RT Journal Article SR Electronic T1 Synthesis and In Vivo Evaluation of 18F-Desbromo-DuP-697 as a PET Tracer for Cyclooxygenase-2 Expression JF Journal of Nuclear Medicine JO J Nucl Med FD Society of Nuclear Medicine SP 1700 OP 1706 VO 44 IS 10 A1 Erik F.J. de Vries A1 Aren van Waarde A1 Anne Rixt Buursma A1 Willem Vaalburg YR 2003 UL http://jnm.snmjournals.org/content/44/10/1700.abstract AB Cyclooxygenase-2 (COX-2) overexpression has been observed in various pathologies, such as inflammation, cancer, ischemia, and Alzheimer’s disease. As an initial step toward a noninvasive PET technique to assay COX-2 expression, this study describes the synthesis and preliminary evaluation of the radiolabeled COX-2 inhibitor 18F-desbromo-DuP-697. Methods: Desbromo-DuP-697 was radiolabeled by a nucleophilic aromatic substitution reaction of the nitro precursor with 18F-fluoride. Biodistribution studies of the tracer were performed in a carrageenan-induced hyperalgesia rat model. Brain uptake was investigated with autoradiography. To confirm the results of the biodistribution, COX activity was determined by a peroxidase assay. Results: Biodistribution studies showed specific binding of the tracer to COX-2 in heart, kidney, brain, and blood cells, but not in the inflamed paw, which was probably due to low COX-2 expression. In the brain, regional differences in tracer uptake were observed, with high uptake in cortical regions. 18F-Desbromo-DuP-697 did not show any binding to COX-1. Nonspecific uptake was high in fat and intestines. Conclusion: Because of its ability to cross the blood-brain barrier, 18F-desbromo-DuP-697 appears to be suitable for COX-2 imaging in the brain. Its high nonspecific uptake in the intestines may limit its use for imaging in the abdominal region.