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Acenocoumarol (United States: Not available): Drug information

Acenocoumarol (United States: Not available): Drug information
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For additional information see "Acenocoumarol (United States: Not available): Patient drug information"

For abbreviations, symbols, and age group definitions show table
Brand Names: Canada
  • Sintrom [DSC]
Pharmacologic Category
  • Anticoagulant;
  • Anticoagulant, Vitamin K Antagonist
Dosing: Adult

Note: Dosage must be individualized. The following information is based on the manufacturer's labeling in Canada.

Prevention/treatment of thrombosis/embolism

Prevention/treatment of thrombosis/embolism: Oral: Initial: 8 to 12 mg on day 1, followed by 4 to 8 mg on day 2. Subsequent dosage should be based on INR measurements. Usual range of maintenance doses: 1 to 10 mg/day. Tapering of dosage is recommended prior to discontinuation.

Dosage adjustment for concomitant therapy: Significant drug interactions exist, requiring dose/frequency adjustment or avoidance. Consult drug interactions database for more information.

Dosing: Kidney Impairment: Adult

Use with caution; the manufacturer's labeling does not provide specific dosing recommendations.

Dosing: Liver Impairment: Adult

Use with caution; the manufacturer's labeling does not provide specific dosing recommendations.

Dosing: Older Adult

Refer to adult dosing. Use with caution; lower dosages may be necessary.

Adverse Reactions

The following adverse drug reactions and incidences are derived from product labeling unless otherwise specified.

As with all anticoagulants, bleeding is the major adverse effect of acenocoumarol. Hemorrhage may occur at virtually any site. Risk is dependent on multiple variables, including the intensity of anticoagulation and patient susceptibility. Frequency not defined.

Dermatologic: Skin necrosis (including hemorrhagic forms) (rare)

Genitourinary: Priapism

Hematologic & oncologic: Hemorrhage may occur at virtually any site that may be predisposed to bleeding. Includes cerebral hemorrhage, gallbladder hemorrhage, hematuria, hemophthalmos, hepatic hemorrhage, melena, menorrhagia, metrorrhagia

Hepatic: Hepatotoxicity

Contraindications

Hypersensitivity to acenocoumarol, related coumarin derivatives, or any component of the formulation; hemorrhagic tendencies and/or blood dyscrasias (eg, hemophilia, thrombocytopenic purpura, leukemia); recent or potential surgery of the eye or CNS; major regional lumbar block anesthesia or surgery resulting in large, open surfaces; bleeding from the GI, respiratory, or GU tract; aneurysm (cerebral or dissecting aortic); cerebrovascular hemorrhage; recent surgical procedures resulting in increased fibrinolytic activity (eg, surgery of the lung, prostate, uterus); polyarthritis; severe hypertension; severe parenchymal lesions of the liver and kidneys; pericarditis or pericardial effusion; subacute bacterial endocarditis; ascorbic acid deficiency; uncooperative patient (eg, patient with alcohol use disorder, unsupervised senile, or psychotic) intramuscular injections; inadequate laboratory facilities; threatened abortion; eclampsia/pre-eclampsia; pregnancy

Warnings/Precautions

Concerns related to adverse effects:

• Anaphylaxis/hypersensitivity: May cause hypersensitivity reactions, including anaphylaxis; use with caution in patients with anaphylactic disorders. Cross-reactivity among coumarin anticoagulants has been described.

• Bleeding: May cause major or fatal bleeding. Risk factors for bleeding include high intensity anticoagulation (INR >4), age (>65 years), variable INRs, history of GI bleeding, hypertension, cerebrovascular disease, serious heart disease, anemia, severe diabetes, malignancy, trauma, renal insufficiency, polycythemia vera, vasculitis, open wound, history of PUD, indwelling catheters, menstruating and postpartum women, and long duration of therapy or known genetic deficiency in CYP2C9 activity. Patient must be instructed to report bleeding, accidents, or falls as well as any new or discontinued medications, herbal or alternative products used, significant changes in smoking or dietary habits. Unrecognized bleeding sites (eg, colon cancer) may be uncovered by anticoagulation. Treatment should be withdrawn at the earliest signs of bleeding.

• Skin necrosis/gangrene: Necrosis or gangrene of the skin and other tissues can occur (rarely) due to early hypercoagulability; risk is increased in patients with protein C or S deficiency. Onset is usually within the first few days of therapy and is frequently localized to the limbs, breast, or penis.

• "Purple toe” syndrome: "Purple toe” syndrome, due to cholesterol microembolization, has been described with coumarin-type anticoagulants.

Disease-related concerns:

• Dietary insufficiency: Use with caution in patients with prolonged dietary insufficiencies (vitamin K deficiency).

• Infection: Use with caution in patients with acute infection or active TB; antibiotics and fever may alter response to acenocoumarol.

• Hepatic impairment: Use with caution in patients with hepatic impairment (undergoes hepatic metabolism).

• Renal impairment: Use with caution in patients with renal impairment.

• Thyroid disease: Use with caution in patients with thyroid disease.

Special populations:

• Older adult: The elderly may be more sensitive to anticoagulant therapy.

• Ovulating women: May be at risk of developing ovarian hemorrhage at the time of ovulation.

• Patients with genomic variants in CYP2C9 and/or VKORC1: Presence of the CYP2C9*3 allele and/or polymorphism of the vitamin K oxidoreductase (VKORC1) gene may increase the risk of bleeding. Lower doses may be required in these patients.

Other warnings/precautions:

• Patient selection: Use care in the selection of patients appropriate for this treatment; ensure patient cooperation.

Product Availability

Not available in the US

Generic Equivalent Available: US

May be product dependent

Dosage Forms: Canada

Excipient information presented when available (limited, particularly for generics); consult specific product labeling. [DSC] = Discontinued product

Tablet, Oral:

Sintrom: 1 mg [DSC], 4 mg [DSC]

Administration: Adult

Administer at the same time each day.

