Acebron
Acebron Uses, Dosage, Side Effects, Food Interaction and all others data.
Acebron is a coumarin derivative used as an anticoagulant. Coumarin derivatives inhibit the reduction of vitamin K by vitamin K reductase. This prevents carboxylation of vitamin K-dependent clotting factors, II, VII, IX and X, and interferes with coagulation. Hematocrit, hemoglobin, international normalized ratio and liver panel should be monitored. Patients on acenocoumarol are prohibited from giving blood.
Acebron inhibits the reduction of vitamin K by vitamin K reductase. This prevents carboxylation of certain glutamic acid residues near the N-terminals of clotting factors II, VII, IX and X, the vitamin K-dependent clotting factors. Glutamic acid carboxylation is important for the interaction between these clotting factors and calcium. Without this interaction, clotting cannot occur. Both the extrinsic (via factors VII, X and II) and intrinsic (via factors IX, X and II) are affected by acenocoumarol.
Trade Name | Acebron |
Generic | Acenocoumarol |
Acenocoumarol Other Names | Acenocoumarin, Acénocoumarol, Acenocoumarol, Acenocoumarolum, Acenocumarol, Acenocumarolo, Acenokumarin, Nicoumalone, Nicumalon, Nitrovarfarian, Nitrowarfarin |
Type | |
Formula | C19H15NO6 |
Weight | Average: 353.3255 Monoisotopic: 353.089937217 |
Protein binding | 98.7% protein bound, mainly to albumin |
Groups | Approved, Investigational |
Therapeutic Class | |
Manufacturer | |
Available Country | Chile |
Last Updated: | September 19, 2023 at 7:00 am |
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Uses
Acebron is an anticoagulant drug used in the prevention of thromboembolic diseases in infarction and transient ischemic attacks, as well as management of deep vein thrombosis and myocardial infarction.
For the treatment and prevention of thromboembolic diseases. More specifically, it is indicated for the prevention of cerebral embolism, deep vein thrombosis, pulmonary embolism, thromboembolism in infarction and transient ischemic attacks. It is used for the treatment of deep vein thrombosis and myocardial infarction.
Acebron is also used to associated treatment for these conditions: Coronary Occlusions, Pulmonary Embolism, Systemic Embolism, Thrombosis, Venous, Transient Ischemic Attack
How Acebron works
Acebron inhibits vitamin K reductase, resulting in depletion of the reduced form of vitamin K (vitamin KH2). As vitamin K is a cofactor for the carboxylation of glutamate residues on the N-terminal regions of vitamin K-dependent clotting factors, this limits the gamma-carboxylation and subsequent activation of the vitamin K-dependent coagulant proteins. The synthesis of vitamin K-dependent coagulation factors II, VII, IX, and X and anticoagulant proteins C and S is inhibited resulting in decreased prothrombin levels and a decrease in the amount of thrombin generated and bound to fibrin. This reduces the thrombogenicity of clots.
Toxicity
The onset and severity of the symptoms are dependent on the individual's sensitivity to oral anticoagulants, the severity of the overdosage, and the duration of treatment. Bleeding is the major sign of toxicity with oral anticoagulant drugs. The most frequent symptoms observed are: cutaneous bleeding (80%), haematuria (with renal colic) (52%), haematomas, gastrointestinal bleeding, haematemesis, uterine bleeding, epistaxis, gingival bleeding and bleeding into the joints. Further symptoms include tachycardia, hypotension, peripheral circulatory disorders due to loss of blood, nausea, vomiting, diarrhoea and abdominal pains.
Food Interaction
- Avoid herbs and supplements with anticoagulant/antiplatelet activity. Examples include garlic, ginger, bilberry, danshen, piracetam, and ginkgo biloba.
- Ensure consistent Vitamin K intake. Changes in vitamin K intake may impact coagulation. Foods containing vitamin K include spinach, kale, and swiss chard.
- Exercise caution with St. John's Wort.
Volume of Distribution
The volume of distribution at steady-state appeared to be significantly dose dependent: 78 ml/kg for doses < or = 20 microg/kg and 88 ml/kg for doses > 20 microg/kg respectively
Elimination Route
Rapidly absorbed orally with greater than 60% bioavailability. Peak plasma levels are attained 1 to 3 hours following oral administration.
Half Life
8 to 11 hours.
Elimination Route
Mostly via the kidney as metabolites
Innovators Monograph
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