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Evidence of deficient glutamatergic signaling through the N-methyl-D-aspartate (NMDA) receptor in schizophrenia has led to attempts to enhance NMDA functioning, mainly through drugs acting on the co-agonist glycine site (e.g., cycloserine and sarcosine), with variable results. A new manufacturer-conducted, phase II study examined the effects of bitopertin, a selective glycine reuptake inhibitor, under the hypothesis that it would produce a more consistent glycine effect. The 323 participants, who had schizophrenia with predominantly negative symptoms, were randomized to placebo or bitopertin (10, 30, or 60 mg) added to ongoing atypical antipsychotic treatment for 8 weeks.
In a completer but not an intent-to-treat analysis, the two lower bito…