Dr Matthew Bull
BSc MSc PhD Auck.
Dr Matthew Bull
Dr Matthew Bull
https://unidirectory.auckland.ac.nz/profile/m-bullResearch Fellow The University of Auckland: Auckland Cancer Society Research Centre
Postdoctoral research fellow at the Auckland Cancer Society Research Centre with the Translational Therapeutics Team, led by Associate Professor Adam Patterson.
Research | Current
- Ongoing development of TH-4000, a hypoxia-selective tyrosine kinase inhibitor (TKI) curently in Phase 2 clincial trials for lung cancer and Head/Neck cancer in USA and Australia
- Development of additional hypoxia-selective TKI prodrugs
- Development of the hypoxia-selective analogues of the prodrug PR-104
Areas of expertise
- In vitro metabolism
- Bioanalysis (HPLC, LC/MS/MS, SPR etc)
- Hypoxia activated prodrugs
- Cancer drug development
Selected publications and creative works (Research Outputs)
- Silva, S., Jackson, V., Guise, C., Abbattista, M., Bull, M., Grey, A., ... Pearce, T. (2015). Preclinical efficacy of tarloxotinib bromide (TH4000), a hypoxiaactivated EGFR/HER2 inhibitor: Rationale for clinical evaluation in EGFR mutant, T790M-negative NSCLC following progression on EGFRTKI therapy. Paper presented at AACR-NCI-EORTC International Conference on Molecular Targets and Cancer Therapeutics, Boston, Massachusetts. 5 November - 9 November 2015. Molecular Cancer Therapeutics. (pp. 2).
Other University of Auckland co-authors: Gus Grey, Maria Abbattista, Christopher Guise, Bob Anderson, Amir Ashoorzadeh, Adam Patterson, Jeffrey Smaill, Victoria Jackson-Patel
- Bull, M., Spicer, J., Huttunen, K., Denny, W., Ciccone, A., Browne, K., ... Helsby, N. (2015). The preclinical pharmacokinetic disposition of a series of perforin-inhibitors as potential immunosuppressive agents. European Journal of Drug Metabolism and Pharmacokinetics, 40 (4), 417-425. 10.1007/s13318-014-0220-y
Other University of Auckland co-authors: Bill Denny, Julie Spicer, Nuala Helsby
- Patterson, A., Silva, S., Jackson, V., Guise, C., Abbattista, M. R., Bull, M., ... Jung, D. (2015). The hypoxia-activated EGFR-TKI TH-4000: Preclinical profile and ongoing clinical studies in NSCLC, SCCHN, and SCCS. Paper presented at 14th International Tumor Microenvironment Workshop: Hypoxia, Angiogensis and Vasculature, Vancouver, Canada. 27 August - 29 August 2015.
Other University of Auckland co-authors: Maria Abbattista, Adam Patterson, Christopher Guise, Amir Ashoorzadeh, Bob Anderson, Jeffrey Smaill, Gus Grey
- Patterson, A. V., Silva, S., Guise, C., Abbattista, M., Bull, M., Hsu, H.-L., ... Ashoorzadeh, A. (2015). Abstract 5358: The hypoxia-activated EGFR-TKI TH-4000 overcomes erlotinib-resistance in preclinical NSCLC models at plasma levels achieved in a Phase 1 clinical trial. Cancer Research. 10.1158/1538-7445.AM2015-5358
Other University of Auckland co-authors: Gus Grey, Adam Patterson, Christopher Guise, Maria Abbattista, Amir Ashoorzadeh, Bob Anderson, Jeffrey Smaill
- Patterson, A. V., Silva, S., Guise, C., Bull, M., Abbattista, M., Hsu, A., ... Smaill, J. B. (2015). TH-4000, a hypoxia-activated EGFR/Her2 inhibitor to treat EGFR-TKI resistant T790M-negative NSCLC. Paper presented at Annual Meeting of the American-Society-of-Clinical-Oncology (ASCO), Chicago, IL. 29 May - 2 June 2015. JOURNAL OF CLINICAL ONCOLOGY. (pp. 1).
Other University of Auckland co-authors: Christopher Guise, Jeffrey Smaill, Adam Patterson, Maria Abbattista
- Spicer, J., Lena, G., Lyons, D., Huttunen, K., Miller, C., O'Connor P, ... Denny, W. (2013). Exploration of a series of 5-arylidene-2-thioxoimidazolidin-4-ones as inhibitors of the cytolytic protein perforin. Journal of Medicinal Chemistry, 56 (23), 9542-9555. 10.1021/jm401604x
Other University of Auckland co-authors: Nuala Helsby, Christian Miller, Bill Denny, Julie Spicer, Stephen Jamieson
- Bull, M. R. (2013). The preclinical pharmacology of novel inhibitors of perforin function The University of Auckland. ResearchSpace@Auckland.
- Bull, M. R. (2009). The presence of illicit drugs on New Zealand currency The University of Auckland. ResearchSpace@Auckland.