Afobazole is a multi-targeted anxiolytic drug with neuroprotective activities.1,2 It binds to the sigma-1, melatonin MT1, and MT3 receptors, as well as monoamine oxidase A (MAO-A; Kis = 5.9, 160, 0.97, and 3.6 ?M, respectively, in a radioligand binding assay).1 Afobazole (5 mg/kg) decreases the latency to enter, as well as increases the number of entries into and percentage of time spent in, the open arms of the elevated plus maze, indicating anxiolytic-like activity in passive stress-coping BALB/c, but not active stress-coping C57BL/6, mice.3 It decreases stroke volume and neuronal and oligodendroglial cell death in the brain in a rat model of ischemia induced by middle cerebral artery occlusion (MCAO) when administered at doses of 0.3 and 3 mg/kg.2
1.Seredenin, S.B., and Voronin, M.V.[Neuroreceptor mechanisms of the afobazole effect]Eksp. Klin. Farmakol.72(1)3-11(2009) 2.Katnik, C., Garcia, A., Behensky, A.A., et al.Treatment with afobazole at delayed time points following ischemic stroke improves long-term functional and histological outcomesNeurobiol. Dis.62354-364(2014) 3.Anderzhanova, E.A., B?chli, H., Buneeva, O.A., et al.Strain differences in profiles of dopaminergic neurotransmission in the prefrontal cortex of the BALB/C vs. C57Bl/6 mice: Consequences of stress and afobazoleEur. J. Pharmacol.708(1-3)95-104(2013)