The assessment is focused on the pharmacological faculties of apixaban in comparison with other NOACs and on the influence of apixaban on the management of VTE prophylaxis in patients undergoing MOS. Activation of factor X to factor Xa plays a key role in the cascade of blood coagulation. FXa straight converts prothrombin to thrombin through the prothrombinase complex, leading to fibrin clot formation and activation of platelets by thrombin. An individual particle of FXa can make more than 1000 molecules of thrombin due to the character of the coagulation cascade. Moreover, the reaction rate of prothrombinase bound FXa increases 300, 000 fold compared with that of free FXa. New orally working elements have now been designed to inhibit FXa selectively, prevent this burst of thrombin generation, or inhibit the excessively made thrombin. Apixaban is really a small particle having a molecular weight of 460 Da, which additionally inhibits trypsin and thrombin generation and inhibits element Xa reversibly. As well as inhibiting circulating factor Xa, apixaban also blocks factor Xa bound within the prothrombinase complex or factor Xa exercise within the clot. After oral absorption, apixaban is rapidly absorbed with bioavailability Eumycetoma in the abdomen and small intestine of around 66% and a high protein binding of 877-546. Maximum concentration levels are seen after 1 3 hours. The half-life of apixaban is 8 15 hours in young subjects after metabolic rate by a cytochrome P-450 3A4 associated path with 25% renal excretion and 55-65 elimination by the feces. Another new oral factor Xa inhibitors rivaroxaban and edoxaban were also found to inhibit free and clotbound factor Xa, which appears to be a class effect of all new oral factor Xa inhibitors. Of note, rivaroxaban does not restrict other serine proteases such as trypsin. The bio-availability of MAPK activity rivaroxaban is around hundreds of with plasma protein binding above 90-point and metabolic process via CYP3A4, CYP2C8, and CYP independent components. Thirty to forty percent of the substance is renally excreted as unchanged drug, whereas 30% is renally excreted as inactive metabolits and the remainder is excreted as unchanged drug in the feces. The intestinal excretion seems to be mediated by p glycoprotein an intestinal drug transporter therefore potent p Gp inhibitors may increase drug concentrations. The half-life ranges between 5 hours and 9 hours in healthy subjects and between 11 hours and 13 hours in elderly subjects. Compared with apixaban and rivaroxaban, edoxaban features a lower bio-availability of around 50,000-1,000,000 and a half-life of 9 11 hours in young healthier subjects with a mixed removal pathway: 35% is renally excreted and 62% is excreted via feces. Edoxaban can also be a substrate of p Gp, so strong inhibitors can lead to an increased concentration of edoxaban.