Amfonelic acid, a derivative of nalidixic acid, was originally developed as a central nervous system stimulant. It is a highly potent nonamphetamine stimulant whose actions are inhibited by reserpine but not by the tyrosine hydroxylase inhibitor, a-methyltyrosine. Additionally, it enhances the impacts of antipsychotic medicines such as haloperidol, trifluoperazine, and spiperone.
Amfonelic acid (AFA) is a dopamine reuptake inhibitor, that has marked effects on brain dopamine metabolism but not noradrenaline metabolism. Experiments on rats have shown that AFA treatment completely prevented the effects of methamphetamine on the dopaminergic system, both morphologically and biochemically. Rats are shown to self-administer amfonelic acid in a dose-dependent manner.
Amfonelic acid (AFA), an inhibitor of dopamine (DA) uptake, has been found to increase the levels of tryptophan (TRYP) and 5-hydroxyindoleacetic acid (5-HIAA) in the rat c. striatum, cerebral cortex, and brain stem. The duration of action of the effect of AFA on TRYP and 5-HIAA appeared to be longer than that of the increase of the striatal DA metabolites homovanillic acid and 3,4-dihydroxyphenylacetic acid[1].
[1] P C Waldmeier. “The effects of amfonelic acid on 5-HT metabolism in rat brain.” Journal of Neural Transmission 57 3 (1983): 149–65.
