Various lines of evidence suggest that hypofunction of glutamatergic transmission via NMDA receptors plays a role in the pathophysiology of CNS disorders such as schizophrenia.  One strategy to normalize the reduced function of NMDA receptor neurotransmission is to increase the availability of the obligatory co-agonist glycine at its modulatory site on the receptor through inhibition of glycine transporter type 1 (GlyT1). We have discovered bitopertin (RG1678), a potent compound highly selective for GlyT1 that has shown a promising effect when added to a stable dose of an antipsychotic in a Phase II trial in patients with schizophrenia characterized by predominant negative symptoms. We will present the discovery and the pharmacological profile of bitopertin as well as the relationship between target receptor occupancy, exposure and efficacy.

Bitopertin (RG1678), a potent and selective glycine re-uptake inhibitor for the treatment of schizophrenia

244th National Meeting (2012)

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