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Chronic Treatment With Addex Therapeutics' Dipraglurant Rescues Impairment Of Long-Term Synaptic Plasticity In Validated Preclinical Model Of Primary Generalized Torsion Dystonia 1


Wednesday, 4 Sep 2013 01:00am EDT 

Addex Therapeutics announced additional positive preclinical data for its mGlu5 negative allosteric modulator (NAM) oral small molecule, dipraglurant, in a validated model for primary generalized torsion dystonia 1 (DYT1), a common and severe genetic form of dystonia, caused by a mutation in the TOR1A gene encoding the torsin A protein. In the study, that is part of an ongoing collaboration with Professor Antonio Pisani, University of Rome Tor Vergata and Fondazione Santa Lucia, chronic treatment with dipraglurant (50 mg/kg i.p. for 8 days) partially restored long-term depression and synaptic de-potentiation which are impaired in the DYT1 mutant mice over expressing the human mutant TOR1A gene. These data together with previously reported results obtained with dipraglurant in in vitro and in in vivo preclinical behavioral models, as well as observations made in the Phase 2a study of dipraglurant in Parkinson's disease patients, further support the hypothesis that inhibition of mGlu5 could be beneficial in counteracting the abnormal electrophysiological function observed in dystonia. In keeping with the Company's rare disease development strategy, Addex plans to initiate a Phase 2a study with dipraglurant in a rare dystonia. 

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