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Active ingredient: Anisindione - Brands, Medical Use, Clinical Data

Brands, Medical Use, Clinical Data

Drug Category

  • Anticoagulants

Dosage Forms

  • Tablet (oral, 50mg)

Brands / Synonyms

Anisin indandione; Miradon; Unidone


For the prophylaxis and treatment of venous thrombosis and its extension, the treatment of atrial fibrillation with embolization, the prophylaxis and treatment of pulmonary embolism, and as an adjunct in the treatment of coronary occlusion.


Anisindione is a synthetic anticoagulant and an indanedione derivative. It is prescribed only if you cannot take coumarin-type anticoagulants such as coumadin as anisindione is a powerful drug with serious potential side effects. Anticoagulants decrease the clotting ability of the blood and therefore help to prevent harmful clots from forming in the blood vessels. These medicines are sometimes called blood thinners, although they do not actually thin the blood. They also will not dissolve clots that already have formed, but they may prevent the clots from becoming larger and causing more serious problems.

Mechanism of Action

Like phenindione, to which it is related chemically, anisindione exercises its therapeutic action by reducing the prothrombin activity of the blood. Anisindione prevents the formation of active procoagulation factors II, VII, IX, and X, as well as the anticoagulant proteins C and S, in the liver by inhibiting the vitamin K–mediated gamma-carboxylation of precursor proteins. Anisindione has no direct thrombolytic effect and does not reverse ischemic tissue damage, although it may limit extension of existing thrombi and prevent secondary thromboembolic complications.


Accumulation does not occur with repeated dosing.


An overdose is likely to cause abnormal bleeding, for which the symptoms include: bleeding from gums or nose, blood in urine or stools, excessive bleeding from minor cuts, patches of discoloration or bruises on the skin.

Biotrnasformation / Drug Metabolism

Not Available


All contraindications to oral anticoagulant therapy are relative rather than absolute. Contraindications should be evaluated for each patient, giving consideration to the need for and the benefits to be achieved by anticoagulant therapy, the potential dangers of hemorrhage, the expected duration of therapy, and the quality of patient monitoring and compliance.

Hemorrhagic Tendencies or Blood Dyscrasias:

In general, oral anticoagulants are contraindicated in patients who are bleeding or who have hemorrhagic blood dyscrasias or hemorrhagic tendencies (eg, hemophilia, polycythemia vera, purpura, leukemia) or a history of bleeding dia-thesis. They are contraindicated in patients with recent cerebral hemorrhage, active ulceration of the gastrointestinal tract, including ulcerative colitis, or open ulcerative, traumatic, or surgical wounds. Oral anticoagulants may be contraindicated in patients with recent or contemplated brain, eye, or spinal cord surgery or prostatec-tomy, and in those undergoing regional or lumbar block anesthesia or continuous tube drainage of the small intestine. Oral anticoagulants may be contraindicated in patients who have severe renal or hepatic disease, subacute bacterial endocar-ditis, pericarditis, polyarthritis, diverticulitis, visceral carcinoma, or aneurysm. Other conditions in which the oral anticoagulants may be contraindicated include severe or malignant hypertension, eclampsia or preeclampsia, threatened abortion, emaciation, malnutrition, and vitamin C or K deficiencies. Since a high degree of patient cooperation is required for the outpatient use of oral anticoagulants, a lack of such cooperation is a relative contraindication to their use.

Pregnancy: Anisindione is contraindicated in pregnancy because the drug crosses the placental barrier. Oral anticoagulants may cause fetal damage when administered to pregnant women. Fetal or neonatal hemorrhage and intrauterine fetal death have occurred even when maternal prothrombin times were within the therapeutically accepted range. Maternal use of warfarin and anisindione during the first trimester of pregnancy has been reported to cause hypoplastic nasal structures or other signs of the Conradi-Hunermann syndrome in the offspring. These patients received other drugs in addition to anticoagulants and a positive causal relationship has not been established. If oral anticoagulants must be used during pregnancy, or if the patient becomes pregnant while taking one of these drugs, the patient should be apprised of the potential hazard to the fetus. The possibility of termination of the pregnancy should be considered in light of these risks.

As an alternative to the use of oral anticoagulants in pregnant patients, the use of heparin, which does not cross the placenta, should be considered.

