Sertindole (brand names: "Serdolect" and "Serlect") is an antipsychotic medication. Sertindole was developed by the Danish pharmaceutical company Lundbeck and marketed under license by Abbott Labs. Like other atypical antipsychotics, it has activity at dopamine and serotonin receptors in the brain. It is used in the treatment of schizophrenia. Sertindole is not approved for use in the United States and was discontinued in Australia in January 2014. In Europe, sertindole was approved and marketed in 19 countries from 1996, but its marketing authorization was suspended by the European Medicines Agency in 1998 and the drug was withdrawn from the market. In 2002, based on new data, the EMA's CHMP suggested that Sertindole could be reintroduced for restricted use in clinical trials, with strong safeguards including extensive contraindications and warnings for patients at risk of cardiac dysrhythmias, a recommended reduction in maximum dose from 24 mg to 20 mg in all but exceptional cases, and extensive ECG monitoring requirement before and during treatment.

Trifluperidol is an antipsychotic butyrophenone derivative. It is a high-affinity sigma receptor blocker and it was strongly selective for NR1a/2B receptors. It exhibit pharmacological effects and a mechanism of action very similar to that of phenothiazines and thioxanthenes in that it blocks dopaminergic receptors. It is more selective with respect to D2 receptors. Trifluperidol is indicated for the treatment of acute and chronic schizophrenia, mania and hypomania, organic psychoses, childhood behavioral disorders, agitation in psychotic illness and motor tics. Trifluperidol has been suspected as a cause of cataract in Japan. Patients receiving trifluperidol treatment may develop a parkinsonian-like syndrome which responds to withdrawal of the drug or concurrent administration of an anti-parkinsonian drug. Acute dystonias and akathisia are other acute extrapyramidal effects; tardive dyskinesia may supervene after longer periods of treatment.

3-CPMT (3α-[(4-Chlorophenyl)phenylmethoxy] tropane) is a dopamine uptake inhibitor. Behavioral studies suggested that it did not display a cocaine-like behavioral profile, despite their ability to inhibit dopamine uptake.

18F-beta-CIT-FP is a cocaine analog with high affinity for the dopamine transporter. The compound is used as an imaging agent for PET studies and was approved in Korea to diagnose Parkinson's disease.

(+)-modafinil is an enantiomer of modafinil, a wake-promoting agent, that primarily affects areas of the brain involved in controlling wakefulness. (+)-enantiomer of modafinil was clarified to be S-configuration. The optical enantiomers of modafinil have similar pharmacological actions. Both modafinil enantiomers bind in vitro to the dopamine transporter and inhibit dopamine reuptake with the R- slightly more potent than the S-enantiomer. As a component of racemic mixture (+)-modafinil is indicated to improve wakefulness in adult patients with excessive sleepiness associated with narcolepsy, obstructive sleep apnea/hypopnea syndrome, and shift work sleep disorder.

Valerian is on the FDA’s list of substances that are generally recognised to be safe (GRAS). The root oil and extracts may be used as spice or seasoning. Valerian is most commonly used for sleep disorders. The essential oil of valerian contains a variety of compounds including valerenic acid and its derivatives, hydroxyvalerenic acid, acetoxyvalerenic acid and valerenal.

Raclopride is a salicylamide neuroleptic, that acts as a selective antagonist of D2 dopamine receptors both in vitro and in vivo. Tritium-labelled raclopride has properties that demonstrate its usefulness as a radioligand for the labelling of dopamine-D2 receptors : 3H-Raclopride has a high affinity for the rat and human dopamine-D2 receptors, the non-specific binding of 3H-raclopride is very low, not exceeding 5% of the total binding and the distribution of the 3H-raclopride binding sites in the brain closely correlates with the dopaminergic innervation. The binding of 3H-raclopride is blocked by dopamine-D2 agonists and antagonists, while the D1 agonist SKF 38393 and the Dl antagonist SCH 23390 have much less potency. The interaction of dopamine with 3H-raclopride binding results in a shallow competition curve, which suggests that 3H-raclopride, similar to other dopamine-D2 radioligands, labels both high and low agonist affinity states of the dopamine-D2 receptor. The in vivo receptor binding studies performed with 3H-raclopride also demonstrate its favorable properties as a dopamine-D2 receptor marker in vivo In contrast to some other compounds used as radioligands, raclopride enters the brain readily and binds with a low component of non-specific binding in all dopamine-rich brain areas. A saturation curve may be achieved in vivo binding studies since injections of increasing concentrations of 3H-raclopride appears to be saturated at concentrations above 25 mkCi (corresponding to approximately 5 nmol/kg). Raclopride antagonizes apomorphine-induced hyperactivity in the rat at low doses (ED50 = 130 nM/kg i.p.) but induces catalepsy only at much higher doses (ED50 = 27 mkM/kg i.p.). Radiolabelled raclopride has been used as a ligand for in vitro and in vivo autoradiography in rat and primate brains. Raclopride C 11 is used with positron emission tomography (PET) as a clinical research tool to determine dopamine type 2 (D 2) receptor density in the human brain under normal and pathological conditions. For example, raclopride C 11 used in PET studies has served to confirm the age-related decrease in striatal dopamine D2 receptor density, which may be associated with a decline in the motor as well as cognitive functions. In patients with Alzheimer's disease, raclopride C 11 may be used to examine neuroreceptor distribution and quantities, which may help in the analysis of degenerative alterations of neuron populations and neuroreceptor systems in patients with this disease. In Huntington's disease, in which degeneration of neostriatal interneurons occurs (postsynaptic to the dopaminergic input), specific binding of raclopride C 11 to D 2 receptors may serve as one of the parameters in predicting performance in cognitive tasks.

Chlorpromazine pamoate (also known as chlorpromazine embonate) is a salt of pamoic acid and a chlorpromazine. Pamoate salts are used in pharmaceutical formulations because they show slow dissolution and are useful in formulations where extended duration of action is required. Chlorpromazine is a phenothiazine antipsychotic. It also exerts sedative and antiemetic activity. The precise mechanism whereby the therapeutic effects of chlorpromazine are produced is not known. It has a wide range of activity arising from its depressant actions on the CNS and its alpha-adrenergic blocking and antimuscarinic activities. Chlorpromazine is a dopamine inhibitor; the turnover of dopamine in the brain is also increased. There is some evidence that the antagonism of central dopaminergic function, especially at the D2-dopaminergic receptor, is related to therapeutic effect in psychotic conditions.

Sulpiride is an atypical antipsychotic drug (although some texts have referred to it as a typical antipsychotic) of the benzamide class used mainly in the treatment of psychosis associated with schizophrenia and major depressive disorder, and sometimes used in low dosage to treat anxiety and mild depression. Sulpiride is commonly used in Europe, Russia and Japan. Sulpiride is a selective antagonist at dopamine D2 and D3 receptors. This action dominates in doses exceeding 600 mg daily. In doses of 600 to 1,600 mg sulpiride shows mild sedating and antipsychotic activity. Its antipsychotic potency compared to chlorpromazine is only 0.2 (1/5). In low doses (in particular 50 to 200 mg daily) its prominent feature is antagonism of presynaptic inhibitory dopamine receptors accounting for some antidepressant activity and a stimulating effect. Therefore, it is in these doses used as a second line antidepressant. Racemic and L-sulpiride significantly decreased stimulated serum gastrin concentration, but they did not affect fasting serum gastrin or basal and stimulated gastric acidity. D-sulpiride significantly decreased gastric acid secretion, without affecting serum gastrin levels.