ArticleCNS neuroscience & therapeutics2014
N-(furan-2-ylmethyl)-N-methylprop-2-yn-1-amine (F2MPA): A potential cognitive enhancer with MAO inhibitor properties.
Article in CNS neuroscience & therapeutics, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 papers.
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Who cites it
3 citing papers in PubMed, 13 citations in OpenAlex.
- Ginkgo Biloba as a niche theme cognitive enhancer agent, 1420 dokumen of Scopus database. A bibliometric study from 1988 to 2024.F1000Research · 2025Article
- Monoaminergic neuropathology in Alzheimer's disease.Progress in neurobiology · 2017Review
- Role(s) of the 5-HT2C receptor in the development of maximal dentate activation in the hippocampus of anesthetized rats.CNS neuroscience & therapeutics · 2014Article
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Authors and funding
12 authors at 7 institutions in 5 countries.
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No grant is acknowledged in the PubMed record.
Abstract
backgroundA considerable body of human and animal experimental evidence links monoaminergic systems and cognition. Monoamine oxidase inhibitors (MAOIs), being able to enhance monoaminergic transmission and having neuroprotective properties, might represent a promising therapeutic strategy in cognitive impairment in Alzheimer's disease (AD) and other dementias.
methodsThe MAO-A and MAO-B inhibition profile of N-(furan-2-ylmethyl)-N-prop-2-yn-1-amine derivates (compounds 1-3) were evaluated by fluorimetric method and their absorption, distribution, metabolism, excretion, and toxicity (ADMET) properties estimated. The effects of the selected compound 1, N-(furan-2-ylmethyl)-N-methylprop-2-yn-1-amine (F2MPA), were evaluated on the basic synaptic transmission, long-term potentiation (LTP), and excitability in the dentate gyrus (DG) of the hippocampus of anesthetized rats.
resultsF2MPA is a partially reversible inhibitor of hMAO-B, with moderate to good ADMET properties and drug-likeness. Intraperitoneal administration of 1 mg/kg F2MPA greatly enhanced basic synaptic transmission, induced LTP, and potentiated electrically induced LTP in the dentate gyrus. Moreover, F2MPA did not modify seizure threshold of pilocarpine-induced convulsion in CD1 mice.
conclusionOur findings suggest that, the MAO-B inhibitor, F2MPA improves DG synaptic transmission without triggering pathological hyperexcitability. Therefore, F2MPA shows promise as a potential cognition-enhancing therapeutic drug.
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