Table 1 Investigational schizophrenia therapeutics with nootropic efficacy in the rodent novel object recognition task do not possess clinical pro-cognitive activity.

From: Beyond antipsychotics: a twenty-first century update for preclinical development of schizophrenia therapeutics

Investigational drug

Mechanism of action

Clinical efficacy

Donepezil

AChE inhibitor

Not significantly different from placebo

Determined by CATIE neurocognitive battery

GTS-21/DMXB-A

α7 nAChR partial agonist

Not significantly different from placebo

Determined by MCCB

CX516

AMPAR PAM

Not significantly different from placebo

Determined by cognitive battery (similar to MCCB)

MK-0777/TPA-023

GABAAR α2/α3 partial agonist

Not significantly different from placebo

Determined by MCCB

Modafinil

DAT inhibitor

Not significantly different from placebo

Determined by COGBAT

Atomoxetine

NET inhibitor

Not significantly different from placebo

Determined by BACS

  1. AChE acetylcholinesterase, AMPAR PAM α-amino-3-hydroxy-5-methyl-4-isoxazolepropionic acid receptor positive allosteric modulator, BACS Brief Assessment of Cognition in Schizophrenia, CATIE Clinical Antipsychotic Trials of Intervention Effectiveness, DAT dopamine transporter, GABAA gamma-aminobutyricacid A receptor, MCCB MATRICS Consensus Cognitive Battery, nAChR nicotinic acetylcholine receptor, NET norepinephrine transporter
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