Adverse Drug Reactions (ADRs) and Individualized ADR Risk Assessment
Adverse drug reactions are a significant concern in clinical practice. Genomic SVs can predispose individuals to ADRs by affecting drug metabolism enzymes’ activity, drug transporters’ function, or drug target genes3. Genes-encoding drug metabolizing enzymes, such as the cytochrome P450 (CYP) family, are susceptible to genomic SVs. CNVs, deletions, or duplications in these genes can lead to variations in enzyme activity, affecting drug metabolism rates and potentially leading to either reduced efficacy or drug toxicity3. For instance, duplications in the CYP2D6 gene can result in ultra-rapid metabolizer phenotypes, increasing the risk of ADRs for drugs metabolized by this enzyme. Incorporating genomic SV analysis into pharmacogenomics allows for the development of predictive models to assess an individual’s risk of experiencing ADRs. Understanding an individual’s genomic SV profile and how it relates to specific drugs can aid in tailoring drug selection, dosing, and monitoring strategies to minimize ADRs and improve treatment outcomes.