Use: Labeled Indications

Note: Not approved in the US

Prophylaxis and treatment of venous thrombosis, pulmonary embolism, and thromboembolic disorders; atrial fibrillation with risk of embolism; adjunct in the treatment of coronary occlusion and transient ischemic attacks

Medication Safety Issues
High alert medication:

The Institute for Safe Medication Practices (ISMP) includes this medication among its list of drug classes (anticoagulants, parenteral and oral; contraindicated during pregnancy) which have a heightened risk of causing significant patient harm when used in error (High-Alert Medications in Acute Care, Community/Ambulatory Care, and Long-Term Care Settings).

Other safety concerns:

Interferes with hepatic synthesis of vitamin K-dependent coagulation factors (II, VII, IX, X)

Metabolism/Transport Effects

Substrate of CYP1A2 (Minor), CYP2C19 (Minor), CYP2C9 (Major); Note: Assignment of Major/Minor substrate status based on clinically relevant drug interaction potential;

Drug Interactions

Note: Interacting drugs may not be individually listed below if they are part of a group interaction (eg, individual drugs within “CYP3A4 Inducers [Strong]” are NOT listed). For a complete list of drug interactions by individual drug name and detailed management recommendations, use the drug interactions program by clicking on the “Launch drug interactions program” link above.

5-Aminosalicylic Acid Derivatives: May increase anticoagulant effects of Vitamin K Antagonists. 5-Aminosalicylic Acid Derivatives may decrease anticoagulant effects of Vitamin K Antagonists. Risk C: Monitor

Abciximab: May increase anticoagulant effects of Vitamin K Antagonists. Risk X: Avoid

Acalabrutinib: May increase anticoagulant effects of Anticoagulants. Risk C: Monitor

Acetaminophen: May increase anticoagulant effects of Vitamin K Antagonists. This appears most likely with daily acetaminophen doses exceeding 1.3 or 2 g/day for multiple consecutive days. Risk C: Monitor

Acoramidis: May increase serum concentration of CYP2C9 Substrates (Narrow Therapeutic Index/Sensitive with Inhibitors). Risk C: Monitor

Adalimumab: May decrease serum concentration of CYP Substrates (Narrow Therapeutic Index/Sensitive with Inducers). Risk C: Monitor

Aducanumab: May increase anticoagulant effects of Anticoagulants. Management: Avoid use of anticoagulants in patients being treated with aducanumab when possible. If concurrent use is necessary, monitor closely for evidence of intracerebral hemorrhage or other bleeding. Risk D: Consider Therapy Modification

Alcohol (Ethyl): May increase anticoagulant effects of Vitamin K Antagonists. Risk C: Monitor

Aldesleukin: May increase serum concentration of CYP Substrates (Narrow Therapeutic Index/Sensitive with Inhibitors). Risk C: Monitor

Alemtuzumab: May increase anticoagulant effects of Anticoagulants. Risk C: Monitor

Allopurinol: May increase anticoagulant effects of Vitamin K Antagonists. Management: Monitor for increased prothrombin times (PT)/therapeutic effects of oral anticoagulants if allopurinol is initiated/dose increased, or decreased effects if allopurinol is discontinued/dose decreased. Reductions in coumarin dosage will likely be needed. Risk D: Consider Therapy Modification

Alteplase: May increase anticoagulant effects of Anticoagulants. Risk X: Avoid

Amiodarone: May increase anticoagulant effects of Vitamin K Antagonists. Amiodarone may increase serum concentration of Vitamin K Antagonists. Management: Monitor patients extra closely for evidence of increased anticoagulant effects if amiodarone is started. Consider empiric reduction of 30% to 50% in warfarin dose, though no specific guidelines on dose adjustment have been published. Risk D: Consider Therapy Modification

Amitriptyline: May increase anticoagulant effects of Vitamin K Antagonists. Risk C: Monitor

Amitriptylinoxide: May increase anticoagulant effects of Vitamin K Antagonists. Risk C: Monitor

Anacaulase: May increase anticoagulant effects of Anticoagulants. Risk C: Monitor

Anagrelide: May increase anticoagulant effects of Anticoagulants. Risk C: Monitor

Androgens: May increase anticoagulant effects of Vitamin K Antagonists. Management: Monitor for increased effects of vitamin K antagonists if an androgen is initiated/dose increased, or decreased effects if androgen is discontinued/dose decreased. Significant reductions in vitamin K antagonist dose are likely required. Risk D: Consider Therapy Modification

Anticoagulants: May increase anticoagulant effects of Vitamin K Antagonists. Risk C: Monitor

Antidepressants with Antiplatelet Effects: May increase anticoagulant effects of Vitamin K Antagonists. Risk C: Monitor

Antiplatelet Agents (P2Y12 Inhibitors): May increase anticoagulant effects of Vitamin K Antagonists. Risk C: Monitor

Antithyroid Agents: May decrease anticoagulant effects of Vitamin K Antagonists. Risk C: Monitor

Aprepitant: May decrease serum concentration of Vitamin K Antagonists. Risk C: Monitor

Aspirin: May increase anticoagulant effects of Vitamin K Antagonists. Risk C: Monitor

AzaTHIOprine: May decrease anticoagulant effects of Vitamin K Antagonists. Risk C: Monitor

Barbiturates: May increase metabolism of Vitamin K Antagonists. Management: Monitor INR more closely. Anticoagulant dose increases of 30% to 60% may be needed after a barbiturate is initiated or given at an increased dose. Anticoagulant dose decreases may be needed following barbiturate discontinuation or dose reduction. Risk D: Consider Therapy Modification

Bicalutamide: May increase serum concentration of Vitamin K Antagonists. Specifically, free concentrations of the vitamin K antagonists may be increased. Risk C: Monitor

Bimekizumab: May decrease serum concentration of CYP Substrates (Narrow Therapeutic Index/Sensitive with Inducers). Risk C: Monitor

Bosentan: May decrease serum concentration of Vitamin K Antagonists. Risk C: Monitor

Bromperidol: May increase adverse/toxic effects of Anticoagulants. Risk C: Monitor

Caplacizumab: May increase anticoagulant effects of Anticoagulants. Management: Avoid coadministration of caplacizumab with antiplatelets if possible. If coadministration is required, monitor closely for signs and symptoms of bleeding. Interrupt use of caplacizumab if clinically significant bleeding occurs. Risk D: Consider Therapy Modification

