Concept:
Several clotting factors (II, VII, IX and X) only work after their glutamate residues are γ-carboxylated, a reaction that needs vitamin K. Blocking vitamin K therefore stops these factors from working.
Step 1: Warfarin inhibits the enzyme vitamin K epoxide reductase, so the body cannot recycle vitamin K back to its active form.
Step 2: Without active vitamin K, the γ-carboxylation of glutamate residues cannot happen, and the clotting factors are produced in a non-functional form. This is exactly the mechanism described in the question.
Why the others are wrong: Heparin works by boosting antithrombin. Rivaroxaban is a direct factor Xa inhibitor, and dabigatran is a direct thrombin (factor IIa) inhibitor. None of these touch the vitamin-K-dependent carboxylation step — only warfarin does.
Answer: Option (4) — Warfarin.