Magnetic Thallium for MRI of Ischemic Heart Disease

Period of Performance: 08/01/1999 - 01/31/2000


Phase 1 SBIR

Recipient Firm

Eagle Vision Pharmaceutical Corporation
Downingtown, PA 19335
Principal Investigator

Research Topics


EVP 1001 is intended to be a unique, intracellular, cardiac specific magnetic resonance imaging (MRI) agent which specifically enhances both the myocardium and the vasculature. It will satisfy currently-unmet needs for the rapid, non-invasive diagnosis and treatment planning of ischemic heart disease, including simultaneous assessment of both structure and function (stenosis, occlusion, wall motion, myocardial perfusion and delineation of viable versus non-viable myocardium). The preclinical research proposed for Phase 1 will augment the cardiac safety of EVP 1001 and will define the relationship between its pharmacokinetics and its MR enhancement. Does regimens which provide effective cardiac and vascular MR enhancements will be delineated from these data. The unique magnetic properties of EVP 1001 are expected to provide enhancement at low doses compared to current gadolinium agents (3-15 versus 100-200 mumol/kg). Phase 2 will assess the safety and efficacy of EVP 1001 in models of cardiac ischemia, laying the foundation for human trials. When approved, this contrast agent will make optimal use of the powerful diagnostic potential of MRI and its rapid technical evolution, becoming the "one-stop shop" for diagnosis of coronary artery disease and replacing more costly and invasive tests. PROPOSED COMMERCIAL APPLICATIONS: The long-term goal of this research is to register EVP 1001 in the U.S. and elsewhere as a contrast agent for cardiovascular MRI. By combining the noninvasive assessment of both cardiac structure and function, this agent should provide more cost-effective diagnosis and treatment planning than echocardiography, nuclear perfusion/functional imaging, and x-ray angiography. In addition, its use as a vascular enhancement agent may be extended to other regions of the body.