CarBAMazepine: May decrease serum concentration of Vitamin K Antagonists. Management: Monitor for decreased INR and effects of vitamin K antagonists if carbamazepine is initiated/dose increased, or increased INR and effects if carbamazepine is discontinued/dose decreased. Vitamin K antagonist dose adjustments will likely be required. Risk D: Consider Therapy Modification

Carbimazole: May increase anticoagulant effects of Vitamin K Antagonists. Risk C: Monitor

Cephalosporins: May increase anticoagulant effects of Vitamin K Antagonists. Risk C: Monitor

Chenodiol: May increase anticoagulant effects of Vitamin K Antagonists. Risk C: Monitor

Chloral Hydrate/Chloral Betaine: May increase serum concentration of Vitamin K Antagonists. Risk C: Monitor

Chloroprocaine (Systemic): Anticoagulants may increase adverse/toxic effects of Chloroprocaine (Systemic). Risk C: Monitor

Cholestyramine Resin: May decrease serum concentration of Vitamin K Antagonists. Management: Separate the administration of vitamin K antagonists and cholestyramine by at least 3 to 4 hours. Monitor patients closely for reduced vitamin K antagonist effects (eg, decreased INR, thrombosis) when these agents are combined. Risk D: Consider Therapy Modification

Chondroitin Sulfate: May increase anticoagulant effects of Vitamin K Antagonists. Risk C: Monitor

Cilostazol: May increase anticoagulant effects of Anticoagulants. Risk C: Monitor

Cimetidine: May increase anticoagulant effects of Vitamin K Antagonists. Management: Avoid coadministration of cimetidine and vitamin K antagonists. If unavoidable, monitor for increased effects of vitamin K antagonists when cimetidine is initiated/dose increased, or decreased effects if cimetidine is discontinued/dose decreased. Risk D: Consider Therapy Modification

Cloxacillin: May decrease anticoagulant effects of Vitamin K Antagonists. Cloxacillin may increase anticoagulant effects of Vitamin K Antagonists. Risk C: Monitor

Coenzyme Q-10: May decrease anticoagulant effects of Vitamin K Antagonists. Coenzyme Q-10 may increase anticoagulant effects of Vitamin K Antagonists. Risk C: Monitor

Collagenase (Systemic): Anticoagulants may increase adverse/toxic effects of Collagenase (Systemic). Specifically, the risk of injection site bruising and/or bleeding may be increased. Risk C: Monitor

Corticosteroids (Systemic): May increase anticoagulant effects of Vitamin K Antagonists. Risk C: Monitor

Cranberry: May increase anticoagulant effects of Vitamin K Antagonists. Risk C: Monitor

CYP2C9 Inducers (Moderate): May decrease serum concentration of Vitamin K Antagonists. Management: Monitor for decreased effects of vitamin K antagonists (eg, decreased INR, thrombosis) if combined with moderate CYP2C9 inducers. Vitamin K antagonist dose adjustments will likely be required. Risk D: Consider Therapy Modification

CYP2C9 Inducers (Weak): May decrease serum concentration of Vitamin K Antagonists. Risk C: Monitor

CYP2C9 Inhibitors (Moderate): May increase serum concentration of Vitamin K Antagonists. Risk C: Monitor

CYP2C9 Inhibitors (Weak): May increase serum concentration of Vitamin K Antagonists. Risk C: Monitor

Dasatinib: May increase anticoagulant effects of Anticoagulants. Risk C: Monitor

Deferasirox: Anticoagulants may increase adverse/toxic effects of Deferasirox. Specifically, the risk for GI ulceration/irritation or GI bleeding may be increased. Risk C: Monitor

Defibrotide: May increase anticoagulant effects of Anticoagulants. Risk X: Avoid

Deoxycholic Acid: Anticoagulants may increase adverse/toxic effects of Deoxycholic Acid. Specifically, the risk for bleeding or bruising in the treatment area may be increased. Risk C: Monitor

Desirudin: Anticoagulants may increase anticoagulant effects of Desirudin. Management: Discontinue treatment with other anticoagulants prior to desirudin initiation. If concomitant use cannot be avoided, monitor patients receiving these combinations closely for clinical and laboratory evidence of excessive anticoagulation. Risk D: Consider Therapy Modification

Dexlansoprazole: May increase serum concentration of Vitamin K Antagonists. Risk C: Monitor

Diazoxide Choline: May increase serum concentration of Vitamin K Antagonists. Diazoxide Choline may decrease serum concentration of Vitamin K Antagonists. Risk C: Monitor

Dicloxacillin: May decrease anticoagulant effects of Vitamin K Antagonists. Risk C: Monitor

Dinutuximab Beta: May increase serum concentration of CYP Substrates (Narrow Therapeutic Index/Sensitive with Inhibitors). Risk C: Monitor

Direct Acting Antiviral Agents (HCV): May decrease anticoagulant effects of Vitamin K Antagonists. Risk C: Monitor

Disulfiram: May increase serum concentration of Vitamin K Antagonists. Risk C: Monitor

Donanemab: May increase anticoagulant effects of Anticoagulants. Management: Avoid use of anticoagulants in patients being treated with donanemab when possible. If concurrent use is necessary, monitor closely for evidence of intracerebral hemorrhage or other bleeding. Risk D: Consider Therapy Modification

Dronedarone: May increase serum concentration of Vitamin K Antagonists. Risk C: Monitor

Econazole: May increase serum concentration of Vitamin K Antagonists. Risk C: Monitor

Efavirenz: May decrease serum concentration of Vitamin K Antagonists. Efavirenz may increase serum concentration of Vitamin K Antagonists. Risk C: Monitor

Elranatamab: May increase serum concentration of CYP Substrates (Narrow Therapeutic Index/Sensitive with Inhibitors). Risk C: Monitor

Epcoritamab: May increase serum concentration of CYP Substrates (Narrow Therapeutic Index/Sensitive with Inhibitors). Risk C: Monitor

