Remoxipride is a substituted
benzamide that acts as a weak but very selective antagonist of
dopamine D2 receptors. It was introduced by Astra (Roxiam) at the end of the eighties and was prescribed as an atypical
antipsychotic. This article reviews its putative selective effects on mesolimbic versus nigrostriatal dopaminergic systems. In animals,
remoxipride has minimal cataleptic effects at doses that block
dopamine agonist-induced hyperactivity. These findings are predictive of
antipsychotic activity with a low likelihood of extrapyramidal symptoms.
Remoxipride also appears to be effective in more recent animal models of
schizophrenia, such as latent inhibition or prepulse inhibition. In clinical studies,
remoxipride shows a relatively low incidence of extrapyramidal side effects and its effects on
prolactin release are short-lasting and generally mild. The clinical efficacy of
remoxipride is similar to that of
haloperidol or
chlorpromazine. Although its clinical use was severely restricted in 1993, due to reports of
aplastic anemia in some patients receiving
remoxipride, this
drug has been found to exhibit relatively high selectivity for
dopamine D2 receptors making
remoxipride an interesting tool for neurochemical and behavioral studies.