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Deutarserine (CTP-692) is a deuterium-modified analog of the endogenous amino acid D-serine. It was developed as an adjunctive treatment for schizophrenia. Deutarserine acts as a co-agonist at the N-methyl-D-aspartate (NMDA) receptor in the brain and is designed to restore NMDA receptor activity in patients with schizophrenia who typically have low levels of D-serine. The modification with deuterium aims to improve metabolic stability and reduce renal toxicity compared to non-deuterated D-serine. Preclinical studies showed that CTP-692 has similar functional activation of NMDA receptors as D-serine but with improved safety and pharmacokinetic properties. Despite promising early data, development was discontinued after a phase 2 trial failed to meet its primary endpoint for efficacy in schizophrenia[1][2][3][4][6].
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