Esomeprazole: May increase serum concentration of Vitamin K Antagonists. Risk C: Monitor

Ethacrynic Acid: May increase anticoagulant effects of Vitamin K Antagonists. Risk C: Monitor

Etoposide Phosphate: May increase anticoagulant effects of Vitamin K Antagonists. Risk C: Monitor

Etoposide: May increase anticoagulant effects of Vitamin K Antagonists. Risk C: Monitor

Fibric Acid Derivatives: May increase anticoagulant effects of Vitamin K Antagonists. Management: Consider reducing the oral anticoagulant dose by 25% to 33% when initiating a fibric acid derivative. Monitor for toxic or reduced anticoagulant effects if a fibric acid derivative is initiated/dose increased, or discontinued/dose decreased, respectively. Risk D: Consider Therapy Modification

Flucloxacillin: May decrease anticoagulant effects of Vitamin K Antagonists. Flucloxacillin may decrease serum concentration of Vitamin K Antagonists. Risk C: Monitor

Fluconazole: May increase serum concentration of Vitamin K Antagonists. Management: Consider alternatives when possible. If combined, consider reducing the vitamin K antagonist dose by 10% to 20% if combined with fluconazole. Monitor for increased anticoagulant effects (ie, increased INR, bleeding) to guide further dose adjustments. Risk D: Consider Therapy Modification

Fluorouracil Products: May increase serum concentration of Vitamin K Antagonists. Management: Monitor INR and for signs/symptoms of bleeding closely when a fluorouracil product is combined with a vitamin K antagonist (eg, warfarin). Anticoagulant dose adjustment will likely be necessary. Risk D: Consider Therapy Modification

FluvoxaMINE: May increase anticoagulant effects of Vitamin K Antagonists. FluvoxaMINE may increase serum concentration of Vitamin K Antagonists. Risk C: Monitor

Fosaprepitant: May decrease serum concentration of Vitamin K Antagonists. Risk C: Monitor

Fosphenytoin-Phenytoin: May increase anticoagulant effects of Vitamin K Antagonists. Fosphenytoin-Phenytoin may decrease anticoagulant effects of Vitamin K Antagonists. Vitamin K Antagonists may increase serum concentration of Fosphenytoin-Phenytoin. Risk C: Monitor

Fusidic Acid (Systemic): May increase serum concentration of Vitamin K Antagonists. Management: Vitamin K antagonist dose adjustments may be required when used with systemic fusidic acid. Patients using this combination should be monitored extra closely for evidence of bleeding and to determine appropriate dose. Risk D: Consider Therapy Modification

Gefitinib: May increase anticoagulant effects of Vitamin K Antagonists. Risk C: Monitor

Ginkgo Biloba: May increase adverse/toxic effects of Vitamin K Antagonists. Management: Consider avoiding the use of this combination of agents. Monitor for signs and symptoms of bleeding if vitamin K antagonists and Ginkgo biloba are used concomitantly. Risk D: Consider Therapy Modification

Glofitamab: May increase serum concentration of CYP Substrates (Narrow Therapeutic Index/Sensitive with Inhibitors). Risk C: Monitor

Glucagon and Glucagon Analogs: May increase anticoagulant effects of Vitamin K Antagonists. Risk C: Monitor

Glucosamine: May increase anticoagulant effects of Vitamin K Antagonists. Risk C: Monitor

Glycoprotein IIb/IIIa Inhibitors: May increase anticoagulant effects of Vitamin K Antagonists. Risk C: Monitor

Goji Berry: May increase anticoagulant effects of Vitamin K Antagonists. Risk C: Monitor

Griseofulvin: May decrease serum concentration of Vitamin K Antagonists. Risk C: Monitor

Hemin: May increase anticoagulant effects of Anticoagulants. Risk X: Avoid

Herbal Products with Anticoagulant/Antiplatelet Effects: May increase adverse/toxic effects of Anticoagulants. Bleeding may occur. Risk C: Monitor

HMG-CoA Reductase Inhibitors (Statins): May increase anticoagulant effects of Vitamin K Antagonists. Risk C: Monitor

Hormonal Contraceptives: May increase serum concentration of Vitamin K Antagonists. Hormonal Contraceptives may decrease serum concentration of Vitamin K Antagonists. Risk C: Monitor

Ibritumomab Tiuxetan: Anticoagulants may increase adverse/toxic effects of Ibritumomab Tiuxetan. Both agents may contribute to an increased risk of bleeding. Risk C: Monitor

Ibrutinib: Anticoagulants may increase adverse/toxic effects of Ibrutinib. Specifically, the risks of bleeding and hemorrhage may be increased. Risk C: Monitor

Icosapent Ethyl: May increase anticoagulant effects of Anticoagulants. Risk C: Monitor

Ifosfamide: May increase anticoagulant effects of Vitamin K Antagonists. Risk C: Monitor

Immune Checkpoint Inhibitors (Anti-PD-1, -PD-L1, and -CTLA4 Therapies): May increase anticoagulant effects of Vitamin K Antagonists. Risk C: Monitor

Inotersen: May increase anticoagulant effects of Anticoagulants. Risk C: Monitor

Interferons (Alfa): May increase anticoagulant effects of Vitamin K Antagonists. Risk C: Monitor

Interleukin-6 (IL-6) Inhibiting Therapies: May decrease serum concentration of CYP2C9 Substrates (Narrow Therapeutic Index/Sensitive with Inducers). Risk C: Monitor

Itraconazole: May increase serum concentration of Vitamin K Antagonists. Risk C: Monitor

Ivermectin (Systemic): May increase anticoagulant effects of Vitamin K Antagonists. Risk C: Monitor

Ivosidenib: May decrease serum concentration of CYP2C9 Substrates (Narrow Therapeutic Index/Sensitive with Inducers). Management: Consider alternatives to this combination when possible. If combined, monitor for decreased effectiveness of these CYP2C9 substrates if combined with ivosidenib. Risk D: Consider Therapy Modification

Kanamycin: May increase anticoagulant effects of Anticoagulants. Risk C: Monitor

Ketoconazole (Systemic): May increase serum concentration of Vitamin K Antagonists. Risk C: Monitor

