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3-(Fur-2-yl)-10-(2-phenylethyl)-[1,2,4]triazino[4,3-a]benzimidazol-4(10H)-one, a Novel Adenosine Receptor Antagonist with A2A-Mediated Neuroprotective Effects
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    3-(Fur-2-yl)-10-(2-phenylethyl)-[1,2,4]triazino[4,3-a]benzimidazol-4(10H)-one, a Novel Adenosine Receptor Antagonist with A2A-Mediated Neuroprotective Effects
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    Dipartimento di Morfologia Umana e Biologia Applicata, Università di Pisa, Via Roma 55, 56126 Pisa, Italy
    Neurobiologia dei disturbi del movimento, IRCCS INM Neuromed, Via Atinense 18, 86077 Pozzilli, Isernia, Italy
    § Department of Drug Discovery and Development, Istituto Italiano di Tecnologia, via Morego, 30, 16163 Genova, Italy
    Dipartimento di Psichiatria, Neurobiologia, Farmacologia e Biotecnologie, Università di Pisa, Via Bonanno 6, 56126 Pisa, Italy
    Dipartimento di Scienze Farmaceutiche, Università di Pisa, Via Bonanno 6, 56126 Pisa, Italy
    # Dipartimento di Scienze Ambientali, Seconda Università di Napoli, Via Vivaldi 43, 81100 Caserta, Italy
    Mailing address: Department of Pharmaceutical Sciences, University of Pisa, Via Bonanno 6, 56126 Pisa, Italy. Telephone: (+39-050) 2219561. Fax: (+39-050) 2219605. E-mail: [email protected]
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    ACS Chemical Neuroscience

    Cite this: ACS Chem. Neurosci. 2011, 2, 9, 526–535
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    https://doi.org/10.1021/cn200036s
    Published June 10, 2011
    Copyright © 2011 American Chemical Society

    Abstract

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    In this study, compound FTBI (3-(2-furyl)-10-(2-phenylethyl)[1,2,4]triazino[4,3-a]benzimidazol-4(10H)-one) was selected from a small library of triazinobenzimidazole derivatives as a potent A2A adenosine receptor (AR) antagonist and tested for its neuroprotective effects against two different kinds of dopaminergic neurotoxins, 1-methyl-4-phenylpyridinium (MPP+) and methamphetamine (METH), in rat PC12 and in human neuroblastoma SH-SY5Y cell lines. FTBI, in a concentration range corresponding to its affinity for A2A AR subtype, significantly increased the number of viable PC12 cells after their exposure to METH and, to a similar extent, to MPP+, as demonstrated in both trypan blue exclusion assay and in cytological staining. These neuroprotective effects were also observed with a classical A2A AR antagonist, ZM241385, and appeared to be completely counteracted by the AR agonist, NECA, supporting A2A ARs are directly involved in FTBI-mediated effects. Similarly, in human SH-SY5Y cells, FTBI was able to prevent cell toxicity induced by MPP+ and METH, showing that this A2A AR antagonist has a neuroprotective effect independently by the specific cell model. Altogether these results demonstrate that the A2A AR blockade mediates cell protection against neurotoxicity induced by dopaminergic neurotoxins in dopamine containing cells, supporting the potential use of A2A AR antagonists in dopaminergic degenerative diseases including Parkinson’s disease.

    Copyright © 2011 American Chemical Society

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    Cited By

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    This article is cited by 7 publications.

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    ACS Chemical Neuroscience

    Cite this: ACS Chem. Neurosci. 2011, 2, 9, 526–535
    Click to copy citationCitation copied!
    https://doi.org/10.1021/cn200036s
    Published June 10, 2011
    Copyright © 2011 American Chemical Society

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