Open Access Articles- Top Results for Edoxaban


Systematic (IUPAC) name
Clinical data
Trade names Lixiana, Savaysa
AHFS/ Monograph
  • US: C (Risk not ruled out)
Pharmacokinetic data
Bioavailability 62%; Tmax 1–2 hours
Protein binding 55%
Metabolism Minimal hepatic
Half-life 10–14 hours
Excretion 50% renal; <50% bile
912273-65-5 7pxY
PubChem CID 25022378
ChemSpider 8456212 7pxN
KEGG D09710 7pxN
Chemical data
Formula C24H30ClN7O4S
548.056 g/mol
 14pxN (what is this?)  (verify)

Edoxaban (DU-176b, trade names Savaysa, Lixiana) is an anticoagulant drug which acts as a direct factor Xa inhibitor. It was developed by Daiichi Sankyo and approved in July 2011 in Japan for prevention of venous thromboembolisms (VTE) following lower-limb orthopedic surgery.[1] It was also approved by the FDA in January 2015 for the prevention of stroke and non–central-nervous-system systemic embolism.[2]

Medical uses

US FDA-labeled indications:

Treatment of deep vein thrombosis (DVT) and pulmonary embolism (PE) following 5 to 10 days of initial therapy with a parenteral anticoagulant.
To reduce the risk of stroke and systemic embolism (SE) in patients with nonvalvular atrial fibrillation (NVAF)

Limitations of use:

Edoxaban should not be used in NVAF patients with CrCl >95 mL/minute because of an increased risk of ischemic stroke compared to warfarin[3]


Premature discontinuation of any oral anticoagulant, including edoxaban, in the absence of adequate alternative anticoagulation increases the risk of ischemic events. If edoxaban is discontinued for reasons other than pathological bleeding or completion of a course of therapy, consider the use of another anticoagulant.[4]

Do not administer to nonvalvular atrial fibrillation (NVAF) patients with CrCl >95 mL/minute. In clinical trials, these patients had an increased rate of ischemic stroke with edoxaban 60 mg once daily compared to patients treated with warfarin; use another anticoagulant in these patients.[4]

Spinal or epidural hematomas resulting in long-term or permanent paralysis may occur with neuraxial anesthesia (epidural or spinal anesthesia) or spinal/epidural puncture; the risk is increased by the use of indwelling epidural catheters, concomitant administration of other drugs that affect hemostasis (eg, NSAIDS, platelet inhibitors, other anticoagulants), in patients with a history of traumatic or repeated epidural or spinal punctures, a history of spinal deformity or surgery, or if optimal timing between the administration of edoxaban and neuraxial procedures is not known. Consider the potential benefit versus risk prior to neuraxial intervention in patients who are anticoagulated or scheduled to be anticoagulated for thromboprophylaxis. Monitor frequently for signs and symptoms of neurologic impairment (eg, numbness/weakness of legs, bowel/bladder dysfunction). If neurologic impairment is noted, prompt treatment is necessary.[4]

Contraindicated in patients with active pathological bleeding.[5]

Adverse effects

More common

  • bloody nose
  • heavy non-menstrual vaginal bleeding
  • pale skin
  • troubled breathing with exertion
  • unusual bleeding or bruising
  • unusual tiredness or weakness

Less common

  • bloody or black, tarry stools
  • vomiting of blood or material that looks like coffee grounds
  • rash


  • confusion
  • cough
  • difficulty with speaking
  • double vision
  • fever
  • headache, sudden, severe
  • inability to move the arms, legs, or facial muscles
  • inability to speak
  • nausea and vomiting
  • slow speech[6]

Mechanism of action

Edoxaban inhibits free factor Xa and prothrombinase activity and inhibits thrombin-induced platelet aggregation. Inhibition of factor Xa in the coagulation cascade reduces thrombin generation and thrombus formation.[4][5]

Factor Xa

Factor Xa (FXa) is an essential blood coagulation factor[7] that is responsible for the initiation of the coagulation cascade. FXa cleaves prothrombin to its active form thrombin, which then acts to convert soluble fibrinogen to insoluble fibrin and to activate platelets. Stabilization of the platelet aggregation by fibrin mesh ultimately leads to clot formation.[8]

Related medications

A number of anticoagulants inhibit the activity of Factor Xa. Unfractionated heparin (UFH), low molecular weight heparin (LMWH), and fondaparinux inhibit the activity of factor Xa indirectly by binding to circulating antithrombin (AT III). These agents must be injected. Warfarin, phenprocoumon, and acenocoumarol are orally active vitamin K antagonists (VKA) which decrease hepatic synthesis of a number of coagulation factors, including Factor X. In recent years, a new series of oral, direct acting inhibitors of Factor Xa have entered clinical development. These include rivaroxaban, apixaban, betrixaban, LY517717, darexaban (YM150), and edoxaban (DU-176b).[9]


  1. ^ "First market approval in Japan for LIXIANA (Edoxaban)". Press Release. Daiichi Sankyo Europe GmbH. 2011-04-22. 
  2. ^ O'Riordan, Michael (9 January 2015). "FDA Approves Edoxaban for Stroke Prevention in AF and DVT/PE Prevention". Medscape. Retrieved 10 January 2015. 
  3. ^
  4. ^ a b c d
  5. ^ a b Savaysa (edoxaban) [prescribing information]. Parsippany, NJ: Daiichi Sankyo; January 2015.
  6. ^
  7. ^ Yoshiyuki, I., et al. "Biochemical and pharmalogical profile of darexaban, an oral direct Xa inhibitor." European Journal of Pharmacology (2011): 49-55
  8. ^ Katsung, B., S. Masters and A. Trevor. Basic and Clinical Pharmacology 11th Edition. United States of America: McGraw-Hill, 2009
  9. ^ Turpie AG (January 2008). "New oral anticoagulants in atrial fibrillation". European Heart Journal 29 (2): 155–65. PMID 18096568. doi:10.1093/eurheartj/ehm575.