Each film-coated tablet contains: Edoxaban (as tosilate) 30 mg or 60 mg.
Pharmacotherapeutic group: Other antithrombotic agents. ATC code: B01AF03.
Pharmacology: Pharmacodynamics: Edoxaban is a highly selective, direct and reversible inhibitor of factor Xa, the serine protease located in the final common pathway of the coagulation cascade. Edoxaban inhibits free factor Xa, and prothrombinase activity. Inhibition of factor Xa in the coagulation cascade reduces thrombin generation, prolongs clotting time and reduces the risk of thrombus formation.
Edoxaban produces rapid onset of pharmacodynamic effects within 1 - 2 hours, which corresponds with peak edoxaban exposure (Cmax). The pharmacodynamic effects measured by anti-factor Xa assay are predictable and correlate with the dose and the concentration of edoxaban. As a result of FXa inhibition, edoxaban also prolongs clotting time in tests such as prothrombin time (PT), and activated partial thromboplastin time (aPTT). Changes observed in these clotting tests are expected at the therapeutic dose, however, these changes are small, subject to a high degree of variability, and not useful in monitoring the anticoagulation effect of edoxaban.
Effects of coagulation markers when switching from rivaroxaban, dabigatran, or apixaban to edoxaban.
In clinical pharmacology studies, healthy subjects received rivaroxaban 20 mg once daily, dabigatran 150 mg twice daily, or apixaban 5 mg twice daily, followed by a single dose of edoxaban 60 mg on Day 4. The effect on prothrombin time (PT) and other coagulation biomarkers (e.g. anti-FXa, aPTT) was measured. Following the switch to edoxaban on Day 4 the PT was equivalent to Day 3 of rivaroxaban and apixaban. For dabigatran higher aPTT activity was observed after edoxaban administration with prior dabigatran treatment compared to that after treatment with edoxaban alone. This is considered to be due to the carry-over effect of dabigatran treatment, however, this did not lead to a prolongation of bleeding time. Based on these data, when switching from these anticoagulants to edoxaban, the first dose of edoxaban can be initiated at the time of the next scheduled dose of the previous anticoagulant.
Pharmacokinetics: Edoxaban is absorbed with peak plasma concentrations within 1 - 2 hours. The absolute bioavailability is approximately 62%. Food increases peak exposure to a varying extent, but has minimal effect on total exposure. Edoxaban was administered with or without food in the ENGAGE AF-TIMI 48 and the Hokusai-VTE studies. Edoxaban is poorly soluble at pH of 6.0 or higher. Co-administration of proton pump inhibitors had no relevant impact on edoxaban exposure Disposition is biphasic. The volume of distribution is 107 (19.9) L mean (SD). In vitro plasma protein binding is approximately 55%. There is no clinically relevant accumulation of edoxaban (accumulation ratio 1.14) with once daily dosing. Steady state concentrations are achieved within 3 days.
Unchanged edoxaban is the predominant form in plasma. Edoxaban is metabolised via hydrolysis (mediated by carboxylesterase 1), conjugation or oxidation by CYP3A4/5 (<10%). Edoxaban has three active metabolites, the predominant metabolite (M-4), formed by hydrolysis, is active and reaches less than 10% of the exposure of the parent compound in healthy subjects. Exposure to the other metabolites is less than 5%. Edoxaban is a substrate for the efflux transporter P-glycoprotein (Pgp), but not a substrate for uptake transporters such as organic anion transporter polypeptide OATP1B1, organic anion transporters OAT1 or OAT3 or organic cation transporter OCT2. Its active metabolite is a substrate for OATP1B1.
In healthy subjects, the total clearance is estimated as 22 (± 3) L/hour; 50% is renally cleared (11 L/hour). Renal clearance accounts for approximately 35% of the administered dose. Metabolism and biliary/intestinal excretion account for the remaining clearance. The t½ for oral administration is 10 - 14 hours. Edoxaban displays approximately dose-proportional pharmacokinetics for doses of 15 mg to 60 mg in healthy subjects.
Toxicology: Preclinical safety data: Non-clinical data reveal no special hazard for humans based on conventional studies of safety pharmacology, repeated dose toxicity, genotoxicity, carcinogenic potential, or phototoxicity.
