonnet, S., Amiel, J., Holder, M., Heggie, A.A., Bamshad, M.J., Nickerson, D.A., Cox, T.C., Hing, A.V., Horst, J.A., Cunningham, M.L. A human homeotic transformation resulting from mutations in PLCB4 and GNAI3 causes auriculocondylar syndrome. Am J Hum Genet. 2012 May 4; 90(5):907-14.

Stamper, B.D., Park, S.S., Beyer, R.P., Bammler, T.K., Farin, F.M., Mecham, B., Cunningham, M.L. Differential expression of extracellular matrix-mediated pathways in single-suture craniosynostosis. PLoS One. 2011;6(10):e26557.

Stamper, B.D., Mohar, I., Kavanagh, T.J., Nelson, S.D. Proteomic analysis of acetaminophen-induced changes in mitochondrial protein expression using spectral counting. Chem Res Toxicol2011, 24(4):549-58.

Stamper, B.D., Bammler, T.K., Beyer, R.P., Farin, F.M., Nelson, S.D. Differential regulation of mitogen-activated protein kinase pathways by acetaminophen and its nonhepatotoxic regioisomer 3'-hydroxyacetanilide in TAMH cells. Toxicol Sci 2010, 116(1):164-73.

Honors & Awards

2014 | AACP Innovations in Teaching Competition Award

2011 | Sage Bionetworks Washington Partner’s Program Award (funded by the Washington Life Sciences Discovery Fund)

2009 | Carl C. Smith Award, Honorable Mention

2004 | University of Washington Drug Metabolism Transport and Pharmacogenomic Research Program Award


By appointment

Area of Study I Teach (Graduate/Professional):