Drug Interactions

Addition or deletion of any drug from the therapeutic regimen of patients receiving oral anticoagulants may affect patient response to the anticoagulant. Frequent determination of prothrombin time and close monitoring of the patient is essential to ascertain when adjustment of dosage of anticoagulant may be needed.

Because of the variability of individual patient response, multiple interacting mechanisms with some drugs, the dependency of the extent of the interaction on the dosage and duration of therapy, and the possible administration of several interacting drugs simultaneously, it is difficult to predict the direction and degree of the ultimate effect of concomitant medications on anticoagulant response. For example, since cholestyramine may reduce the gastrointestinal absorption of both the oral anticoagulants and vitamin K, the net effects are unpredictable. Chloral hydrate may cause an increased prothrombin response by displacing the anticoagulant from protein binding sites or a diminished prothrombin response through increased metabolism of the unbound drug by hepatic enzyme induction, thus leading to inter-patient variation in ultimate prothrombin effect. An interacting drug which leads to a decrease in prothrombin time necessitating an increased dose of oral anticoagulant to maintain an adequate degree of anticoagulation may, if abruptly discontinued, increase the risk of subsequent bleeding.

Drugs that have been reported to diminish oral anticoagulant response, ie, decreased prothrom-bin time response, in man significantly include: adrenocortical steroids; alcohol*; antacids; antihistamines; barbiturates; carbamazepine; chloral hydrate*; chlordiazepoxide; cholestyramine; diet high in vitamin K; diuretics*; ethchlorvynol; glu-tethimide; griseofulvin; haloperidol; meprobamate; oral contraceptives; paraldehyde; primidone; ranitidine*; rifampin; unreliable prothrombin time determinations; vitamin C; warfarin sodium under-dosage.

Drugs that reportedly may increase oral anticoagulant response, ie, increased prothrombin response, in man include:alcohol*; allopurinol; aminosalicylic acid; amiodarone; anabolic steroids; antibiotics; bromelains; chloral hydrate*; chlorpro-pamide; chymotrypsin; cimetidine; cinchophen; clofibrate; dextran; dextrothyroxine; diazoxide; die-tarydeficiencies; diflunisal; diuretics*; disulfiram; drugs affecting blood elements; ethacrynic acid; fenoprofen; glucagon; hepatotoxic drugs; ibuprofen; indomethacin; influenza virus vaccine; inhalation anesthetics; mefenamic acid; methyldopa; methylphenidate; metronidazole; miconazole; monoamine oxidase inhibitors; nalidixic acid; naproxen; oxolinic acid; oxyphenbutazone; pent-oxifylline; phenylbutazone; phenyramidol; pheny-toin; prolonged hot weather; prolonged narcotics; pyrazolones; quinidine; quinine; ranitidine*; sali-cylates;sulfinpyrazone; sulfonamides, long acting; sulindac; thyroid drugs; tolbutamide; triclofos sodium; trimethoprim/sulfamethoxazole; unreliable prothrombin time determinations; warfarin sodium overdosage.

Oral anticoagulants may potentiate the hypoglycemic action of hypoglycemic agents, eg, tolbut-amide and chlorpropamide, by inhibiting their metabolism in the liver. Because oral anticoagulants may interfere with the hepatic metabolism of phenytoin, toxic levels of the anticonvulsant may occur when an oral anticoagulant and pheny-toin are administered concurrently.

Drugs that reduce the number of blood platelets by causing bone marrow depression (such as antineoplastic agents) or drugs which inhibit platelet function (eg, aspirin and other non-steroidal anti-inflammatory drugs, dipyridamole, hydrochloroquine, clofibrate, dextran) may increase the bleeding tendency produced by anticoagulants without altering prothrombin time determinations. The beneficial effects on arterial thrombus formation from combined therapy with antiplatelet and anticoagulant medication must be weighed against an increased risk of inducing hemorrhage.

*Increased and decreased prothrombin time responses have been reported.

Drug/Laboratory Test Interferences: Dicu-marol and indanedione anticoagulants, including anisindione, or their metabolites may color alkaline urine red-orange, which may interfere with spectrophotometrically determined urinary laboratory tests. The color reverses when the test sample is acidified in vitro to a pH below 4.

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