Prevention of stroke and systemic embolism in adult patients with nonvalvular atrial fibrillation (NVAF) with one or more risk factors, such as congestive heart failure, hypertension, age ≥ 75 years, diabetes mellitus, prior stroke or transient ischaemic attack (TIA). Treatment of deep vein thrombosis (DVT) and pulmonary embolism (PE), and prevention of recurrent DVT and PE in adults (see Precautions).
Patients with Renal insufficiency: In patients with mild renal impairment (CrCL > 50 - 80 mL/min), the recommended dose is 60 mg Lixiana once daily.
In patients with moderate or severe renal impairment (CrCL 15 - 50 mL/min), the recommended dose is 30 mg Lixiana once daily.
In patients with end stage renal disease (ESRD) (CrCL < 15 mL/min) or on dialysis, the use of Edoxaban (Lixiana) is not recommended.
Patients with Hepatic insufficiency: Lixiana is contraindicated in patients with hepatic disease associated with coagulopathy and clinically relevant bleeding risk.
In patients with severe hepatic impairment Edoxaban (Lixiana) is not recommended.
In patients with mild to moderate hepatic impairment the recommended dose is 60 mg Edoxaban (Lixiana) once daily. Edoxaban (Lixiana) should be used with caution in patients with mild to moderate hepatic impairment.
Elderly: No dose deduction is required.
Children and Adolescents: The safety and efficacy of Edoxaban (Lixiana) in children and adolescents less than 18 years of age have not been established. No data are available.
Patients undergoing cardioversion: Edoxaban (Lixiana) can be initiated or continued in patients who may require cardioversion. For transoesophageal echocardiogram (TEE) guided cardioversion in patients not previously treated with anticoagulants, Edoxaban (Lixiana) treatment should be started at least 2 hours before cardioversion to ensure adequate anticoagulation. Cardioversion should be performed no later than 12 hours after the dose of Edoxaban (Lixiana) on the day of the procedure.
For all patients undergoing cardioversion: Confirmation should be sought prior to cardioversion that the patient has taken Edoxaban (Lixiana) as prescribed. Decisions on initiation and duration of treatment should follow established guidelines for anticoagulant treatment in patients undergoing cardioversion.
Elderly: No dose adjustment is required since uptitration to the maximum tolerated dose is individually adjusted.
Children and Adolescents: The safety and efficacy of Edoxaban (Lixiana) in children and adolescents less than 18 years of age have not been established. No data are available.
Method of administration: For oral use.
Edoxaban (Lixiana) can be taken with or without food.
Overdose with edoxaban may lead to haemorrhage. Experience with overdose cases is very limited.
Treatment: In case of overdosage or hypersensitivity, the patient should be kept under close supervision and be treated in an intensive care ward. A specific antidote antagonising the pharmacodynamic effect of edoxaban is not available. Early administration of activated charcoal may be considered in case of edoxaban overdose to reduce absorption. This recommendation is based on standard treatment of drug overdose and data available with similar compounds, as the use of activated charcoal to reduce absorption of edoxaban has not been specifically studied in the edoxaban clinical programme.
Management of bleeding: Should a bleeding complication arise in a patient receiving edoxaban, the next edoxaban administration should be delayed or treatment should be discontinued as appropriate.
Edoxaban has a half-life of approximately 10 to 14 hours. Management should be individualised according to the severity and location of the haemorrhage. Appropriate symptomatic treatment could be used as needed, such as mechanical compression (e.g. for severe epistaxis), surgical haemostasis with bleeding control procedures, fluid replacement and haemodynamic support, blood products (packed red cells or fresh frozen plasma, depending on associated anaemia or coagulopathy) or platelets.
For life-threatening bleeding that cannot be controlled with the measures such as transfusion or haemostasis, the administration of a 4-factor prothrombin complex concentrate (PCC) at 50 IU/kg has been shown to reverse the effects of Lixiana 30 minutes after completing the infusion. Recombinant factor VIIa (r-FVIIa) can also be considered. However, there is limited clinical experience with the use of this product in individuals receiving edoxaban.
Depending on local availability, a consultation with a coagulation expert should be considered in case of major bleedings. Protamine sulfate and vitamin K are not expected to affect the anticoagulant activity of edoxaban.
There is no experience with antifibrinolytic agents (tranexamic acid, aminocaproic acid) in individuals receiving edoxaban. There is neither scientific rationale for benefit nor experience with the use of systemic haemostatics (desmopressin, aprotinin) in individuals receiving edoxaban. Due to the high plasma protein binding edoxaban is not expected to be dialysable.
