FARIN-1
Warfarin Tablets BP 1 mg
What it does
Warfarin is a medication that helps prevent blood clots.
Commonly used for: prevention of blood clots, treatment of deep vein thrombosis (DVT), treatment of pulmonary embolism, prevention of stroke in people with atrial fibrillation
Read more in plain English ↓Plain-language summary for general understanding - not medical advice. Always follow your pharmacist/doctor.
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Sourcing - Kenya onlyRegistration & product details
Source: Rwanda Food and Drugs Authority · fetched 2026-03-11 22:07:23 · updated 2026-09-17 02:30:44
Drug Interactions
98Pharmacodynamic Warnings
Warfarin appears in TABLE 3: Drugs with anticoagulant effects
Severe (6)
Coumarins - increases anticoagulant effect
Glucosamine potentially increases the anticoagulant effect of coumarins (warfarin). Avoid. Anecdotal Glycerol phenylbutyrate
Coumarins - affects exposure
Mexiletinepotentiallyaffectstheexposuretocoumarins (warfarin).Avoid.qTheoretical
Warfarin - increases exposure
Ceritinibispredictedtoincreasetheexposuretocoumarins (warfarin).Avoid.rTheoretical
Warfarin - increases anticoagulant effect
Glucosamine potentially increases the anticoagulant effect of warfarin. Avoid.
Warfarin - affects exposure
Mexiletinepotentiallyaffectstheexposuretowarfarin.Avoid. qTheoretical
Warfarin - affects exposure
Pralsetinibmightaffecttheexposuretowarfarin.Avoid. oTheoretical
Moderate (25)
Coumarins - decreases exposure
Enzalutamide potentially decreases the exposure to coumarins. Avoid or adjust dose and monitor INR.
Coumarins - increases anticoagulant effect
Propafenoneincreasestheanticoagulanteffectofcoumarins. MonitorINRandadjustdose.oStudy 1xidneppA|snoitcaretnI A1 https://www.facebook.c (Books-Courses-Medic
Coumarins - decreases effects
Carbamazepine decreases the effects of coumarins. Monitor and adjust dose.
Coumarins - increases anticoagulant effect
Fluconazole increases the anticoagulant effect of coumarins. Monitor INR and adjust dose.
Coumarins - increases anticoagulant effect
Ketoconazole potentially increases the anticoagulant effect of coumarins (warfarin). Monitor INR and adjust dose.
Unknown (67)
Coumarins - decreases efficacy
Alpelisibispredictedtodecreasetheefficacyofcoumarins (warfarin).oTheoretical
Coumarins - decreases exposure
Apalutamide is predicted to decrease the exposure to coumarins. Avoid or monitor.
Coumarins - increases anticoagulant effect
Amiodarone increases the anticoagulant effect of coumarins.
Coumarins - increases anticoagulant effect
Itraconazole potentially increases the anticoagulant effect of coumarins.
Coumarins - increases exposure
Asciminibslightlytomoderatelyincreasestheexposureto coumarins(warfarin).rTheoretical
Data from BNF 85 (British National Formulary). This is not a substitute for professional medical advice. Matched via: class
About this medicine
Warfarin is a medication that helps prevent blood clots.
What it treats
- prevention of blood clots
- treatment of deep vein thrombosis (DVT)
- treatment of pulmonary embolism
- prevention of stroke in people with atrial fibrillation
How it works
Warfarin works by reducing the ability of your blood to clot, which helps prevent the formation of dangerous clots.
Who it's for
Warfarin is for people at risk of developing blood clots, such as those with certain heart conditions or previous clotting issues.
Drug class
Coumarins
Cautions
- • Be careful if you are taking other medications that also thin the blood.
AI-assisted summary grounded in BNF data - general information only, not medical advice. Always confirm with your pharmacist or doctor.
Clinical monograph: warfarin
BNF-referencedWarfarin is an oral anticoagulant belonging to the coumarin class, primarily used to prevent and treat thromboembolic disorders. It functions by inhibiting the synthesis of vitamin K-dependent clotting factors, thereby reducing the formation of blood clots. Commonly prescribed for conditions such as deep vein thrombosis, pulmonary embolism, and atrial fibrillation, warfarin plays a crucial role in the management of thromboembolic events.
Indications
- Prevention of venous thromboembolism (e.g., deep vein thrombosis, pulmonary embolism)
- Management of atrial fibrillation to reduce stroke risk
- Treatment of thromboembolic complications associated with cardiac valve disease
- Secondary prevention of myocardial infarction
Dosage
Children: Refer to the BNF for Children for specific paediatric dosing information.
