# Development and Translation of Generator-Produced PET Tracer for Myocardial Perfusion Imaging > **NIH NIH R01** · WASHINGTON UNIVERSITY · 2020 · $727,792 ## Abstract Abstract. Myocardial perfusion imaging (MPI), a versatile tool for clinical diagnosis, plays an important role in noninvasive identification of obstructive CAD. Currently, single-photon emission computed tomography (SPECT) MPI agents include 201Tl or 99mTc-complexes, such as 99mTc-sestamibi and 99mTc-tetrofosmin, for determining myocardial perfusion in patients with suspicion of or known CAD. However, SPECT imaging agents have inherent limitations, including the potential 99mMo/99mTc-generator shortage. Additionally, current SPECT tracers also suffer from shortcomings in pharmacokinetics, myocardial extraction, redistribution of the radiotracer to non-targeted tissues over time, and non-linearity of uptake at elevated blood flow (the “roll-off” phenomenon). Of note, SPECT MPI does not afford the routine clinical calculation of myocardial blood flow (MBF) in ml/g/min as is possible with positron emission tomography (PET). Thus, PET assessment of MBF or myocardial flow reserve (MFR) enables better identification and characterization of both subclinical and clinically-manifest CAD processes and provides important prognostic and therapeutic information, not achievable with SPECT MPI. Commonly employed PET MPI tracers are: 82RbCl, 13NH3, and H215O. Apart from their strengths and weaknesses, these tracers have limited utility for PET imaging due to short half- lives, and restricted access to imaging facilities located within nearby cyclotrons. To enhance access to PET MPI, few promising 18F-labeled agents such as18F-BnTP, a mitochondrial membrane potential probe, and 18F-BMS-747158,18F- 10, 18F-RP1004, and 18F-MCI27, mitochondrial complex I inhibitors, have been investigated in preclinical models. Among these agents, 18F-BMS-747158 (Flurpiridaz, the mitochondrial complex I targeted tracer) has advanced to phase 3 studies. Importantly, complex I deficiency, which is clinically and genetically heterogeneous, can present with hypertrophic cardiomyopathy that could either be isolated or associated with other comorbid multi-organ diseases. Thus, the lower uptake of a given mitochondrial complex I targeted tracer, such as 18F-Flurpiridaz could also be susceptible to these complications. However, these tracers depend on an 18F-radiopharmaceutical distribution business model, which may not readily apply to all sites within the U.S. or other countries in the world. Therefore, PET tracers demonstrating high myocardial first pass extraction, sustained myocardium retention and rapid liver clearance, in vivo stability, and a sufficiently long half-lives to enable PET myocardium imaging with quantification, while incorporating radionuclides that could potentially be generator-produced (rather than cyclotron produced) on site would facilitate wide access to PET MPI technology. To meet this unmet diagnostic clinical nuclear medicine need, we have developed 68Ga- Galmydar which demonstrates high extraction into the myocardium of mice, rats, and rabbits, while displayin... ## Key facts - **NIH application ID:** 9859464 - **Project number:** 5R01HL142297-02 - **Recipient organization:** WASHINGTON UNIVERSITY - **Principal Investigator:** Thomas Hellmut Schindler - **Activity code:** R01 (R01, R21, SBIR, etc.) - **Funding institute:** NIH - **Fiscal year:** 2020 - **Award amount:** $727,792 - **Award type:** 5 - **Project period:** 2019-03-01 → 2023-02-28 ## Primary source NIH RePORTER: https://reporter.nih.gov/project-details/9859464 ## Citation > US National Institutes of Health, RePORTER application 9859464, Development and Translation of Generator-Produced PET Tracer for Myocardial Perfusion Imaging (5R01HL142297-02). Retrieved via AI Analytics 2026-05-23 from https://api.ai-analytics.org/grant/nih/9859464. Licensed CC0. --- *[NIH grants dataset](/datasets/nih-grants) · CC0 1.0*