Hypersensitivity to the active substance or to any of the excipients.
Clinically significant active bleeding.
Hepatic disease associated with coagulopathy and clinically relevant bleeding risk.
Lesion or condition, if considered to be a significant risk for major bleeding. This may include current or recent gastrointestinal ulceration, presence of malignant neoplasms at high risk of bleeding, recent brain or spinal injury, recent brain, spinal or ophthalmic surgery, recent intracranial haemorrhage, known or suspected oesophageal varices, arteriovenous malformations, vascular aneurysms or major intraspinal or intracerebral vascular abnormalities.
Uncontrolled severe hypertension.
Concomitant treatment with any other anticoagulants e.g. unfractionated heparin (UFH), low molecular weight heparins (enoxaparin, dalteparin, etc.), heparin derivatives (fondaparinux, etc.), oral anticoagulants (warfarin, dabigatran etexilate, rivaroxaban, apixaban etc.) except under specific circumstances of switching oral anticoagulant therapy or when UFH is given at doses necessary to maintain an open central venous or arterial catheter.
Pregnancy and breast-feeding.
Edoxaban (Lixiana) 15 mg is not indicated as monotherapy, as it may result in decreased efficacy. It is only indicated in the process of switching from Edoxaban (Lixiana) 30 mg (patients with one or more clinical factors for increased exposure) to VKA, together with an appropriate VKA dose.
Haemorrhagic risk: Edoxaban increases the risk of bleeding and can cause serious, potentially fatal bleeding. Edoxaban (Lixiana), like other anticoagulants, is recommended to be used with caution in patients with increased risk of bleeding. Edoxaban (Lixiana) administration should be discontinued if severe haemorrhage occurs. In the clinical studies mucosal bleedings (e.g. epistaxis, gastrointestinal, genitourinary) and anaemia were seen more frequently during long term edoxaban treatment compared with VKA treatment. Thus, in addition to adequate clinical surveillance, laboratory testing of haemoglobin/haematocrit could be of value to detect occult bleeding, as judged to be appropriate.
Several sub-groups of patients, as detailed as follows, are at increased risk of bleeding. These patients are to be carefully monitored for signs and symptoms of bleeding complications and anaemia after initiation of treatment. Any unexplained fall in haemoglobin or blood pressure should lead to a search for a bleeding site. The anticoagulant effect of edoxaban cannot be reliably monitored with standard laboratory testing. A specific anticoagulant reversal agent for edoxaban is not available.
Haemodialysis does not significantly contribute to edoxaban clearance. The co-administration of Edoxaban (Lixiana) with ASA in elderly patients should be used cautiously because of a potentially higher bleeding risk.
Renal impairment: The plasma AUC for subjects with mild (CrCL > 50 - 80 mL/min), moderate (CrCL 30 - 50 mL/min) and severe (CrCL< 30 mL/min but not undergoing dialysis) renal impairment was increased by 32%, 74%, and 72%, respectively, relative to subjects with normal renal function. In patients with end stage renal disease or on dialysis, Edoxaban (Lixiana) is not recommended.
Renal function in NVAF: A trend towards decreasing efficacy with increasing creatinine clearance was observed for edoxaban compared to well-managed warfarin. Therefore, edoxaban should only be used in patients with NVAF and high creatinine clearance after a careful evaluation of the individual thromboembolic and bleeding risk.
Assessment of renal function: CrCL should be monitored at the beginning of the treatment in all patients and afterwards when clinically indicated.
Hepatic impairment: Patients with elevated liver enzymes (ALT/AST > 2 x ULN) or total bilirubin ≥ 1.5 x ULN were excluded in clinical trials.
Therefore Edoxaban (Lixiana) should be used with caution in this population. Prior to initiating Lixiana, liver function testing should be performed.
Periodic hepatic monitoring is recommended for patients on Edoxaban (Lixiana) treatment beyond 1 year.
Discontinuation for surgery and other interventions: If anticoagulation must be discontinued to reduce the risk of bleeding with surgical or other procedures, Edoxaban (Lixiana) should be stopped as soon as possible and preferably at least 24 hours before the procedure.
