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| ECHA InfoCard | 100.229.925 |
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| Formula | C22H21N3O3S |
| Molar mass | 407.49 g·mol−1 |
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ANA-12 is aselective,small-moleculenon-competitiveantagonist ofTrkB, the mainreceptor ofbrain-derived neurotrophic factor (BDNF).[1] ANA-12 was originally discovered and developed by Cazorla M. and colleagues atUniversité Paris andInserm in 2011.[1] The compound crosses theblood-brain-barrier and exerts central TrkB blockade, producing effects as early as 30 minutes (~400 nM) and as long as 6 hours (~10 nM) followingintraperitoneal injection in mice.[1] It blocks theneurotrophic actions of BDNF without compromisingneuron survival.[1]
ANA-12 has two binding sites on TrkB, a high- and low-affinity site (Kd = 10 nM and 12 μM, respectively).
ANA-12 produces rapidantidepressant- andanxiolytic-like effects inanimal models,[1] the former of which have been elucidated to be mediated by blockade of BDNF signaling in thenucleus accumbens.[2][3] It has also been found to alleviatemethamphetamine-induced depression-like behavior (includinganhedonia),behavioral sensitization, and nucleus accumbensneuroplasticity changes with subchronic (14-day) administration in mice, whereas the TrkB agonist7,8-dihydroxyflavone was ineffective in doing so.[4]
ANA-12 blocks thecognitive-enhancing effects ofenvironmental enrichment andcalorie restriction in rodents, which are mediated byBDNF signaling through TrkB in thehippocampus.[5][6] It also blocks hippocampal neurogenesis induced byphysical exercise in rodents, and may block the cognitive-enhancing effects of exercise as well.[7]
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