Warfarin is an anticoagulant available as a racemic mixture. The R- and 
S-isomers differ with respect to relative plasma concentrations, clearance, 
potency, sites of metabolism, and cytochrome P450 (CYP) isoenzymes responsible 
for metabolism. S-Warfarin, the more potent isomer, is metabolized primarily by 
CYP2C9. Genetic polymorphisms resulting from single amino acid substitutions 
reduce the metabolic capability of 2C9. A reduction in warfarin metabolism due 
to genetic polymorphism may explain the increased warfarin response and bleeding 
episodes in some patients. Clinical studies showed an increased plasma level of 
S-warfarin, decreased clearance of S-warfarin, increased frequency of bleeding, 
and prolongation of hospitalization in patients with variant CYP2C9 alleles. 
Adverse outcomes associated with warfarin possibly could be avoided by 
identifying patients with variant alleles before therapy and starting therapy at 
low dosages.