Adults: The initial dose of warfarin is typically 5 mg once daily, with adjustments made based on INR monitoring to achieve the desired therapeutic range.
Mechanism of action
Warfarin acts as a vitamin K antagonist, inhibiting vitamin K epoxide reductase, which is essential for the recycling of vitamin K. This inhibition prevents the γ-carboxylation of vitamin K-dependent coagulation factors, such as factors II, VII, IX, X, and proteins C and S, rendering them biologically inactive and interrupting the coagulation cascade.
Pharmacodynamics
As an anticoagulant, warfarin reduces the frequency and extent of thrombus formation, particularly in patients at increased risk due to conditions like deep vein thrombosis, atrial fibrillation, or cardiac valve disease. However, its use can lead to adverse effects, including bleeding complications and the potential for atheroemboli formation in patients with atherosclerosis.
Pharmacokinetics
Warfarin is well-absorbed after oral administration, with peak plasma concentrations typically occurring within 1 to 4 hours. It has a half-life of approximately 36 hours, but this can vary significantly between individuals due to genetic factors and drug interactions. The drug is extensively metabolized in the liver via cytochrome P450 enzymes, and its anticoagulant effect is monitored through prothrombin time (PT) and international normalized ratio (INR) measurements.
Contra-indications
- Pregnancy (especially in the first trimester due to teratogenic effects)
- Active bleeding disorders (e.g., hemorrhagic stroke, gastrointestinal bleeding)
- Severe liver impairment
- Recent surgery or trauma with high bleeding risk
- Known hypersensitivity to warfarin
Adverse effects
- Hemorrhage
- Gastrointestinal bleeding
- Skin necrosis
- Purple toe syndrome
- Allergic skin reactions
- Liver dysfunction
- Transient hair loss
Interactions
- ceritinib: Severe (increases exposure)
- glucosamine: Severe (increases anticoagulant effect)
- mexiletine: Potentially severe (affects exposure)
- pralsetinib: Severe (affects exposure)
- ketoconazole: Moderate (increases anticoagulant effect)
- letermovir: Moderate (decreases concentration)
- lomitapide: Moderate (increases exposure)
- monoclonal antibodies: Moderate (decreases exposure)
- rucaparib: Moderate (increases exposure)
- sarilumab: Potentially moderate (affects exposure)
Precautions
- Regular monitoring of INR (International Normalized Ratio)
- Caution in patients with renal impairment
- Avoid sudden changes in dietary vitamin K intake
- Assess for potential drug interactions before prescribing
- Use cautiously in elderly patients due to increased bleeding risk
Pregnancy
Warfarin is contraindicated in pregnancy, particularly during the first trimester, as it can cause fetal malformations and complications such as fetal hemorrhage.
Breast-feeding
Warfarin is excreted in breast milk, but generally is considered compatible with breastfeeding; however, monitoring of the infant may be necessary.
Storage
Store at room temperature, away from moisture and heat. Keep out of reach of children.
Formulations
- Tablets: 1 mg, 2 mg, 2.5 mg, 3 mg, 4 mg, 5 mg, 6 mg, 7.5 mg, 10 mg
AI-synthesized from BNF references - general information only, not a substitute for professional medical advice or the current BNF. Verify doses with a pharmacist.
Clinical monograph: Warfarinsodium
BNF-referencedWarfarin sodium is an anticoagulant medication primarily used to prevent thromboembolic events in various medical conditions, including atrial fibrillation, mechanical heart valves, and venous thromboembolism. It works by inhibiting vitamin K-dependent coagulation factors, thereby reducing the ability of blood to clot. As a widely used anticoagulant, it requires careful monitoring of prothrombin time, expressed as INR, to ensure therapeutic effectiveness while minimizing the risk of bleeding complications.
Indications
- Prophylaxis of embolisation in rheumatic heart disease
- Atrial fibrillation
- Prophylaxis after insertion of prosthetic heart valves
- Prophylaxis and treatment of venous thrombosis and pulmonary embolism
- Prevention of transient ischaemic attacks
Dosage
Adults: Initially, 5–10 mg
Mechanism of action
Warfarin sodium functions as a vitamin K antagonist. It inhibits the enzyme vitamin K epoxide reductase, which is crucial for the regeneration of reduced vitamin K. This action reduces the synthesis of vitamin K-dependent clotting factors II, VII, IX, and X in the liver, which are essential for normal blood coagulation. The decreased levels of these factors lead to an anticoagulant effect, thereby preventing thrombus formation.
Pharmacodynamics
The anticoagulant effect of warfarin is dose-dependent and influenced by various factors, including age, body weight, diet, and concurrent medications. The onset of action typically requires several days due to the existing levels of clotting factors, and the therapeutic range is monitored through INR measurements. The ideal INR is usually between 2.0 and 3.0 for most indications, but this can vary based on the specific condition being treated.
