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Harrison College of Pharmacy

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Peter Panizzi headshot

Peter Panizzi

Unit: Drug Discovery and Development
Auburn University
Harrison College of Pharmacy
247 Pharmacy Research Building
Auburn, AL 36849
Phone: 334-844-7941
Fax: 334-844-8331

Curriculum Vitae



  • B.S. - Montevallo, 1996
  • M.S., Biochemistry - Vanderbilt, 1999
  • Ph.D., Cellular and Molecular Pathology - Vanderbilt, 2004

Current Funding

Roles of fibrin(ogen) in conformational activation of hemostatic proteinase precursors
National Institutes of Health - 1 R01 HL158918-01A1
05/10/22 – 04/30/26
Role: Co-Principal Investigator
This project focuses on the tracking and treatment of Gram-positive infections with monoclonal antibody therapies.

Laboratory Personnel

Graduate Students

  • Charlotte Muse, Pharm.D.

External Links

Research Interests

Overview – I am a Professor with Tenure at Auburn University. I have been at Auburn since Fall 2010, and my lab uses state-of-the-art molecular imaging technologies to monitor disease progression and to aid in the evaluation of currently approved and novel drugs. We primarily focus on the identification and treatment of Gram-positive infections of various types. We have both murine and porcine models of acute bacterial endocarditis that we use to better understand this rapidly progressing and often deadly disease.

Molecular imaging strategies aid us in tracking disease progression and identification of the casual pathogens. Our results are often confirmed via host organ homogenization followed by colony forming unit determination by serial dilution plating. Tissue histology on adjacent sections using Gram- and hematoxylin & eosin staining is done to assessment abscess architecture. In situ hybridization and fluorescence immunostaining studies performed in the lab help to assess host cellular response and virulence factor expression by the pathogens. One of our secondary lab focuses to investigate melanoma development and to better understand how these cancers cells metastasize in vivo.

Selected Publications

80+ publications, 8461 citations; H-index of 31; i10 of 43

My research uncovered the molecular mechanisms that staphylocoagulase uses to activate human clotting in the pathogenesis of acute bacterial endocarditis. In a series of collaborative study with the late Dr. Paul E. Bock and Ingrid Verhamme (Vanderbilt), Wolfram Bode, Robert Huber, and Pablo Fuentes-Prior (Max Planck Institute, Germany), we proved the "molecular sexuality" mechanism of staphylocoagulase-induced activation of host prothrombin by solving the X-ray crystal structures of various complexes of staphylocoagulase fragment with either human prethrombin 2 and thrombin. These new structures along with prothrombin activation studies employing N-terminal deletion mutants of staphylocoagulase proved the “molecular sexuality” mechanism was indeed valid. In more recent year, our studies have focused on the specificity of the activation pocket for different N-terminal SC residues. We also investigated the nature of fibrinogen binding by the C-terminal tandem repeats on SC.

  • Friedrich R, Panizzi P, Fuentes-Prior P, Richter K, Verhamme I, Anderson PJ, Kawabata S, Huber R, Bode W, Bock PE.(2003) “Staphylocoagulase is a Prototype for the Mechanism of Cofactor-induced Zymogen Activation.” Nature 425, 535-9. PMID: 14523451
  • Kroh H, Panizzi P, Bock PE. (2009) “von Willebrand Factor Binding Protein is a Novel Hysteretic Conformational Activator of Prothrombin.” Proc. Natl. Acad. Sci. USA. 106, 7786-91. PMCID: PMC2683071
  • Panizzi P, Nahrendorf M, Figueiredo JL, Panizzi JR, Marinelli B, Iwamoto Y, Keliher E, Waterman P, Kroh HK, Maddur AA, Aikawa E, Hackeng T, Fuentes-Prior P, Bock PE and Weissleder R (2011) “In vivo Detection of Staphylococcus aureus Endocarditis by targeting Pathogen-specific Prothrombin Activation” Nature Medicine 17, 1142-6. PMCID: PMC21857652
  • Maddur-Appajaiah A, Voehler M, Panizzi P, Meiler J, Bock PE and Verhamme I, “Mapping of the Fibrinogen-Binding Site on the Staphylocoagulase C-Terminal Repeat Region.” (2022), J Biol Chem., 298(1):101493. PMCID: PMC8761706

We have developed non-invasive molecular imaging technology to track pathogens during endocarditis, meningitis, and sepsis. As proof of principle, we began our studies with S. aureus, which has the unique ability to wall itself off from host blood and tissue cells, avoiding immune detection and causing localized inflammation at the surrounding infection site. In the pathology of endocarditis, the protective endothelium layer is damaged, and circulating bacteria adhere to these sites of exposed host basement matrix through bacterial surface receptors. In recent years, we have expanded to detection of endocarditis in our new piglet models for both right and left-sided endocarditis. We have also begun to study the mechanism of bacterial meningitis development by Strep. pneumonia via novel host skull channels.