In deciding whether a procedure should be delayed until 24 hours after the last dose of Edoxaban (Lixiana), the increased risk of bleeding should be weighed against the urgency of the intervention. Edoxaban (Lixiana) should be restarted after the surgical or other procedures as soon as adequate haemostasis has been established; noting that the time to onset of the edoxaban anticoagulant therapeutic effect is 1-2 hours. If oral medicinal products cannot be taken during or after surgical intervention, consider administering a parenteral anticoagulant and then switch to oral once daily Edoxaban (Lixiana).
Interaction with other medicinal products affecting haemostasis: Concomitant use of medicines affecting haemostasis may increase the risk of bleeding. These include acetylsalicylic acid (ASA), P2Y12 platelet inhibitors, other antithrombotic agents, fibrinolytic therapy, selective serotonin reuptake inhibitors (SSRIs) or serotonin norepinephrine reuptake inhibitors (SNRIs), and chronic nonsteroidal anti-inflammatory drugs (NSAIDs).
Prosthetic heart valves and moderate to severe mitral stenosis: Edoxaban has not been studied in patients with mechanical heart valves, in patients during the first 3 months after implantation of a bioprosthetic heart valve, with or without atrial fibrillation, or in patients with moderate to severe mitral stenosis. Therefore, use of edoxaban is not recommended in these patients.
Haemodynamically unstable PE patients or patients who require thrombolysis or pulmonary embolectomy: Edoxaban (Lixiana) is not recommended as an alternative to unfractionated heparin in patients with pulmonary embolism who are haemodynamically unstable or may receive thrombolysis or pulmonary embolectomy since the safety and efficacy of edoxaban have not been established in these clinical situations.
Patients with active cancer: Efficacy and safety of edoxaban in the treatment and/or prevention of VTE in patients with active cancer have not been established.
Patients with antiphospholipid syndrome: Direct acting Oral Anticoagulants (DOACs) including edoxaban are not recommended for patients with a history of thrombosis who are diagnosed with antiphospholipid syndrome. In particular for patients that are triple positive (for lupus anticoagulant, anticardiolipin antibodies, and anti-beta 2-glycoprotein I antibodies), treatment with DOACs could be associated with increased rates of recurrent thrombotic events compared with vitamin K antagonist therapy.
Laboratory coagulation parameters: Although treatment with edoxaban does not require routine monitoring, the effect on anticoagulation can be estimated by a calibrated quantitative anti-Factor Xa assay which may help to inform clinical decisions in particular situations as, e.g. overdose and emergency surgery Edoxaban prolongs standard clotting tests such as prothrombin time (PT), INR, and activated partial thromboplastin time (aPTT) as a result of FXa inhibition. Changes observed in these clotting tests at the expected therapeutic dose are, however, small, subject to a high degree of variability, and not useful in monitoring the anticoagulation effect of edoxaban.
Effects On Ability to Drive and Use Machines: Edoxaban (Lixiana) has no or negligible influence on the ability to drive and use machines.
Use in pregnancy: Safety and efficacy of edoxaban have not been established in pregnant women. Studies in animals have shown reproductive toxicity. Due to the potential reproductive toxicity, the intrinsic risk of bleeding and the evidence that edoxaban passes the placenta, Edoxaban (Lixiana) is contraindicated during pregnancy.
Use in lactation: Safety and efficacy of edoxaban have not been established in breast-feeding women. Data from animals indicate that edoxaban is secreted into breast milk. Therefore Edoxaban (Lixiana) is contraindicated during breast-feeding. A decision must be made whether to discontinue breastfeeding or to discontinue/abstain from therapy.
The safety of edoxaban has been evaluated in two Phase 3 studies including 21,105 patients with NVAF (ENGAGE AF-TIMI 48 study), and 8,292 patients with VTE (DVT and PE) (Hokusai-VTE study).
The average exposure to edoxaban 60 mg (including 30 mg dose reduced) was 2.5 years among 7,012 patients in ENGAGE AF-TIMI 48 and 251 days among 4,118 patients in Hokusai-VTE. Adverse reactions were experienced by 2,256 (32.2%) of the patients treated with edoxaban 60 mg (30 mg dose reduced) in the ENGAGE AF-TIMI 48 study and 1,249 (30.3%) in the Hokusai-VTE study.
In both studies, the most common adverse reactions related to bleeding with edoxaban 60 mg based on adjudicated terms included cutaneous soft tissue haemorrhage (up to 5.9%) and epistaxis (up to 4.7%), while vaginal haemorrhage (9.0%) was the most common bleeding-related adverse reaction in Hokusai-VTE only.
