Rasagiline is a selective and irreversible inhibitor of monoamine oxidase type B with neuroprotective effect, indicated for the management of Parkinson's disease. The aim of this work was to evaluate the impact of seven alleles and of 120 additional variants located in other CYP enzymes (e.g., ), UGT enzymes (e.g., ) or other enzymes (e.g., ), and transporters (e.g., ) on the pharmacokinetic variability and safety of rasagiline. A total of 118 healthy volunteers enrolled in four bioequivalence clinical trials consented to participate in this pharmacogenetic study. alleles were not associated with the pharmacokinetic variability of rasagiline. Patients with rs1045642 G/A+A/A genotypes presented higher area under the curve adjusted by dose per weight (AUC/DW) than those with the G/G genotype ( = 0.012) and lower volume of distribution (V/F) and clearance (Cl/F) ( = 0.001 and = 0.012, respectively). Subjects with the rs2273697 A/A genotype presented lower t (i.e., the time to reach the maximum concentration, C) compared to those with G/G+G/A genotypes ( = 0.001). Volunteers with the *1/*5 genotype exhibited lower C/DW and higher t ( = 0.003 and = 0.018, respectively) than subjects with the *1/*1 diplotype. Only one adverse drug reaction was reported: headache. Our results suggest the genetic polymorphism of drug transporters, rather than metabolizing enzymes, conditions the pharmacokinetics of rasagiline.