Evaluates a novel MAO-B PET tracer in a rat model, suggesting potential for neurodegenerative disease imaging.
Monoamine oxidase B (MAO-B), upregulated in reactive astrogliosis, represents a promising positron emission tomography (PET) target for neurodegenerative disorders. In this study, 37 fluorinated indazole carboxamide derivatives were designed and synthesized as MAO-B inhibitors. Among them, compound 32 showed outstanding MAO-B inhibitory activity (IC 50 = 0.07 nM) and excellent selectivity over MAO-A. Automated radiosynthesis offered [ 18 F] 32 with high molar activity (135.8 GBq/μmol) and radiochemical yield (36.5%, decay-corrected to end-of-bombardment). Dynamic PET imaging revealed efficient blood–brain barrier penetration of [ 18 F] 32 (SUV 1 min = 1.40 in rat), with specific binding confirmed by selegiline blocking. Ex vivo autoradiography revealed region-specific binding of [ 18 F] 32 to MAO-B in rat brain. Metabolism studies showed that 62 ± 4% of brain radioactivity remained as the parent fraction at 30 min post-injection. Altogether, this work provides a novel MAO-B PET tracer based on an indazole carboxamide scaffold, potentially providing inspiration for future tracer development.
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