Pharmacology · Direct oral anticoagulants (DOACs)
Rivaroxaban !
An oral anticoagulant that blocks factor Xa directly. It needs no routine INR, and andexanet alfa can reverse it.
Updated 2026-11-01
The figure shows human factor Xa with rivaroxaban in its active site.
Mechanism of action
Rivaroxaban is a selective factor Xa inhibitor that needs no cofactor such as antithrombin. It blocks free factor Xa and the Xa inside the prothrombinase complex, so far less prothrombin is turned into thrombin. Less thrombin means less fibrin and, indirectly, less thrombin-driven platelet aggregation.
- Rivaroxaban binds factor Xa, free or in prothrombinase
- Prothrombinase cannot turn prothrombin into thrombin
- Less thrombin: less fibrin and less platelet aggregation
- Clots form and grow less: lower risk of stroke and VTE
Pharmacokinetics
- Absorption
- Well absorbed at low strengths; the higher strengths are absorbed better with food.
- Distribution
- Highly bound to plasma proteins (mainly albumin), so dialysis does not remove it.
- Metabolism
- By CYP3A4/5 and CYP2J2 and by hydrolysis; a P-glycoprotein and BCRP substrate.
- Elimination
- About a third of a dose leaves unchanged in the urine.
- Half-life
- Short: about 5 to 9 hours in young adults and 11 to 13 hours in older adults.
- Onset and duration
- Peak levels 2 to 4 hours after a dose.
Indications
- Prevention of stroke and embolism in atrial fibrillation without a mechanical valve. Atrial fibrillation →
- Treatment and prevention of deep vein thrombosis. Deep vein thrombosis →
- Treatment and prevention of pulmonary embolism. Pulmonary embolism →
Adverse effects
Common
- Bleeding (nose, gums, bruising, urine, stool)
- Pain in the arms or legs and muscle spasms
- Abdominal pain
Contraindications
- Active pathological bleeding
- Severe allergy to rivaroxaban
- Prosthetic heart valves (not recommended)
- Moderate or severe liver disease, or liver disease with clotting problems
- Pregnancy and breastfeeding
- Triple-positive antiphospholipid syndrome (not recommended)
Key interactions
- Combined P-glycoprotein and strong CYP3A inhibitors (ketoconazole, ritonavir)
- Raise rivaroxaban levels and bleeding risk; the combination is avoided.
- Combined P-glycoprotein and strong CYP3A inducers (rifampicin, carbamazepine, phenytoin, St John's wort)
- Lower levels and the protection against clots; the combination is avoided.
- Aspirin, clopidogrel, NSAIDs and SSRIs
- Add to bleeding risk.
What is monitored
- Kidney and liver function
- Signs of bleeding
- Standard tests such as the INR do not reliably measure its effect
Test yourself
Think of the answer, then tap the question to see it.
Which reversal agent is designed for factor Xa inhibitors such as rivaroxaban?
Andexanet alfa, a modified factor Xa without clotting activity that binds and holds the drug. Prothrombin complex concentrate may be considered as an alternative.
A patient with a mechanical mitral valve and atrial fibrillation needs anticoagulation. Is rivaroxaban an option?
No. Rivaroxaban is not recommended with prosthetic heart valves; warfarin is the anticoagulant used with mechanical valves.
Why does rivaroxaban not need antithrombin, unlike heparin?
It is a direct inhibitor: the molecule itself blocks factor Xa, while heparin only works by activating antithrombin.
Related drugs
Related conditions
← Back to the class: Direct oral anticoagulants (DOACs)
Educational content on how drugs work; not a prescribing guide and no substitute for a health professional's advice. No doses are given.
Sources: DailyMed - RIVAROXABAN tablet (DailyMed (U.S. National Library of Medicine), 2026); Rivaroxaban: MedlinePlus Drug Information (MedlinePlus (U.S. National Library of Medicine), 2026); Rivaroxaban: medicine to help prevent blood clots - NHS (NHS (UK), 2026).
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Representative model, for educational purposes only.