Pharmacokinetics
Warfarin sodium is well-absorbed from the gastrointestinal tract, with peak plasma concentrations occurring 1 to 4 hours post-administration. It is highly protein-bound (approximately 97%) and has a long half-life of about 36 hours. Warfarin is metabolized extensively in the liver via cytochrome P450 enzymes, primarily CYP2C9, and its metabolites are excreted in urine. Factors such as liver function, age, and concurrent medications can significantly affect warfarin metabolism, requiring careful dose adjustment.
Contra-indications
- Significant bleeding disorders
- Recent ischaemic stroke
- Recent surgery
- Uncontrolled hypertension
- Postpartum (within 48 hours of delivery)
- Bacterial endocarditis (unless indicated)
- History of gastrointestinal bleeding
- Hyperthyroidism
- Hypothyroidism
Adverse effects
- Hemmorrhage
- Alopecia
- Nausea
- Vomiting
- Calciphylaxis (rare)
Interactions
- Concomitant medications affecting hepatic function
- Drugs that influence INR levels
- Vitamin K-containing foods or supplements
Precautions
- Monitor INR levels regularly
- Adjust doses based on INR results
- Caution in elderly patients and those with hepatic impairment
- Delay use in postpartum patients until hemorrhage risk is low (usually 5-7 days after delivery)
Pregnancy
Babies of mothers taking warfarin at the time of delivery need immediate prophylaxis with intramuscular phytomenadione (vitamin K1).
Breast-feeding
Not present in milk in significant amounts and appears safe.
Storage
Store at room temperature, away from moisture and heat.
Formulations
- Warfarin sodium 500 microgram tablets
- Warfarin sodium 1 mg tablets
- Warfarin sodium 3 mg tablets
- Warfarin sodium 5 mg tablets
- Warfarin sodium 4 mg Coumadin tablets
- Warfarin sodium 1 mg/ml oral suspension
AI-synthesized from BNF references - general information only, not a substitute for professional medical advice or the current BNF. Verify doses with a pharmacist.
Molecular reference: warfarin
PubChem CID 54678486Molecular formula: C19H16O4
Mechanism of action
Warfarin is a [vitamin K] antagonist which acts to inhibit the production of vitamin K by vitamin K epoxide reductase. The reduced form of vitamin K, vitamin KH<sub>2</sub> is a cofactor used in the γ-carboxylation of coagulation factors VII, IX, X, and thrombin. Carboxylation induces a conformational change allowing the factors to bind Ca<sup>2+</sup> and to phospholipid surfaces. Uncarboxylated factors VII, IX, X, and thrombin are biologically inactive and therefore serve to interrupt the coagulation cascade. The endogenous anticoagulation proteins C and S also require γ-carboxylation to function. This is particularly true in the case of thrombin which must be activated in order to form a thrombus. vitamin KH<sub>2</sub> is converted to vitamin K epoxide as part of the γ-carboxylation reaction catalyzed by γ-glutamyl carboxylase. Vitamin K epoxide is then converted to vitamin K<sub>1</sub> by vitamin K epoxide reductase then back to vitamin KH<sub>2</sub> by vitamin K reductase. Warfarin binds to vitamin K epoxide reductase complex subunit 1 and irreversibly inhibits the enzyme thereby stopping the recycling of vitamin K by preventing the conversion of vitamin K epoxide to vitamin K<sub>1</sub>. This process creates a hypercoagulable state for a short time as proteins C and S degrade first with half lives of 8 and 24 hours, with the exception of factor VII which has a half life of 6 hours. Factors IX, X, and finally thrombin degrade later with half lives of 24, 36, and 50 hours resulting in a dominant anticoagulation effect. In order to reverse this anticoagulation vitamin K must be supplied, either exogenously or by removal of the vitamin K epoxide reductase inhibition, and time allowed for new coagulation factors to be synthesized. It takes approximately 2 days for new coagulation factors to be synthesized in the liver. Vitamin K<sub>2</sub>, functionally identical to vitamin K<sub>1</sub>, is synthesized by gut bacteria leading to interactions with antibiotics as elimination of these bacteria can reduce vitamin K<sub>2</sub supply and result in a greater anticoagulation effect. Animals poisoned by warfarin ... die of tissue hypoxia resulting from massive internal bleeding of 2-5 days onset. Bleeding is due to incr capillary permeability & decr blood coagulability. The exact cause of capillary damage is not known, but its presence is evidenced by the fact that hemorrhages occur in tissues not subjected to much mechanical stress. The coagulation defect is the result decreased blood concentrations of the coagulation proteins factor II (prothrombin), factor VII (proconvertin, autoprothrombin I), factor IX (Christmas factor, autoprothrombin II, PTC), and factor X (Stuart factor, autoprothrombin III). These coagulation factors are decreased because their synthesis in the liver has been