ABSTRACT
Thioridazine (THD), a phenothiazine drug, is a very commonly prescribed neuroleptic for the treatment of psychoses. After oral adsorption, THD is extensively metabolized by side-chain oxidation leading to mesoridazine and sulforidazine, by N-demethylation to northioridazine, and by ring sulfoxidation to thioridazine 5-sulfoxide (THD 5-SO). THD is believed to act mainly via antidopaminergic functions in the central nervous system. THD 5-SO, which is the metabolite found in largest concentrations in serum after chronic THD administration, seems to be devoid of antipsychotic effects but contributes to cardiotoxicity and is more potent than the parent drug. Due to the impossibility of obtaining pure isomeric THD 5-SO pairs during their isolation processes, solvent pH, and temperature conditions were checked to avoid racemization.