Bleeding can occur at any site and may be severe and even fatal.
Common other adverse reactions for edoxaban were anaemia, rash and abnormal liver function tests.
Tabulated list of adverse reactions:
Table as follows provides the list of adverse reactions from the two pivotal Phase 3 studies in patients with VTE (DVT and PE) (Hokusai-VTE study) and AF (ENGAGE AF-TIMI 48 study) combined for both indications. The adverse reactions are classified by System Organ Class and frequency, using the following convention: Very common (≥ 1/10), Common (≥ 1/100 to < 1/10), Uncommon (≥ 1/1,000 to < 1/100), Rare (≥ 1/10,000 to < 1/1,000), Very rare (< 1/10,000), not known (cannot be estimated from the available data). (See table.)
Click on icon to see table/diagram/image
Due to the pharmacological mode of action, the use of Lixiana may be associated with an increased risk of occult or overt bleeding from any tissue or organ which may result in post haemorrhagic anaemia. The signs, symptoms, and severity (including fatal outcome) will vary according to the location and degree or extent of the bleeding and/or anaemia (see Management of bleeding under Overdosage). In the clinical studies mucosal bleedings (e.g. epistaxis, gastrointestinal, genitourinary) and anaemia were seen more frequently during long term edoxaban treatment compared with VKA treatment. Thus, in addition to adequate clinical surveillance, laboratory testing of haemoglobin/haematocrit could be of value to detect occult bleeding, as judged to be appropriate. The risk of bleedings may be increased in certain patient groups e.g. those patients with uncontrolled severe arterial hypertension and/or on concomitant treatment affecting haemostasis. Menstrual bleeding may be intensified and/or prolonged.
Haemorrhagic complications may present as weakness, paleness, dizziness, headache or unexplained swelling, dyspnoea, and unexplained shock.
Known complications secondary to severe bleeding such as compartment syndrome and renal failure due to hypoperfusion have been reported for Edoxaban (Lixiana).
Therefore, the possibility of haemorrhage is to be considered in evaluating the condition in any anticoagulated patient.
Reporting of suspected adverse reactions:
Reporting suspected adverse reactions after authorisation of the medicinal product is important. It allows continued monitoring of the benefit/risk balance of the medicinal product.
Please seek medical attention immediately at the first sign of any adverse drug reaction.
Edoxaban is predominantly absorbed in the upper gastrointestinal (GI) tract. Thus, medicines or disease conditions that increase gastric emptying and gut motility have the possibility of reducing edoxaban dissolution and absorption.
P-gp inhibitors: Edoxaban is a substrate for the efflux transporter P-gp. In pharmacokinetic (PK) studies, concomitant administration of edoxaban with the P-gp inhibitors: ciclosporin, dronedarone, erythromycin, ketoconazole, quinidine, or verapamil resulted in increased plasma concentrations of edoxaban.
Concomitant use of edoxaban with ciclosporin, dronedarone, erythromycin, or ketoconazole requires dose reduction to 30 mg once daily.
Concomitant use of edoxaban with quinidine, verapamil, or amiodarone does not require dose reduction based on clinical data. The use of edoxaban with other P-gp inhibitors including HIV protease inhibitors has not been studied.
Lixiana 30 mg once daily must be administered during concomitant use with the following P-gp inhibitors: Ciclosporin: Concurrent administration of a single dose of ciclosporin 500 mg with a single dose of edoxaban 60 mg increased edoxaban AUC and Cmax by 73% and 74%, respectively.
Dronedarone: Dronedarone 400 mg twice daily for 7 days with a single concomitant dose of edoxaban 60 mg on Day 5 increased edoxaban AUC and Cmax by 85% and 46%, respectively.
Erythromycin: Erythromycin 500 mg four times daily for 8 days with a single concomitant dose of edoxaban 60 mg on Day 7 increased the edoxaban AUC and Cmax by 85% and 68%, respectively.
Ketoconazole: Ketoconazole 400 mg once daily for 7 days with a single concomitant dose of edoxaban 60 mg on Day 4, increased edoxaban AUC and Cmax by 87% and 89%, respectively.