inhibited. Biosynthesis of these particular proteins is inhibited becaused each one requires adequate activity of vitamin K for biosynthesis, but the rodenticide interferes with the normal function of vitamin K. Hepatic synthesis of prothrombin and factors VII, IX, and X is dependent upon adequate supplies of vitamin K. The molecular and even the cellular mechanism of the anti-vitamin K action of the coumarin compounds remain uncertain. These drugs seem to act as antimetabolites in synthesis of affected clotting factors. Since large doses of vitamin K can overcome or surmount action of dicumarol, competitive type of interaction is thought to be involved. Perhaps coumarin anticoagulants simply inhibit transport of vitamin K to the cellular sites wheresynthesis takes place. In any event, there is some evidence that dicumarol interferes with involvement of vitamin K in synthesis of a prothrombin precursor that may also be common to factors VII, IX, and X. Anticoagulants interfere with fibrin formation and are used to prevent thrombus development and extension. Their major therapeutic application has traditionally been for venous thromboembolic diso
Pharmacodynamics
Warfarin is an anticoagulant, as such it disrupts the coagulation cascade to reduce frequency and extent of thrombus formation. In patients with deep vein thrombosis or atrial fibrillation there is an increased risk of thrombus formation due to the reduced movement of blood. For patients with cardiac valve disease or valve replacements this increased coagulability is due to tissue damage. Thrombi due to venous thrombosis can travel to the lungs and become pulmonary emboli, blocking circulation to a portion of lung tissue. Thrombi which form in the heart can travel to the brain and cause ischemic strokes. Prevention of these events is the primary goal of warfarin therapy. Limitation of thrombus formation is also a source of adverse effects. In patients with atheroscelotic plaques rupture typically results in thrombus formation. When these patients are anticoagulated plaque rupture can allow the escape of cholesterol from the lipid core in the form of atheroemboli or cholesterol microemboli. These emboli are smaller than thrombi and block smaller vessels, usually less than 200 μm in diameter. The consequences of this are varied and depend on the location of the blockage. Effects include visual disturbances, acute kidney injury or worsening of chronic kidney disease, central nervous system ischemia, and purple or blue toe syndrome. Blue toe syndrome can be reversed if it has not progressed to tissue necrosis but the other effects of microemboli are often permanent. Antocoagulation appears to mediate warfarin-related nephropathy, a seemingly spontaneous kidney injury or worsening of chronic kidney disease associated with warfarin therapy. Nephropathy in this case appears to be due to increased passage of red blood cells through the glomerulus and subsequent blockage of renal tubules with red blood cell casts. This is worsened or possibly triggered by pre-existing kidney damage. Increased risk of warfarin-related nephropathy occurs at INRs over 3.0 but risk does not increase as a function of INR beyond this point. Warfarin has been linked to the development of calciphylaxis. This is thought to be due to warfarin's inhibition of [vitamin K](VKA) recycling as VKA is needed for the carboxylation of matrix Gla protein. This protein is an anti-calcification factor and its inhibition through preventing the carboxylation step in its production leads to a shift in calcification balance in favor of calciphylaxis. Tissue necrosis can occur early on in warfarin therapy. This is attributable to half lives of the clotting factors impacted by inhibition of vitamin K recycling. Proteins C and S are anticoagulation factors with half lives of 8 and 24 hours respectively. The coagulation factors IX, X, VII, and thrombin (factor II) have half lives of 24, 36, 6, and 50 hours respectively. This means proteins C and S are inactivated sooner than pro-coagulation proteins, with the exception of factor VII, resulting in a pro-thrombotic state for the first few days of therapy. Thrombi which form in this time period can occlude arterioles in various locations, blocking blood flow and causing tissue necrosis due to ischemia.
Biological pathways
Source: PubChem (NCBI) · pathways from PathBank, Reactome, WikiPathways & PharmGKB.
Molecular reference: Warfarinsodium
PubChem CID 54695721Molecular formula: C19H16NaO4
Source: PubChem (NCBI) · pathways from PathBank, Reactome, WikiPathways & PharmGKB.
This drug in other countries
The same active ingredient registered across other registries we cover - including different brands.
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- WARFARIN 1 mg AUSTELL
- WARFARIN 1 mg APEX
- WARFARIN 1 mg CAMOX
- WARFARIN 3 mg APEX
- WARFARIN 3 mg AUSTELL