Lactulose: May increase anticoagulant effects of Vitamin K Antagonists. Risk C: Monitor

Lansoprazole: May increase anticoagulant effects of Vitamin K Antagonists. Risk C: Monitor

Lecanemab: May increase adverse/toxic effects of Anticoagulants. Specifically, the risk of hemorrhage may be increased. Management: Avoid use of lecanemab in patients who are being treated with an anticoagulant when possible. If concurrent use is necessary, monitor closely for evidence of intracerebral hemorrhage or other bleeding. Risk D: Consider Therapy Modification

LevOCARNitine: May increase anticoagulant effects of Vitamin K Antagonists. Risk C: Monitor

Limaprost: May increase adverse/toxic effects of Anticoagulants. The risk for bleeding may be increased. Risk C: Monitor

Linezolid: May increase anticoagulant effects of Vitamin K Antagonists. Risk C: Monitor

Lipid Emulsion (Fish Oil and Plant Based): May decrease anticoagulant effects of Vitamin K Antagonists. Risk C: Monitor

Lipid Emulsion (Fish Oil Based): May increase anticoagulant effects of Anticoagulants. Lipid Emulsion (Fish Oil Based) may decrease anticoagulant effects of Anticoagulants. Risk C: Monitor

Lornoxicam: May increase anticoagulant effects of Vitamin K Antagonists. Lornoxicam may increase serum concentration of Vitamin K Antagonists. Management: Consider alternatives to this combination when possible. If the combination must be used, monitor coagulation status closely and advise patients to promptly report any evidence of bleeding or bruising. Risk D: Consider Therapy Modification

Lumacaftor and Ivacaftor: May decrease serum concentration of CYP2C9 Substrates (High Risk with Inhibitors or Inducers). Lumacaftor and Ivacaftor may increase serum concentration of CYP2C9 Substrates (High Risk with Inhibitors or Inducers). Risk C: Monitor

Macrolide Antibiotics: May increase anticoagulant effects of Vitamin K Antagonists. Risk C: Monitor

Mavacamten: May decrease serum concentration of CYP2C9 Substrates (Narrow Therapeutic Index/Sensitive with Inducers). Risk C: Monitor

Megestrol: May increase serum concentration of Vitamin K Antagonists. Risk C: Monitor

Menadiol Diphosphate: May decrease anticoagulant effects of Vitamin K Antagonists. Risk C: Monitor

Menatetrenone: May decrease anticoagulant effects of Vitamin K Antagonists. Management: Coadministration is not recommended. If concomitant use of menatetrenone and vitamin K antagonists cannot be avoided, monitor coagulation parameters, such as PT/INR. Risk D: Consider Therapy Modification

Mercaptopurine: May decrease anticoagulant effects of Vitamin K Antagonists. Risk C: Monitor

Mesoglycan: May increase anticoagulant effects of Anticoagulants. Risk C: Monitor

MetFORMIN: May decrease anticoagulant effects of Vitamin K Antagonists. Vitamin K Antagonists may increase hypoglycemic effects of MetFORMIN. Risk C: Monitor

MetroNIDAZOLE (Systemic): May increase serum concentration of Vitamin K Antagonists. Management: Consider alternatives to concomitant therapy with these agents. If concomitant therapy cannot be avoided, consider reducing the dose of the vitamin K antagonist and monitor for increased INR/bleeding. Risk D: Consider Therapy Modification

Mianserin: May increase anticoagulant effects of Vitamin K Antagonists. Risk C: Monitor

Miconazole (Topical): May increase serum concentration of Vitamin K Antagonists. Management: Avoid using any miconazole-containing preparation in patients who are taking warfarin. If coadministration is unavoidable, consider reducing warfarin dose 10% to 20% and monitor for increased warfarin effects (eg, INR, bleeding). Risk D: Consider Therapy Modification

MiFEPRIStone: May increase adverse/toxic effects of Vitamin K Antagonists. Specifically, the risk of bleeding may be increased. MiFEPRIStone may increase serum concentration of Vitamin K Antagonists. Risk X: Avoid

Mirikizumab: May decrease serum concentration of CYP Substrates (Narrow Therapeutic Index/Sensitive with Inducers). Risk C: Monitor

Miscellaneous Antiplatelets: May increase anticoagulant effects of Vitamin K Antagonists. Management: Consider avoiding coadministration of vitamin K antagonists with these therapeutic antiplatelet agents. If coadministered, monitor patients closely for signs (eg, PT, INR) and symptoms of bleeding. Risk D: Consider Therapy Modification

Mitapivat: May decrease serum concentration of CYP2C9 Substrates (Narrow Therapeutic Index/Sensitive with Inducers). Risk C: Monitor

Mosunetuzumab: May increase serum concentration of CYP Substrates (Narrow Therapeutic Index/Sensitive with Inhibitors). Risk C: Monitor

Multivitamins/Fluoride (with ADE): May increase anticoagulant effects of Vitamin K Antagonists. Risk C: Monitor

Multivitamins/Minerals (with ADEK, Folate, Iron): May increase anticoagulant effects of Vitamin K Antagonists. Multivitamins/Minerals (with ADEK, Folate, Iron) may decrease anticoagulant effects of Vitamin K Antagonists. Risk C: Monitor

Multivitamins/Minerals (with AE, No Iron): May increase anticoagulant effects of Vitamin K Antagonists. Risk C: Monitor

Nafcillin: May decrease anticoagulant effects of Vitamin K Antagonists. Management: Consider choosing an alternative antibiotic. Monitor for decreased therapeutic effects and need for dose adjustments of vitamin K antagonists if nafcillin is initiated/dose increased, or increased effects if nafcillin is discontinued/dose decreased. Risk D: Consider Therapy Modification

Nemolizumab: May decrease serum concentration of CYP Substrates (Narrow Therapeutic Index/Sensitive with Inducers). Risk C: Monitor

Neomycin (Systemic): May increase anticoagulant effects of Vitamin K Antagonists. Risk C: Monitor

