[1][2] It was shown to possess central α2-adrenoceptor antagonist activity after oral doses in man and was patented as an antidepressant by Glaxo in the early 1980s, but its development was discontinued when the compound failed to show a clear clinical advantage over existing therapies.

Blockade of α2-adrenoreceptors, particularly presynaptic autoreceptors in noradrenergic neurons by fluparoxan, produces an increase in the synaptic concentrations of noradrenaline,[4] by blocking the autoinhibitory feedback mechanism.

Fluparoxan has been shown to possess central α2-adrenoceptor antagonist activity after both single and repeated oral doses in man, significantly attenuating all responses to the agonist clonidine (growth hormone secretion, bradycardia, hypotension, xerostomia) apart from the measures of sedation.

[8] Fluparoxan has shown positive effects in the treatment of cognitive dysfunction in schizophrenia patients when orally dosed with fluparoxan,[1] and in the treatment of central neurodegenerative disorders in models of Alzheimer's disease where it prevented age-related decline in spatial working memory in transgenic mice, although it had no effect in other memory tasks such as object recognition or the Morris water maze and occurred in the absence of obvious concomitant change in pathology such as β-amyloid plaque load and astrocytosis.

[3] The excellent pharmacokinetics exhibited by fluparoxan in animals also translated into man [1] where it has a superior bioavailability (97%) and longer duration of action (6-7hrs).

[12] In contrast however, recent interest in fluparoxan has increased with its positive effects in treating cognitive dysfunction in central neurodegenerative diseases.