{"database":"biostudies-literature","file_versions":[],"scores":null,"additional":{"submitter":["Kantrowitz JT"],"funding":["NCATS NIH HHS","Taisho Toyama Pharmaceutical Company","NIDA NIH HHS","NIMH NIH HHS","U.S. Department of Health & Human Services | NIH | National Institute of Mental Health","U.S. Department of Health & Human Services | NIH | National Institute of Mental Health (NIMH)"],"pagination":["1842-1850"],"full_dataset_link":["https://www.ebi.ac.uk/biostudies/studies/S-EPMC7608251"],"repository":["biostudies-literature"],"omics_type":["Unknown"],"volume":["45(11)"],"pubmed_abstract":["Glutamate neurotransmission is a prioritized target for antipsychotic drug development. Two metabotropic glutamate receptor 2/3 (mGluR2/3) agonists (pomaglumetad [POMA] and TS-134) were assessed in two Phase Ib proof of mechanism studies of comparable designs and using identical clinical assessments and pharmacoBOLD methodology. POMA was examined in a randomized controlled trial under double-blind conditions for 10-days at doses of 80 or 320 mg/d POMA versus placebo (1:1:1 ratio). The TS-134 trial was a randomized, single-blind, 6-day study of 20 or 60 mg/d TS-134 versus placebo (5:5:2 ratio). Primary outcomes were ketamine-induced changes in pharmacoBOLD in the dorsal anterior cingulate cortex (dACC) and symptoms reflected on the Brief Psychiatric Rating Scale (BPRS). Both trials were con"],"journal":["Neuropsychopharmacology : official publication of the American College of Neuropsychopharmacology"],"pubmed_title":["Proof of mechanism and target engagement of glutamatergic drugs for the treatment of schizophrenia: RCTs of pomaglumetad and TS-134 on ketamine-induced psychotic symptoms and pharmacoBOLD in healthy volunteers."],"pmcid":["PMC7608251"],"funding_grant_id":["HHSN271201200007C","U01 MH094247","Taisho Pharmaceutical R&D Inc","FAST-PS contract (HHSN271201200007I)","UL1 TR001863"],"pubmed_authors":["Sobeih T","Girgis RR","Green MF","Kegeles LS","Goff DC","Choo TH","Lee J","Grinband J","Javitt DC","Horga G","Wall MM","Krystal JH","Yang YS","Marder SR","Lieberman JA","Lahti AC","Potter WZ","Kantrowitz JT"],"additional_accession":[]},"is_claimable":false,"name":"Proof of mechanism and target engagement of glutamatergic drugs for the treatment of schizophrenia: RCTs of pomaglumetad and TS-134 on ketamine-induced psychotic symptoms and pharmacoBOLD in healthy volunteers.","description":"Glutamate neurotransmission is a prioritized target for antipsychotic drug development. Two metabotropic glutamate receptor 2/3 (mGluR2/3) agonists (pomaglumetad [POMA] and TS-134) were assessed in two Phase Ib proof of mechanism studies of comparable designs and using identical clinical assessments and pharmacoBOLD methodology. POMA was examined in a randomized controlled trial under double-blind conditions for 10-days at doses of 80 or 320 mg/d POMA versus placebo (1:1:1 ratio). The TS-134 trial was a randomized, single-blind, 6-day study of 20 or 60 mg/d TS-134 versus placebo (5:5:2 ratio). Primary outcomes were ketamine-induced changes in pharmacoBOLD in the dorsal anterior cingulate cortex (dACC) and symptoms reflected on the Brief Psychiatric Rating Scale (BPRS). Both trials were con","dates":{"release":"2020-01-01T00:00:00Z","publication":"2020 Oct","modification":"2026-05-03T04:51:52.727Z","creation":"2020-11-08T09:45:32Z"},"accession":"S-EPMC7608251","cross_references":{"pubmed":["32403118"],"doi":["10.1038/s41386-020-0706-z"]}}