Histone methylation is associated with the pathophysiology of neurodevelopmental disorders. Lysine-specific demethylase 1 (LSD1) catalyzes histone demethylation in a flavin adenine dinucleotide (FAD)-dependent manner. Thus, inhibiting LSD1 enzyme activity could offer a novel way to treat neurodevelopmental disorders. Assessing LSD1 target engagement using positron-emission tomography (PET) imaging could aid in developing therapeutic LSD1 inhibitors. In this study, PET probes based on 4-(2-aminocyclopropyl)benzamide derivatives that bind irreversibly to FAD found in LSD1 were examined. By optimizing the profiles of brain penetrance and brain-penetrant metabolites, T-914 (1g) was identified as a suitable PET tracer candidate. PET studies in nonhuman primates demonstrated that [18F]1g had heterogeneous brain uptake, which corresponded to known LSD1 expression levels. Moreover, brain uptake of [18F]1g was reduced by coadministration of unlabeled 1g, demonstrating blockable binding. These data suggest that [18F]1g warrants further investigation as a potential PET tracer candidate for assessing target engagement of LSD1.