Edoxaban (Lixiana) 60 mg once daily is recommended during concomitant use with the following P-gp inhibitors: Quinidine: Quinidine 300 mg once daily on Days 1 and 4 and three times daily on Days 2 and 3, with a single concomitant dose of edoxaban 60 mg on Day 3, increased edoxaban AUC over 24 hours by 77% and Cmax by 85%, respectively.
Verapamil: Verapamil 240 mg once daily for 11 days with a single concomitant dose of edoxaban 60 mg on Day 10 increased the edoxaban AUC and Cmax by approximately 53%.
Amiodarone: Co-administration of amiodarone 400 mg once daily with edoxaban 60 mg once daily increased AUC by 40% and Cmax by 66%. This was not considered clinically significant. In ENGAGE AF-TIMI 48 study in NVAF, efficacy and safety results were similar for subjects with and without concomitant amiodarone use.
P-gp inducers: Co-administration of edoxaban with the P-gp inducer rifampicin led to a decrease in mean edoxaban AUC and a shortened half-life, with possible decreases in its pharmacodynamic effects. The concomitant use of edoxaban with other P-gp inducers (e.g. phenytoin, carbamazepine, phenobarbital or St. John's Wort) may lead to reduced edoxaban plasma concentrations. Edoxaban should be used with caution when co-administered with P-gp inducers.
Digoxin: Edoxaban 60 mg once daily on days 1 to 14 with coadministration of multiple daily doses of digoxin 0.25 mg twice daily (days 8 and 9) and 0.25 mg once daily (days 10 to 14) increased the Cmax of edoxaban by 17%, with no significant effect on AUC or renal clearance at steady state. When the effects of edoxaban on digoxin PK were also examined, the Cmax of digoxin increased by approximately 28% and AUC by 7%. This was not considered clinically relevant. No dose modification is necessary when Lixiana is administered with digoxin.
Anticoagulants, antiplatelets, NSAIDs and SSRIs/SNRIs Anticoagulants: Co-administration of edoxaban with other anticoagulants is contraindicated due to increased risk of bleeding.
Acetylsalicylic acid (ASA): Co-administration of ASA (100 mg or 325 mg) and edoxaban increased bleeding time relative to either medicine alone. Co-administration of high dose ASA (325 mg) increased the steady state Cmax and AUC of edoxaban by 35% and 32%, respectively. The concomitant chronic use of high dose ASA (325 mg) with edoxaban is not recommended.
Concomitant administration of higher doses than 100 mg ASA should only be performed under medical supervision. In clinical studies concomitant use of ASA (low dose ≤ 100 mg/day), other antiplatelet agents, and thienopyridines was permitted and resulted in approximately a 2-fold increase in major bleeding in comparison with no concomitant use, although to a similar extent in the edoxaban and warfarin groups.
Co-administration of low dose ASA (≤ 100 mg) did not affect the peak or total exposure of edoxaban either after single dose or at steady-state.
Edoxaban can be co-administered with low dose ASA (≤ 100 mg/day).
Platelet inhibitors: In ENGAGE AF-TIMI 48 concomitant use of thienopyridines (e.g. clopidogrel) monotherapy was permitted and resulted in increased clinically relevant bleeding although with a lower risk of bleeding on edoxaban compared to warfarin. There is very limited experience on the use of edoxaban with dual antiplatelet therapy or fibrinolytic agents.
NSAIDs: Co-administration of naproxen and edoxaban increased bleeding time relative to either medicine alone. Naproxen had no effect on the Cmax and AUC of edoxaban. In clinical studies, co-administration of NSAIDs resulted in increased clinically relevant bleeding. Chronic use of NSAIDs with edoxaban is not recommended.
SSRIs/SNRIs: As with other anticoagulants the possibility may exist that patients are at increased risk of bleeding in case of concomitant use with SSRIs or SNRIs due to their reported effect on platelets.
Effect of edoxaban on other medicines: Edoxaban increased the Cmax of concomitantly administered digoxin by 28%; however, the AUC was not affected. Edoxaban had no effect on the Cmax and AUC of quinidine.
Edoxaban decreased the Cmax and AUC of concomitantly administered verapamil by 14% and 16%, respectively.
Store at temperatures not exceeding 30°C.
B01AF03 - edoxaban ; Belongs to the class of direct factor Xa inhibitors. Used in the treatment of thrombosis.
FC tab 30 mg x 28's. 60 mg x 28's.