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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 a selective, small-molecule non-competitive antagonistofTrkB, the main receptorofbrain-derived neurotrophic factor (BDNF).[1] ANA-12 was originally discovered and developed by Cazorla M. and colleagues at Université Paris and Inserm in 2011.[1] The compound crosses the blood-brain-barrier and exerts central TrkB blockade, producing effects as early as 30 minutes (~400 nM) and as long as 6 hours (~10 nM) following intraperitoneal injection in mice.[1] It blocks the neurotrophic actions of BDNF without compromising neuron 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 rapid antidepressant- and anxiolytic-like effects in animal models,[1] the former of which have been elucidated to be mediated by blockade of BDNF signaling in the nucleus accumbens.[2][3] It has also been found to alleviate methamphetamine-induced depression-like behavior (including anhedonia), behavioral sensitization, and nucleus accumbens neuroplasticity changes with subchronic (14-day) administration in mice, whereas the TrkB agonist 7,8-dihydroxyflavone was ineffective in doing so.[4]
ANA-12 blocks the cognitive-enhancing effects of environmental enrichment and calorie restriction in rodents, which are mediated by BDNF signaling through TrkB in the hippocampus.[5][6] It also blocks hippocampal neurogenesis induced by physical exercise in rodents, and may block the cognitive-enhancing effects of exercise as well.[7]
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