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  • Acitrom®
  • MOA

Mechanism of Action (MOA)4-6

  • Vitamin K1 is essential for normal blood coagulation.
  • Coagulation factors II, VII, IX and X and the anticoagulant proteins C and S are synthesized mainly in the liver and are biologically inactive unless 9 to 13 of the γ-amino-terminal glutamate residues are carboxylated to form the Ca2+-binding γ-carboxyglutamate residues.
  • This reaction requires carbon dioxide, molecular oxygen and reduced vitamin K, and is catalyzed by γ-glutamyl carboxylase in the rough endoplasmic reticulum.
  • Carboxylation is directly coupled to the oxidation of vitamin K to its corresponding vitamin K epoxide or oxidized vitamin K.
  • For the continued synthesis of activated clotting factors, vitamin K1 must be regenerated from the biologically inactive epoxide by vitamin K1 epoxide reductase.
  • Acenocoumarol and the coumarin anticoagulants are structurally similar to vitamin K and competitively inhibit the enzyme vitamin K-epoxide reductase. Hence, they are called vitamin K antagonists.
  • These drugs exert their anticoagulant action by preventing the regeneration of reduced vitamin K by interfering with action of vitamin K epoxide reductase.
  • Oral anticoagulants have no effect on the activity of fully carboxylated molecules in the circulation. Thus, the time required for the activity of each factor in plasma to reach a new steady state after therapy is initiated or adjusted depends on its individual rate of clearance. The approximate half-lives of these factors (in hours) are shown below
  • Half-lives of clotting factors inhibited by coumarins
  • Factor VII - 6 hours
  • Factor IX - 24 hours
  • Factor X - 36 hours
  • Factor II - 50 hours