All anticoagulant rodenticides have the same mode of action, i.e. interference with the synthesis of clotting factors, which results in haemorrhaging and death. In the liver cells, the biologically inactive vitamin K1-2,3 epoxide is reduced by a microsomal enzyme into biologically active vitamin K, which is essential for the synthesis of prothrombin and other clotting factors. Anticoagulant rodenticides antagonize the enzyme vitamin K1-epoxide reductase in the liver causing a gradual depletion of the vitamin and consequently of vitamin K-dependent clotting factors. This results in an increase in blood-clotting time until the point where the clotting mechanism fails. The principal use of anticoagulants worldwide has been for control of commensal rodents, primarily Norway rats, ship rats, and house mice. About ten anticoagulant rodenticides have been brought to the market. Some are reviewed below to illustrate their properties. A number have been registered for commensal rodent control.
The second-generation anticoagulants are more acutely toxic than first-generation anticoagulant rodenticides. Their superior potency is related to their greater affinity for vitamin K-epoxide reductase. Bromadiolone and difenacoum were the first compounds of the second generation introduced to the market.The three most potent anticoagulants are Brodifacoum, Flocoumafen and Difethialone.
No practical resistance is known in Norway rats and house mice against the three most potent second generation anticoagulants.