The vitamin K antagonists can cause birth defects ( teratogens). However, in the case of the second generation superwarfarins intended to kill warfarin resistant rodents, the time of vitamin K administration may need to be prolonged to months, in order to combat the long residence time of the poison. The action of this class of anticoagulants may be reversed by administering vitamin K for the duration of the anticoagulant's residence in the body, and the daily dose needed for reversal is the same for all drugs in the class. Without these residues carboxylated, the protein will not form the appropriate conformation of thrombin, which is needed to produce the fibrin monomers that are polymerized to form clots.

For example, it is needed to carboxylate specific glutamic acid residues on prothrombin. Vitamin K is required for the proper production of certain proteins involved in the blood clotting process. The term 'vitamin K antagonist' is a misnomer, as the drugs do not directly antagonise the action of vitamin K in the pharmacological sense, but rather the recycling of vitamin K. The drugs are structurally similar to vitamin K and act as competitive inhibitors of the enzyme. These drugs deplete the active form of the vitamin by inhibiting the enzyme vitamin K epoxide reductase and thus the recycling of the inactive vitamin K epoxide back to the active reduced form of vitamin K.

They are used as anticoagulant medications in the prevention of thrombosis, and in pest control, as rodenticides. Vitamin K antagonists (VKAs) have been the mainstay of anticoagulation therapy for more than 50 years. The term 'vitamin K antagonist' is technically a misnomer, as the drugs do not directly antagonize the action of vitamin K in the pharmacological sense, but rather the recycling of vitamin K. Vitamin K antagonists ( VKA) are a group of substances that reduce blood clotting by reducing the action of vitamin K. In menaquinone the side chain is composed of a varying number of isoprenoid residues.

Antidote for vitamin k toxicity