Matt Lopper

Dr. Matthew Lopper is an Associate Professor in the Chemistry Department at the University of Dayton, where he also earned his B.S. in Biochemistry (1998) and later returned after completing his Ph.D. in Biomolecular Chemistry at the University of Wisconsin-Madison (2003). He serves dual affiliations with the College of Arts and Sciences and the School of Engineering's Bioengineering Graduate Program. His research focuses on combating bacterial multi-drug resistance by discovering novel inhibitors of bacterial efflux pumps.

Education:

• B.S., Biochemistry, University of Dayton (1998)
• Ph.D., Biomolecular Chemistry, University of Wisconsin-Madison (2003)

Research Interests: Dr. Lopper's work bridges structural biology and microbiology. He investigates mechanisms of DNA replication restart in bacteria and develops small-molecule inhibitors targeting bacterial helicases like PriA. His research emphasizes understanding protein interactions critical for bacterial survival and applying this knowledge to antibiotic development. Key areas include bacterial efflux pumps, DNA repair pathways, and viral membrane fusion processes.

Teaching & Mentoring: He teaches advanced biochemistry courses (CHM 420, 451, 452, 454) and emphasizes communication skills for scientists. He believes mentorship is foundational to student success, fostering independent thinkers through active engagement. His teaching philosophy prioritizes student curiosity and confidence in scientific inquiry.

Grants & Awards: While specific awards are not listed, his publications reflect sustained grant-funded research in bacterial molecular mechanisms. His work has been supported through competitive grants for studies on primosome assembly and helicase inhibitors.

Lab & Collaborations: Though not explicitly named, his projects involve interdisciplinary collaborations in biochemistry, microbiology, and structural biology. His research contributes to both academic and applied fields, addressing urgent challenges in antibiotic resistance and viral pathogenesis.