NIFEdipine (Topical): May increase anticoagulant effects of Vitamin K Antagonists. Risk C: Monitor

Nintedanib: Anticoagulants may increase adverse/toxic effects of Nintedanib. Specifically, the risk for bleeding may be increased. Risk C: Monitor

Nirmatrelvir and Ritonavir: May decrease serum concentration of Vitamin K Antagonists. Nirmatrelvir and Ritonavir may increase serum concentration of Vitamin K Antagonists. Risk C: Monitor

Nonsteroidal Anti-Inflammatory Agents (COX-2 Selective): May increase anticoagulant effects of Anticoagulants. Risk C: Monitor

Nonsteroidal Anti-Inflammatory Agents (Nonselective): May increase anticoagulant effects of Vitamin K Antagonists. Management: Consider alternatives to this combination when possible. If the combination must be used, monitor coagulation status closely and advise patients to promptly report any evidence of bleeding or bruising. Risk D: Consider Therapy Modification

Nonsteroidal Anti-Inflammatory Agents (Ophthalmic): May increase anticoagulant effects of Anticoagulants. Risk C: Monitor

Nonsteroidal Anti-Inflammatory Agents (Topical): May increase anticoagulant effects of Anticoagulants. Risk C: Monitor

Noscapine: May increase anticoagulant effects of Vitamin K Antagonists. Risk C: Monitor

Obinutuzumab: Anticoagulants may increase adverse/toxic effects of Obinutuzumab. Specifically, the risk of serious bleeding-related events may be increased. Management: Consider avoiding coadministration of obinutuzumab and anticoagulants, especially during the first cycle of obinutuzumab therapy. Risk D: Consider Therapy Modification

Omacetaxine: Anticoagulants may increase adverse/toxic effects of Omacetaxine. Specifically, the risk for bleeding-related events may be increased. Management: Avoid concurrent use of anticoagulants with omacetaxine in patients with a platelet count of less than 50,000/uL. Risk X: Avoid

Omega-3 Fatty Acids: May increase anticoagulant effects of Anticoagulants. Risk C: Monitor

Omeprazole: May increase serum concentration of Vitamin K Antagonists. Risk C: Monitor

Oritavancin: May increase serum concentration of Vitamin K Antagonists. Risk C: Monitor

Orlistat: May increase anticoagulant effects of Vitamin K Antagonists. Risk C: Monitor

Ornidazole: May increase anticoagulant effects of Vitamin K Antagonists. Risk C: Monitor

Oxatomide: May increase anticoagulant effects of Vitamin K Antagonists. Risk X: Avoid

Ozagrel: May increase anticoagulant effects of Anticoagulants. Management: Avoid coadministration of ozagrel and anticoagulants if possible. If coadministration is required, use caution, monitor patients closely for signs and symptoms of bleeding, and consider ozagrel or anticoagulant dose reductions. Risk D: Consider Therapy Modification

Penicillins: May increase anticoagulant effects of Vitamin K Antagonists. Risk C: Monitor

Pentosan Polysulfate Sodium: May increase anticoagulant effects of Anticoagulants. Risk C: Monitor

Pentoxifylline: May increase anticoagulant effects of Vitamin K Antagonists. Risk C: Monitor

Phytonadione: May decrease anticoagulant effects of Vitamin K Antagonists. Risk C: Monitor

Pirtobrutinib: May increase anticoagulant effects of Anticoagulants. Risk C: Monitor

Posaconazole: May increase serum concentration of Vitamin K Antagonists. Risk C: Monitor

Proguanil: May increase anticoagulant effects of Vitamin K Antagonists. Risk C: Monitor

Propacetamol: May increase anticoagulant effects of Vitamin K Antagonists. This appears most likely with higher doses (equivalent to acetaminophen doses exceeding 1.3 to 2 g/day) for multiple consecutive days. Risk C: Monitor

Propafenone: May increase serum concentration of Vitamin K Antagonists. Risk C: Monitor

Protein C Concentrate (Human): May increase adverse/toxic effects of Vitamin K Antagonists. Specifically, the risk of warfarin-induced skin necrosis may be increased. Protein C Concentrate (Human) may decrease therapeutic effects of Vitamin K Antagonists. This is effect is transient and occurs at the initiation of vitamin K antagonist therapy. Risk C: Monitor

QuiNIDine: May increase anticoagulant effects of Vitamin K Antagonists. Risk C: Monitor

QuiNINE: May increase anticoagulant effects of Vitamin K Antagonists. Risk C: Monitor

Quinolones: May increase anticoagulant effects of Vitamin K Antagonists. Risk C: Monitor

Raloxifene: May decrease anticoagulant effects of Vitamin K Antagonists. Raloxifene may increase serum concentration of Vitamin K Antagonists. Risk C: Monitor

Reteplase: May increase anticoagulant effects of Anticoagulants. Risk C: Monitor

Ribavirin (Systemic): May decrease anticoagulant effects of Vitamin K Antagonists. Risk C: Monitor

Rifamycin Derivatives: May decrease serum concentration of Vitamin K Antagonists. Management: Consider alternatives if possible. If combined, monitor for reduced anticoagulant effects if a rifamycin derivative is initiated in a vitamin K antagonist treated patient. Vitamin K antagonist dose adjustments will likely be required. Risk D: Consider Therapy Modification

Ritonavir: May decrease serum concentration of Vitamin K Antagonists. Risk C: Monitor

Salicylates: May increase anticoagulant effects of Anticoagulants. Risk C: Monitor

Selumetinib: May increase anticoagulant effects of Vitamin K Antagonists. Risk C: Monitor

Soybean: May decrease anticoagulant effects of Vitamin K Antagonists. Risk C: Monitor

Sparsentan: May decrease serum concentration of CYP2C9 Substrates (Narrow Therapeutic Index/Sensitive with Inducers). Risk C: Monitor

Spinach: May decrease therapeutic effects of Vitamin K Antagonists. Risk C: Monitor

St John's Wort: May increase metabolism of Vitamin K Antagonists. Management: Consider avoiding coadministration of St John's Wort and vitamin K antagonists. If combined, monitor for decreased anticoagulant therapeutic effects (eg, decreased INR, thromboembolic events) if St John's Wort is initiated/dose increased. Risk D: Consider Therapy Modification

