Mechanism of action<unk>  is an inhibitor of the enzyme vitamin K epoxide reductase (VKOR). Vitamin K is needed to activate the coagulation factors II, VII, IX and X and the anticoagulation factors protein C and protein S, in which process it turns into vitamin K 2,3-epoxide. This is then recycled to vitamin K in a process involving VKOR. Inhibiting this enzyme effectively creates a vitamin K deficiency, blocking activation of the coagulation factors. After 36 to 72 hours, the available activated factors have been depleted (used up) by the coagulation system, and the anticoagulation takes effect. Pharmacokinetics Metabolism of S(−)‑phenprocoumon: known positions of hydroxylation by liver enzymes The drug is taken by mouth and quickly and completely absorbed from the gut. When in the bloodstream, 99% are bound to plasma proteins (mainly albumin). The substance is metabolized by the liver enzymes CYP2C9 and CYP3A4 to various hydroxyl derivatives, and subsequently conjugated to glucuronic acid to a small extent. The glucuronide metabolites partly undergo enterohepatic circulation. All metabolites, as well as the parent substance, are excreted predominantly via the kidney and urine, only 15% in unchanged form. The terminal half-life is 150 hours (6 to 7 days) on average with large differences between people. The long half-life means that drug concentrations take about four weeks to reach a steady state after therapy is started; the anticoagulation lasts at least 7 to 10 days after therapy is stopped; and dose changes need several days to take effect. The drug passes the placenta and also into breast milk. Pharmacogenomics Genetic polymorphisms of CYP2C9 can change the metabolization speed of<unk> . Polymorphisms of VKORC1, the gene coding for subunit 1 of vitamin K epoxide reductase, can influence the dose needed to achieve the desired INR.
Phenprocoumon
Warfarin
Prasugrel
Elinogrel
Palladin
Dabigatran
Apixaban
Alteplase