D-kynurenine is metabolite of the amino acid D-tryptophan. D-kynurenine is an agonist for GPR109B (HM74), a putative G protein-coupled receptor. D-kynurenine elicits chemotactic responses in human neutrophils through GPR109B. D-amino acid oxidase can metabolize D-kynurenine to produce the fluorescent compound kynurenic acid.

(S)-Etifoxine is a first in class pain-relieving drug candidate, with the power of morphine and oxycodone, but without the addictive, sedative and GI side effects. (S)-etifoxine is an isomer, chemically isolated from Etifoxine (Stresam), an approved racemic drug (off patent) prescribed in Europe. Preclinical studies determined that the (S)-isomer of Stresam® ((S)-etifoxine) is a non-sedating anxiolytic. It was also discovered that (S)-etifoxine possesses highly potent analgesic activity comparable to morphine (the gold standard) which is consistent with Stresam®’s TSPO-mediated effects on chemotherapy-induced neuropathy and peripheral nerve injury. However, (S)-etifoxine does not display any of the negative side-effects associated with morphine. Even more notably, Stresam® has demonstrated peripheral nerve regeneration and functional recovery. It is believed that (S)-etifoxine will retain these same properties.

PNU-282987 is a potent and selective a7 nAChR agonist. This compound showed high affinity for the rat a7 nAChR (Ki = 26 nM) and activity at the a7–5-HT3 chimera (EC50 = 128 nM). In addition, PNU-282987 was found to be inactive at all tested monoamine, muscarine, glutamate, and GABA receptors at 1 uM concentration, except 5-HT3 receptors (Ki = 930 nM). The highly selective and potent a7 nAChR agonist PNU-282987 enhances GABAergic synaptic activity in the hippocampus in vitro, and reverses amphetamine induced auditory gating deficit in anesthetized rats. In addition, PNU-282987 improves the inherent gating deficit observed in a subset of rats and enhances amphetamine induced hippocampal activity. These results support the concept that a7 nAChR agonists represent a novel, potential pharmacotherapy in treatment of schizophrenia. It also has being shown that acute lung injury is reduced by PNU-282987 through changes in the macrophage profile.

PF-670462 is a selective inhibitor of the δ- and ε-isoforms of casein kinase I, with IC50 values of 7.7 and 14 nM respectively, and >30 selectivity relative to 42 other kinases tested. Casein kinase Iε phosphorylates PER proteins, which are involved in setting the period of the circadian pacemaker or clock. PF-670462 is potent (IC50 7.7 nM) and effective in vivo (i.e. it induces profound phase delays in circadian periodicity). PF-670462 has being shown to have an ability to induce phase delays in circadian rhythms in rats, in which it is rapidly metabolized, and in monkeys. A potential pharmacological use of the compounds like PF-670462 could be for therapy of cognitive deficits in shift workers, mood changes in bipolar disorders, and phase advances in the sleep–wake cycle in elderly people. It has also being shown that Inhibition of the casein-kinase-1-ε/δ/ with PF-670462 prevents relapse-like alcohol drinking in rats, suggesting that CK1 inhibitors may be candidates for drug treatment development for alcoholism.

PF-4778574 is a potent AMPA receptor positive allosteric modulator (PAM) that has been shown to enhance cognition in animal models.Displacement studies using [3 H]PF-04725379 in rat cortical tissue determined a Ki of 85 nM for PF-4778574. The AMPAR potentiator PF-4778574 was characterized in a series of in vitro assays and acute-dose animal studies evaluating AMPAR-mediated mechanism, safety, and nootropism. Potentiator-induced animal effects were likely purely AMPAR-dependent since PF-4778574 (10 uM) only affected the dopamine transporter (IC50 of 910 nM) in a broad human-based receptor/enzyme selectivity panel.

PF-3845 is a selective covalent inhibitor of fatty acid amide hydrolase. It results in increased levels of anandamide and results in cannabinoid receptor-based effects. PF-3845 demonstrated cannabinoid receptor-dependent antinociceptive effects in models of inflammatory and neuropathic pain. In mouse model PF-3845 attenuated withdrawal from morphine dependence. PF3845 reversed traumatic brain injury (TBI)-induced impairments in fine motor movement, hippocampus dependent working memory and anxiety-like behavior in a tramatic brain injury model.

PCI-34051 is a potent and specific HDAC8 inhibitor with IC50 of 10 nM in a cell-free assay. PCI-34051 inhibits ovarian tumor line OVCAR-3 with a GI50 of 6 μM and 15% cell death. Neither significant tubulin nor histone acetylation is observed in the sensitive cell lines treated with PCI-34051 at concentrations less than 25 μM at 24 hours nor at earlier timepoints. PCI-34051 induces a selective cytotoxic effect in cell lines derived only from T-cell malignancies. PCI-34051 induces caspase-dependent apoptosis. PCI-34051 undergoes preclinical studies for cancer

Naltrindole is a highly potent, highly selective delta opioid receptor antagonist. It is predominantly used as a molecular probe in biomedical studies exploring the manipulation of delta opioid receptors. Naltrindole was shown to inhibit cancer cell growth in vitro; potentially through a nonopioid receptor-dependant mechanism.

3-(2-Carboxypiperazin-4-yl)Propyl-1-Phosphonic acid (also known as CPP) is neuro active amino acid and antagonist of the N-methyl-D-aspartate receptor (NMDA). It has been studied in rat models for memory, learning, and pain. Although it did show some efficacy in reducing pain it also appears to significantly impair working memory.

ABT-239 is a selective, nonimidazole H3 receptor antagonist/inverse agonist, which was investigated by Abbott laboratory as a potential drug for treatment of a variety of cognitive disorders including attention deficit/hyperactivity disorder, Alzheimer's disease, and schizophrenia.