The hepatic enzymes CYP2D6 and CYP3A4 are primarily accountable for the transformation of the atypical antipsychotic medication aripirazole. It is recommended that CYP2D6-poor metabolizers adjust their dosage. Most adult patients handle aripiprazole well; however, occasionally, some people may experience negative side effects that lead to the medication being stopped. According to recent research, the effectiveness and safety of pharmacological therapy may be correlated with additional genes implicated in drug metabolism, transport, and excretion. The goal of this research was to compare the genetic variations of patients who had good treatment tolerance and those who had side effects that caused them to stop taking the medication. 20 genes were genetically profiled using the MassARRAY technique. The ABCB1, COMT, CYP2D6, CYP3A4, and CYP3A5 polymorphisms did not differ between the two groups. Suddenly, we found that the group with negative effects had a higher frequency of CYP1A2 ultra-rapid metabolizers, as well as homozygous CYP1A21F/*1F (78% vs. 45%) and CYP2B6*1/*1 (80% vs. 45%). Furthermore, the only individuals experiencing negative effects have been found to have a mixed homozygous condition (CYP1A2*1F/*1F/CYP2B6*1/*1). The potential involvement of CYP1A2 and CYP2B6 enzymes in the aripiprazole metabolism has not yet been explored. Accordingly, our first findings suggest that the CYP1A2*F and/or CYP2B6*1 alleles could be involved in the negative effects of aripiprazole. Therefore, further studies with larger sample sizes are needed to validate our results.
