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A specialist may request a quantitative factor Xa assay in a situation of overdose. [2] Andexanet alfa, a specific antidote to reverse the anticoagulant activity of direct Xa inhibitors in the event of major bleeding, was approved by the FDA in 2018. [9] It is also available in the UK. [10]
This study reports results on 352 people and demonstrates a reduction of anti-Xa-activity while also showing an excellent or good hemostatic efficacy in 82%. While people who were expected to die in 30 days were excluded from the study, 14% of participants died. There was no relationship between hemostatic efficacy and reduced anti-Xa-activity ...
The formation of draculin-factor Xa is a two-stage process. The first reversible stage is characterized by the following constants: k1 = 1.117*106 M-1*sec-1, k-1 = 15.388*10-1 sec-1. The second irreversible (concentration-independent) stage is characterized by the forward reaction rate constant k2 = 0.072 sec-1.
Factor Xa was identified as a promising target for the development of new anticoagulants in the early 1980s. In 1987 the first factor Xa inhibitor, the naturally occurring compound antistasin, was isolated from the salivary glands of the Mexican leech Haementeria officinalis. Antistasin is a polypeptide and a potent Xa inhibitor.
Rivaroxaban inhibits both free and bound Factor Xa in the prothrombinase complex. [33] It is a selective direct factor Xa inhibitor with an onset of action of 2.5 to 4 hours. [34] Inhibition of Factor Xa interrupts the intrinsic and extrinsic pathway of the blood coagulation cascade, inhibiting both thrombin formation
Edoxaban is a direct, selective, reversible and competitive inhibitor of human factor Xa, with an inhibitory constant (K i) value of 0.561 nM. In coagulation, uninhibited factor Xa forms a prothrombinase complex with factor Va on platelet surfaces. Prothrombinases turn prothrombins to thrombins.
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Factor Xa also plays a role in other biological processes that are not directly related to coagulation, like wound healing, tissue remodelling, inflammation, angiogenesis and atherosclerosis. Inhibition of the synthesis or activity of Factor X is the mechanism of action for many anticoagulants in use today.
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