Streptokinase: May increase anticoagulant effects of Anticoagulants. Risk X: Avoid

Sugammadex: May increase anticoagulant effects of Anticoagulants. Risk C: Monitor

Sulfinpyrazone: May decrease protein binding of Vitamin K Antagonists. Sulfinpyrazone may decrease metabolism of Vitamin K Antagonists. Risk C: Monitor

Sulfonamide Antibiotics: May increase anticoagulant effects of Vitamin K Antagonists. Management: Consider reducing the vitamin K antagonist dose by 10% to 20% prior to starting the sulfonamide antibiotic. Monitor INR closely to further guide dosing. Risk D: Consider Therapy Modification

Sulfonylureas: Vitamin K Antagonists may increase hypoglycemic effects of Sulfonylureas. Sulfonylureas may increase anticoagulant effects of Vitamin K Antagonists. Risk C: Monitor

Sulodexide: May increase anticoagulant effects of Anticoagulants. Risk C: Monitor

Talquetamab: May increase serum concentration of CYP Substrates (Narrow Therapeutic Index/Sensitive with Inhibitors). Risk C: Monitor

Tamoxifen: May increase serum concentration of Vitamin K Antagonists. Management: Use of a vitamin K antagonist (VKA) is contraindicated when tamoxifen is used to reduce breast cancer incidence and for ductal carcinoma in situ. Monitor VKA closely when tamoxifen is used to treat metastatic breast cancer or as adjuvant therapy. Risk D: Consider Therapy Modification

Tarlatamab: May increase serum concentration of CYP Substrates (Narrow Therapeutic Index/Sensitive with Inhibitors). Risk C: Monitor

Teclistamab: May increase serum concentration of CYP Substrates (Narrow Therapeutic Index/Sensitive with Inhibitors). Risk C: Monitor

Telavancin: May decrease therapeutic effects of Anticoagulants. Specifically, telavancin may artificially increase the results of laboratory tests commonly used to monitor anticoagulant effectiveness, which could lead to incorrect decisions to decrease anticoagulant doses. Risk C: Monitor

Tenecteplase: May increase anticoagulant effects of Anticoagulants. Risk X: Avoid

Tetracyclines: May increase anticoagulant effects of Vitamin K Antagonists. Risk C: Monitor

Thyroid Products: May increase anticoagulant effects of Vitamin K Antagonists. Risk C: Monitor

Tibolone: May increase anticoagulant effects of Anticoagulants. Risk C: Monitor

Tilidine: May increase anticoagulant effects of Vitamin K Antagonists. Risk C: Monitor

Tipranavir: May increase anticoagulant effects of Anticoagulants. Risk C: Monitor

Tobacco (Smokeless): May decrease therapeutic effects of Vitamin K Antagonists. Risk C: Monitor

Toremifene: May increase serum concentration of CYP2C9 Substrates (Narrow Therapeutic Index/Sensitive with Inhibitors). Risk C: Monitor

TraMADol: May increase anticoagulant effects of Vitamin K Antagonists. Risk C: Monitor

TraZODone: May increase anticoagulant effects of Vitamin K Antagonists. Risk C: Monitor

Urokinase: May increase anticoagulant effects of Anticoagulants. Management: Consider avoiding this combination due to an increased risk of hemorrhage. If anticoagulants are coadministered with urokinase, monitor patients closely for signs and symptoms of bleeding. Risk D: Consider Therapy Modification

Ustekinumab: May decrease serum concentration of CYP Substrates (Narrow Therapeutic Index/Sensitive with Inducers). Risk C: Monitor

Valproic Acid and Derivatives: May increase anticoagulant effects of Vitamin K Antagonists. Risk C: Monitor

Vanzacaftor, Tezacaftor, and Deutivacaftor: May increase serum concentration of CYP2C9 Substrates (High risk with Inhibitors). Risk C: Monitor

Vedolizumab: May decrease serum concentration of CYP Substrates (Narrow Therapeutic Index/Sensitive with Inducers). Risk C: Monitor

Vitamin K Antagonists: Anticoagulants may increase anticoagulant effects of Vitamin K Antagonists. Risk C: Monitor

Volanesorsen: May increase anticoagulant effects of Anticoagulants. Risk C: Monitor

Vorapaxar: May increase adverse/toxic effects of Anticoagulants. More specifically, this combination is expected to increase the risk of bleeding. Risk X: Avoid

Vorinostat: May increase anticoagulant effects of Vitamin K Antagonists. Risk C: Monitor

Zanubrutinib: May increase adverse/toxic effects of Anticoagulants. Risk C: Monitor

Food Interactions

Ethanol: Acute ethanol ingestion (binge drinking) decreases the metabolism of oral anticoagulants and increases PT/INR. Chronic daily ethanol use increases the metabolism of oral anticoagulants and decreases PT/INR. Management: Limit alcohol consumption; monitor INR closely.

Food: Vitamin K can reverse the anticoagulation effects of acenocoumarol; large amounts of food high in vitamin K (such as beef liver, pork liver, green tea, and green leafy vegetables) may reverse acenocoumarol, decrease prothrombin time, and lead to therapeutic failure. Management: Patients should not change dietary habits once stabilized on acenocoumarol therapy. A balanced diet with a consistent intake of vitamin K is essential. High doses of vitamin A, E, or C may alter PT. Cranberry juice or other cranberry products may increase the INR in patients receiving a similar agent (warfarin) and cause severe bleeding (flavonoids found in cranberries may inhibit cytochrome P450 isoenzyme CYP2C9 which metabolize warfarin). Similar risks might be anticipated with acenocoumarol as it also undergoes CYP2C9 metabolism. Management: Use caution with fish oils or omega-3 fatty acids; cranberry juice or other cranberry products.

Reproductive Considerations

Women of childbearing potential are advised to use effective contraception during treatment.

Pregnancy Considerations

Acenocoumarol crosses the placenta.

