- The primary mechanism of action of warfarin is the inhibition of vitamin K epoxide reductase.
- This enzyme is crucial for the recycling of vitamin K in the liver. Vitamin K is a necessary cofactor for the post-translational gamma-carboxylation of certain glutamate residues on clotting factors II, VII, IX, and X, as well as proteins C and S. By inhibiting vitamin K epoxide reductase, warfarin prevents the activation of these vitamin K-dependent clotting factors, leading to a decrease in the blood's ability to form clots.

- It is important to note that warfarin's anticoagulant effect is indirect and requires several days to manifest because it affects the synthesis of new clotting factors rather than the activity of existing ones.

Explanation of other options:
- Option 2: Direct inhibition of thrombin is the mechanism of action of agents like dabigatran, not warfarin.
- Option 3: Activation of antithrombin III is the mechanism of heparin's anticoagulant effect.
- Option 4: Blockade of platelet glycoprotein IIb/IIIa receptors is the mechanism of action of certain antiplatelet drugs like abciximab.

Reference: Harrison's Principles of Internal Medicine, 20th Edition, Volume 2, Chapter 89.