  • Panizzi P, Stone JR, Nahrendorf M. (2014) “Endocarditis and molecular imaging.” J Nucl Cardiol. 21, 486-95. PMCID: PMC4106242
  • Panizzi P, Krohn-Grimberghe M*, Keliher E, Grune J, Frodermann V, Sun Y, Muse CG#, Begins K, Iwamoto Y, van Leent MMT, Meerwaldt A, Toner YC, Munitz J, Maier A, Soultanidis G, Calcagno C, Pérez-Medina C, Carlucci G, Riddell KP, Barney S, Horne G, Anderson B, Appajaiah AM, Verhamme IM, Bock PE, Wojtkiewicz GR, Courties G, Swirski FK, Church WR, Walz PH, D. Tillson M, Mulder WJM, and Nahrendorf M. “Multimodal Imaging of Bacterial-Host Interface in Mice and Piglets with Staphylococcus aureus Endocarditis.” (2020), Science Translational Medicine, Nov 4;12(568): eaay2104. - PMCID: PMC7818516
  • Pulous PE, Cruz-Hernández JC, Yang C, Kaya Z, Paccalet A, Wojtkiewicz G, Capen D, Brown D, Wu JW, Schloss MJ, Vinegoni C, Richter D, Yamazoe M, Hulsmans M, Momin N, Grune J, Rohde D, McAlpine CS, Panizzi P, Weissleder R, Kim DE, Swirski FP, Lin CP, Moskowitz MA, Nahrendorf M, “Cerebrospinal fluid outflow through skull channels instructs cranial hematopoiesis” (2022), Nature Neuroscience. 022 May; 25(5):567-576. doi: 10.1038/s41593-022-01060-2. PMCID: PMC9081225.

We use minimally invasive imaging agents to measure the increased inflammatory burden experienced by mice in models of cancer, atherosclerosis, and rheumatoid arthritis. Our results indicated that mice with atherosclerosis experienced imparted wound healing following myocardial infraction due to a large reduction in their ejection fractions caused by an increased scar formation. We have also developed new tools to assess inflammation and cancer progression and therapy.

  • Panizzi P, Swirski FK, Figueiredo JL, Waterman P, Sosnovik DS, Aikawa E, Libby P, Pittet M, Weissleder R, and Nahrendorf M. (2010) “Atherosclerosis-associated Ly-6Chi Blood Monocytosis Impairs Wound Healing in Mice with Myocardial Infarction” J. Am. Coll. Cardiol. 55, 1629-1638. PMCID: PMC2852892
  • Cortez-Retamozo V, Etzrodt M, Newton A, Ryan R, Pucci F, Sio SW, Kuswanto W, Rauch PJ, Chudnovskiy A, Iwamoto Y, Kohler R, Marinelli B, Gorbatov R, Wojtkiewicz G, Panizzi P, Mino-Kenudson M, Forghani R, Figueiredo JL, Chen JW, Xavier R, Swirski FK, Nahrendorf M, Weissleder R, Pittet MJ. (2013) “Angiotensin II drives the production of tumor-promoting macrophages.” Immunity 38, 296-308 PMCID: PMC3582771
  • Brannen A, Eggert M, Nahrendorf M, Arnold R, Panizzi P. (2018) “Correlation of 360-degree Surface Mapping In Vivo Bioluminescence with Multi-Spectral Optoacoustic Tomography in Human Xenograft Tumor Models.” Sci Rep. 8(1); 3321 PMCID: PMC5820276
  • Anani T#, Brannen A#, Panizzi P, Duin E, and David A, “Validation of Multispectral Optoacoustic Tomography (MSOT) Imaging for Quantitative, Real-time Tracking of Nanoparticle Pharmacokinetics and Biodistribution.” 2020, Journal of Pharmaceutical and Biomedical Analysis; 178:112951 - PMID: 31718983

In studies imaging cancer and rheumatoid arthritis, we wanted to assess the mediators of inflammatory burden, with the focus on myeloperoxidase, a central enzyme to inflammation. We developed a sensor of myeloperoxidase activity that can be used in mice to monitor disease pathology. Currently, we are developing novel ways to inhibit the myeloperoxidase enzyme by use of high throughput imaging, biochemical characterization, and toxicity screening in zebrafish. In two recent ABB papers, we report that potent myeloperoxidase inhibitors like benzoic acid hydrazide and its analogs cause disruption of these important ester linkages that link the heme to the body of the peroxidase.

  • Panizzi P, Nahrendorf M, Wildgruber M, Figueiredo JL, McCarthy, Weissleder R, and Hilderbrand S. (2009) “Oxazine Conjugated Iron Oxide Nanoparticle Detects In Vivo Reactive Oxygen Species Generation” J. Am. Chem. Society 131, 15739-44. PMCID: PMC2773134
  • Huang J, Smith F, Panizzi P. (2014) “Ordered Cleavage of Myeloperoxidase Ester Bonds Releases Active site Heme Leading to Inactivation of Myeloperoxidase by Benzoic Acid Hydrazide Analogs” Arch Biochem Biophys 548,74-85, PMCID:  PMC4336777
  • Huang J, Smith F, Panizzi JR, Goodwin DC, Panizzi P. (2015) “Inactivation of myeloperoxidase by     benzoic acid hydrazide.” Arch Biochem Biophys. 570, 14-22 PMCID: PMC4779370

Last Updated: January 18, 2023