[21][22] Warfarin is indicated for the prophylaxis and treatment of venous thrombosis and its extension, pulmonary embolism;[9] prophylaxis and treatment of thromboembolic complications associated with atrial fibrillation and/or cardiac valve replacement;[9] and reduction in the risk of death, recurrent myocardial infarction, and thromboembolic events such as stroke or systemic embolization after myocardial infarction.

[9] Warfarin is used to decrease the tendency for thrombosis, or as secondary prophylaxis (prevention of further episodes) in those individuals who have already formed a blood clot (thrombus).

Prevention of clotting in arteries is usually undertaken with antiplatelet drugs, which act by a different mechanism from warfarin (which normally has no effect on platelet function).

[25] It can be used to treat people following ischemic strokes due to atrial fibrillation, though direct oral anticoagulants (DOACs) may offer greater benefits.

[28] Recommendations by many national bodies, including the American College of Chest Physicians,[30] have been distilled to help manage dose adjustments.

Currently available self-testing/self-management devices give INR results that are comparable with those obtained in laboratory testing.A 2006 systematic review and meta-analysis of 14 randomized trials showed home testing led to a reduced incidence of complications (thrombosis and major bleeding), and improved the time in the therapeutic range.

The most common congenital abnormalities associated with warfarin use in late pregnancy are central nervous system disorders, including spasticity and seizures, and eye defects.

[54] A 2006 retrospective study of 14,564 Medicare recipients showed that warfarin use for more than one year was linked with a 60% increased risk of osteoporosis-related fracture in men, but no association in women was seen.

[13] While PCC has been found in lab tests to be better than FFP, when rapid reversal is needed,[60] as of 2018, whether a difference in outcomes such as death or disability exists is unclear.

[27] Apart from the metabolic interactions, highly protein bound drugs can displace warfarin from serum albumin and cause an increase in the INR.

Other broad-spectrum antibiotics can reduce the amount of the normal bacterial flora in the bowel, which make significant quantities of vitamin K1, thus potentiating the effect of warfarin.

[11] The Cleveland Clinic suggests that when taking warfarin one should not drink more than "one beer, 6 oz of wine, or one shot of alcohol per day".

[72] Warfarin also interacts with many herbs and spices,[73] some used in food (such as ginger and garlic) and others used purely for medicinal purposes (such as ginseng and Ginkgo biloba).

All may increase bleeding and bruising in people taking warfarin; similar effects have been reported with borage (starflower) oil.

[75] Between 2003 and 2004, the UK Committee on Safety of Medicines received several reports of increased INR and risk of haemorrhage in people taking warfarin and cranberry juice.

[76][77][78] Data establishing a causal relationship are still lacking, and a 2006 review found no cases of this interaction reported to the USFDA;[78] nevertheless, several authors have recommended that both doctors and patients be made aware of its possibility.

Heparin can also cause a prothrombotic condition, heparin-induced thrombocytopenia (an antibody-mediated decrease in platelet levels), which increases the risk for thrombosis.

When this occurs, the coagulation factors are no longer carboxylated at certain glutamic acid residues, and are incapable of binding to the endothelial surface of blood vessels, and are thus biologically inactive.

When warfarin is newly started, it may promote clot formation temporarily, because the level of proteins C and S are also dependent on vitamin K activity.

"[96] A 2014 meta-analysis showed that using genotype-based dosing did not confer benefit in terms of time within therapeutic range, excessive anticoagulation (as defined by INR greater than 4), or a reduction in either major bleeding or thromboembolic events.

[99] In 1921, Frank Schofield, a Canadian veterinary pathologist, determined that the cattle were ingesting moldy silage made from sweet clover, and that this was functioning as a potent anticoagulant.

[98] Only spoiled hay made from sweet clover (grown in northern states of the US and in Canada since the turn of the century) produced the disease.

In 1933, Karl Paul Link and his laboratory of chemists working at the University of Wisconsin set out to isolate and characterize the haemorrhagic agent from the spoiled hay.

[99] They are present notably in woodruff (Galium odoratum, Rubiaceae), and at lower levels in licorice, lavender, and various other species.

[103] However, coumarins themselves do not influence clotting or warfarin-like action, but must first be metabolized by various fungi into compounds such as 4-hydroxycoumarin, then further (in the presence of naturally occurring formaldehyde) into dicoumarol, to have any anticoagulant properties.

Over the next few years, numerous similar chemicals (specifically 4-hydroxycoumarins with a large aromatic substituent at the 3 position) were found to have the same anticoagulant properties.

Karl Link continued working on developing more potent coumarin-based anticoagulants for use as rodent poisons, resulting in warfarin in 1948.

The name "warfarin" stems from the acronym WARF, for Wisconsin Alumni Research Foundation + the ending "-arin" indicating its link with coumarin.

Warfarin as a drug is marketed under many brand and generic names, including Aldocumar, Anasmol, Anticoag, Befarin, Cavamed, Cicoxil, Circuvit, Cofarin, Coumadin, Coumadine, Cumar, Farin, Foley, Haemofarin, Jantoven, Kovar, Lawarin, Maforan, Marevan, Marfarin, Marivanil, Martefarin, Morfarin, Orfarin, Panwarfin, Scheme, Simarc, Varfarin, Varfarins, Varfine, Waran, Warcok, Warf, Warfareks, Warfarin, Warfarina, Warfarine, Warfarinum, Warfen, Warfin, Warik, Warin, Warlin, and Zyfarin.

[109] Other 4-hydroxycoumarins used as rodenticides include coumatetralyl and brodifacoum, which is sometimes referred to as "super-warfarin", because it is more potent, longer-acting, and effective even in rat and mouse populations that are resistant to warfarin.