Teratogenic effects have been reported with coumarin derivative anticoagulants following first trimester exposure and may include coumarin embryopathy (nasal hypoplasia and/or stippled epiphyses; limb hypoplasia may also be present). Adverse events to the fetus have also been observed following second and third trimester exposure with coumarin derivative anticoagulants and may include CNS abnormalities (including ventral midline dysplasia, dorsal midline dysplasia). Fatal hemorrhage in the fetus has been reported even when the mother’s acenocoumarol levels were in the therapeutic range. Acenocoumarol should not be used during pregnancy because of significant risks.

Breastfeeding Considerations

Very small quantities of acenocoumarol can be detected in breast milk and undesirable effects in nursing infants are not anticipated. The manufacturer recommends prophylaxis therapy with phytonadione (1 mg administered once weekly) and monitoring of the infant for signs of bleeding. The American College of Chest Physicians (ACCP) considers acenocoumarol to be safe to use in breast-feeding women (Guyatt, 2012).

Dietary Considerations

Foods high in vitamin K (eg, beef liver, pork liver, green tea, and leafy green vegetables) inhibit anticoagulant effect. Do not change dietary habits once stabilized on acenocoumarol therapy. A balanced diet with a consistent intake of vitamin K is essential. Avoid large amounts of alfalfa, asparagus, broccoli, Brussels sprouts, cabbage, cauliflower, green teas, kale, lettuce, spinach, turnip greens, watercress; these decrease efficacy of oral anticoagulants. It is recommended that an adult diet contain a consistent vitamin K content of 75-120 mcg/day. Check with healthcare provider before changing diet. Avoid using multivitamins that contain vitamin K.

Monitoring Parameters

PT/INR (Note: To obtain a valid PT in patients receiving heparin, allow 4 to 5 hours after last IV dose and 12 to 24 hours after last SubQ dose before blood is drawn); hepatic function, CBC

Mechanism of Action

Hepatic synthesis of coagulation factors II, VII, IX, and X, as well as proteins C and S, requires the presence of vitamin K. These clotting factors are biologically activated by the addition of carboxyl groups to key glutamic acid residues within the proteins’ structure. In the process, “active” vitamin K is oxidatively converted to an “inactive” form, which is then subsequently reactivated by vitamin K epoxide reductase complex 1 (VKORC1). Coumarins are thought to inhibit VKORC1, thus depleting functional vitamin K reserves and hence reduce synthesis of active clotting factors.

Pharmacokinetics (Adult Data Unless Noted)

Onset of action: Peak anticoagulant effect: Oral: 36-48 hours

Absorption: Rapid

Distribution: Vd: 0.16-0.34 L/kg

Protein binding: 99%

Metabolism: Hepatic, via oxidation: R-enantiomer (by CYP2C9 [primary], 1A2, and 2C19; S-enantiomer primarily by CYP2C9) and via keto-reduction to inactive metabolites; also undergoes nitro-reduction via gut flora. (Thijssen, 2000)

Bioavailability: 60%

Half-life elimination: R-enantiomer: ~11 hours; S-enantiomer: <2 hours (Thijssen, 1986)

Time to peak, plasma: 1-3 hours

Excretion: Urine (60% as metabolites; minimal amount as unchanged drug); feces (29% as metabolites)

Brand Names: International
International Brand Names by Country
For country code abbreviations (show table)

  • (AE) United Arab Emirates: Acitrom;
  • (AR) Argentina: Acenocoumarol Rospaw | Acenocumarol Gen Med | Acenotromb | Antitrom | Azecar | Cumarol | Fortonol | Saxiom | Saxion | Sintrom;
  • (AT) Austria: Sintrom;
  • (BE) Belgium: Sintrom;
  • (BG) Bulgaria: Acenocumarol | Sintrom | Sintrom merus labs;
  • (CH) Switzerland: Sintrom;
  • (CL) Chile: Acebron | Acenox | Coarol | Isquelium | Neo-sintrom;
  • (DE) Germany: Sintrom;
  • (EE) Estonia: Syncumar;
  • (ES) Spain: Sintrom;
  • (FR) France: Minisintrom | Sintrom;
  • (GB) United Kingdom: Sinthrome;
  • (GR) Greece: Sintrom;
  • (HR) Croatia: Sintrom;
  • (HU) Hungary: Syncumar;
  • (IE) Ireland: Sinthrome;
  • (IL) Israel: Sintrom;
  • (IN) India: Aceno | Acenomac | Acitrom | Artiflo | Cenorol | Cgtrom | Nicotrom | Nicoz | Nistrom | Numalia;
  • (IT) Italy: Sintrom;
  • (JO) Jordan: Sintrom;
  • (LB) Lebanon: Sintrom;
  • (LT) Lithuania: Acenocumarol | Niffcumar | Sintrom | Syncumar;
  • (LU) Luxembourg: Sintrom;
  • (LV) Latvia: Acenocumarol | Niffcumar | Sintrom | Syncumar;
  • (MA) Morocco: Sintrom;
  • (MX) Mexico: Acenocumarol | Fitromtec | Moll | Sintrom;
  • (NL) Netherlands: Acenocoumarol CF | Acenocoumarol Merck | Acenocoumarol pch | Acenocoumarol ratiopharm | Sintrom;
  • (NO) Norway: Sintrom;
  • (NZ) New Zealand: Sinthrome;
  • (PL) Poland: Acenocumarol | Acenocumarol wzf | Sintrom | Syncumar;
  • (PT) Portugal: Acenocumarol generis | Sintrom;
  • (PY) Paraguay: Azecar | Sintrom | Venohem;
  • (RO) Romania: Acenocumarol;
  • (RU) Russian Federation: Acenocumarol | Syncumar;
  • (SI) Slovenia: Sintrom;
  • (SR) Suriname: Acenocoumarol CF | Acenocoumarol sandoz;
  • (TN) Tunisia: Acenocumarol wzf | Mini sintrom | Sintrom;
  • (UA) Ukraine: Syncumar;
  • (UY) Uruguay: Sintrom;
  • (VN) Viet Nam: Azenmarol | Darius | Tegrucil | Vincerol
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