Pharmacology and Pharmacogenomics of Anti-Migraine Drugs

Migraine is the most prevalent neurological condition, which affects 1.16 million individuals globally, ranking first among adolescents and children and second in the case of adults aged under 60 years. Both genetic and environmental factors contribute to its pathophysiology, influencing treatment outcomes and drug responses. Pharmacogenomics has emerged as a critical field in understanding interindividual variability in migraine therapy. Genetic variants in pharmacokinetic and pharmacodynamic pathways impact the metabolism, efficacy, and adverse drug reactions of drugs used in migraine. Variants in genes such as PLCE1, SRP72, CACNA1D, and CACNA1C affect calcium channel blockers' efficacy, while polymorphisms in GNB3 and DRD2 influence triptan response. CYP3A4 and CYP2D6 polymorphisms influence the metabolism of ergot alkaloids and beta blockers, impacting their efficacy and toxicity. The TSPAN2 gene is associated with reduced ergotamine response in patients with migraines without aura. Moreover, CGRP receptor antagonists exhibit varying effectiveness based on the receptor gene variants. This review compiles current pharmacogenetic insights to optimize migraine treatment through personalized medicine. Understanding these genetic markers could lead to improved therapeutic strategies, reducing trial-anderror prescribing and improving patient outcomes. Further research is warranted to verify these associations and translate outcomes into clinical practice.