Brallobarbital possessed the sedative and hypnotic properties and was a component of Vesparax that was used to treat sleep disorders. However, was revealed that brallobarbital was responsible for the problems in Vesparax intoxication.

Bometolol is a cardiospecific beta-adrenergic blocking drug that was never marketed.

Bisorcic is an N-acetyl-L-amino acid that is L-ornithine was developed as a hepatoprotective agent and was studied as a psychostimulant.

Guaiactamine was developed as antispasmodic therapeutic agents, and it has never been marketed.

Maroxepin is a tetracyclic compound antagonizing activity of dopamine receptors. Maroxepin has a potent central nervous action and a strong sedative potential. Maroxepin exerts both antipsychotic and antidepressant properties.

Odapipam is a benzazepine with high affinity and selectivity for D1-dopamine receptors. Labeled with C-11, it has been used as a PET radiotracer to visualize D1 receptors both in striatal and extrastriatal areas, such as the prefrontal cortex. Odapipam inhibits dopamine D1 receptor binding in vitro with low nanomolar to picomolar dissociation constants. The affinity of [11C]NNC 756 for D1 receptors is 0.18 nM. Odapipam was tested in phase I of clinical trials for the treatment of psychotic disorders, but failed.

Tonazocine is a nonpeptide, partial delta-opioid agonist with mu antagonist properties and weak k agonist activity. Tonazocine augmented the efficacy of L-DOPA in the reserpine model. Tonazocine evoked a dose-related, ipsilateral rotation, consistent with augmentation of dopaminergic function on the unlesioned side. Tonazocine has a narcotic antagonist activity which is 90 times that of pentazocine and 5 times less than that of naloxone as measured by the antagonism of morphine analgesia in the rat tail-flick test. Total pain relief scores for tonazocine 4 mg were nearly identical with that of morphine sulfate 10 mg while 8 mg of tonazocine were superior to 10 mg of morphine. Drowsiness was the main adverse reaction of tonazocine. Tonazocine has undergone phase II clinical trials for postoperative pain and appeared to possess reasonable efficacy.

Dexefaroxan is a selective alpha 2-adrenergic receptor antagonist. Вexefaroxan improved TgCRND8 (protein-transgenic mouse model of Alzheimer's disease) behavioral phenotypes and increased BDNF mRNA expression without affecting amyloid-β peptide levels. Dexefaroxan treatment also enhanced the number and complexity of the dendritic arborizations of polysialated neural cell adhesion molecule-positive neurons. The trophic effects of dexefaroxan on newborn cells might involve an increase in brain-derived neurotrophic factor, which was upregulated in afferent noradrenergic fiber projection areas and in neurons in the granule cell layer. By promoting the survival of new endogenously formed neurons, dexefaroxan treatment represents a potential therapeutic strategy for maintaining adult neurogenesis in neurodegenerative conditions, such as Alzheimer's disease, that affect the hippocampus. Dexefaroxan increases neuron survival in the olfactory bulb of the adult rat in vivo, putatively as a result of reducing the apoptotic fate of telencephalic stem cell progenies.

Declenperone is an antagonist of 5-HT2 receptors, developed by Janssen Pharmaceutica. The compound is claimed to have strong neuroleptic activity, as evidenced by experimental data obtained in apomorphine-tryptamine and norepinephrine test in rats, and the apomorphine test in dogs. Declenperone was used in a veterinary as a sedative.

Carabersat is an anticonvulsant devoid of cardiovascular side effects with minimal central nervous system adverse actions. Carabersat does not bind to ion channels, purinergic, aminergic, opioid and other peptidergic receptors. It selectively interacts with its own binding site, which is not yet elucidated. Carabersat has no effect on sodium channels, GABAergic or glutamate pathways. Carabersat had been in phase II clinical trials for the treatment of epilepsy. It has a potential action in preventing migraines because it acts through an inhibition of the cortical spreading depression trigeminal nerve-induced vasodilatation in cats. Its good therapeutic index and the markedly reduced neurological impairments could make it a useful agent for migraine prophylaxis pending efficacy parameters of controlled studies, which are underway.