Warfarin is an anticoagulant drug normally used to prevent blood clot formation as well as migration. Warfarin is marketed under the brand name Coumadin among others. Coumadin (crystalline warfarin sodium) is an anticoagulant which acts by inhibiting vitamin K-dependent coagulation factors. Chemically, it is 3-(α-acetonylbenzyl)-4-hydroxycoumarin and is a racemic mixture of the R- and S-enantiomers. Coumadin is indicated for the prophylaxis and/or treatment of venous thrombosis and its extension, and pulmonary embolism. It is also indicated for the prophylaxis and/or treatment of the thromboembolic complications associated with atrial fibrillation and/or cardiac valve replacement. Warfarin is thought to interfere with clotting factor synthesis by inhibition of the C1 subunit of the vitamin K epoxide reductase (VKORC1) enzyme complex, thereby reducing the regeneration of vitamin K1 epoxide. The degree of depression is dependent upon the dosage administered and, in part, by the patient’s VKORC1 genotype. Therapeutic doses of warfarin decrease the total amount of the active form of each vitamin K dependent clotting factor made by the liver by approximately 30% to 50%.

Warfarin, (S)- is an oral anticoagulant, S-enantiomer of warfarin, that having a greater pharmacologic potency than the R-enantiomer. Clinically available warfarin is a racemic mixture of (R)- and (S)-warfarin, and the (S)-enantiomer has 3 to 5 times greater anticoagulation potency than its optical congener. Both enantiomers are eliminated extensively via hepatic metabolism with low clearance relative to hepatic blood flow. The scientific debate on the contribution of the R- Warfarin -to-S- Warfarin effect is a long and conflictual story. It has shown that the pharmacodynamic response to (R/S)-Warfarin 25 mg (a mixture of equal amounts of S-Warfarin and R- Warfarin) was nearly twice that of S-Warfarin 12.5 mg given alone, thus indicating the substantial contribution of R-Warfarin to the (R/S)-Warfarin effect. (R/S)-Warfarin is indicated for the prophylaxis and/or treatment of venous thrombosis and its extension, and pulmonary embolism. It is also indicated for the prophylaxis and/or treatment of the thromboembolic complications associated with atrial fibrillation and/or cardiac valve replacement. Warfarin is thought to interfere with clotting factor synthesis by inhibition of the C1 subunit of the vitamin K epoxide reductase (VKORC1) enzyme complex, thereby reducing the regeneration of vitamin K1 epoxide.

Warfarin, (R)- is R-enantiomer of warfarin, an oral anticoagulant, with relatively low potency compared to S-enantiomer. Clinically available warfarin is a racemic mixture of (R)- and (S)-warfarin, and the (S)-enantiomer has 3 to 5 times greater anticoagulation potency than its optical congener. Both enantiomers are eliminated extensively via hepatic metabolism with low clearance relative to hepatic blood flow. The scientific debate on the contribution of the R- Warfarin -to-S- Warfarin effect is a long and conflictual story. It has shown that the pharmacodynamic response to (R/S)-Warfarin 25 mg (a mixture of equal amounts of S-Warfarin and R- Warfarin) was nearly twice that of S-Warfarin 12.5 mg given alone, thus indicating the substantial contribution of R-Warfarin to the (R/S)-Warfarin effect. (R/S)-Warfarin is indicated for the prophylaxis and/or treatment of venous thrombosis and its extension, and pulmonary embolism. It is also indicated for the prophylaxis and/or treatment of the thromboembolic complications associated with atrial fibrillation and/or cardiac valve replacement. Warfarin is thought to interfere with clotting factor synthesis by inhibition of the C1 subunit of the vitamin K epoxide reductase (VKORC1) enzyme complex, thereby reducing the regeneration of vitamin K1 epoxide.