Brendan D. Stamper, PhD
I teach the fundamental principles of medicinal chemistry, toxicology, and natural products predominantly to first-year pharmacy students. In the classroom, I enjoy finding creative ways to relate chemical structure to drug action in order to foster an engaging yet rigorous learning environment for my students. Brendan Stamper’s Vimeo Channel (PharmSongs)
PHRM 580 | Gastrointestinal & Nutrition
PHRM 581 | Endocrine & Sex Hormones
PHRM 583 | Immunology & Toxicology
PHRM 586 | Infectious Diseases
PHRM 648 | Gastrointestinal
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 technologies 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 exploring hepatotoxicity associated with exposure to acetaminophen, herbicides, and 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 (Tylenol) 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 levels increase, resulting in glutathione depletion, protein adduct formation, oxidative stress, and eventually liver injury. 3-hydroxyacetanilide can be used as a comparative tool to identify biologic targets and pathways unique to acetaminophen overdose. Efforts are currently underway to understand how these targets mediate drug-induced liver injury.
In other words: Acetaminophen and 3-hydroxyacetanilide 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.
Nguyen NU & Stamper BD. Polyphenols reported to shift APAP-induced changes in MAPK signaling and toxicity outcomes. Chem Biol Interact 2017 277:129-136.
Stamper BD, Buhler AV, Harrelson JP, Roberts SC, Malhotra A, Elbarbry FA, Rao D, Karimi R, Turner R, Marlow C, Devaud LL. Implementation of online prerequisite review tutorials for first year pharmacy students for predicting academic success. Curr Pharm Teach Learn 2017 9(2):261-271.
Davis M & Stamper BD. TAMH: a useful in vitro model for assessing hepatotoxic mechanisms. BioMed Res Int 2016, 2016:4780872.
Kyriakides M, Maitre L, Stamper BD, Mohar I, Kavanagh TJ, Foster J, Wilson ID, Holmes E, Nelson SD, Coen M. Comparative metabonomic analysis of hepatotoxicity induced by acetaminophen and its less toxic meta-isomer. Arch Toxicol 2016 90(12):3073-3085.
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
2016 | AACP Excellence in Assessment Award
2015 | Pacific University Junior Faculty Award
2015 | Pacific University School of Pharmacy Dean’s Faculty Excellence Award
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