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Anti-Clotting / Anticoagulants

Our Anti-Clotting/Anticoagulants class of Heart Health medications are used to prevent blood clot formation or thrombosis, and reduce risk of heart attack stroke and pulmonary embolism.

Use the search feature to quickly find the product you are looking for, by entering either the active ingredient, e.g. clopidogrel or the product name, e.g. Clopivas. 

Our Anti-Clotting/Anticoagulants class of Heart Health medications are used to prevent blood clot formation or thrombosis, and reduce risk of heart attack stroke and pulmonary embolism.

Use the search feature to quickly find the product you are looking for, by entering either the active ingredient, e.g. clopidogrel or the product name, e.g. Clopivas. 
...Read more

Branded Product
Generic Alternative
Brilinta 90mg (Ticagrelor)
Brilinta 90mg (Ticagrelor)
Ticagrelor 90mg
Also known as Brilique or Possia
From $2.00 per Tablet
Xarelto (Rivaroxaban 20mg) Tablets (Sourced from Turkey)
Xarelto (Rivaroxaban 20mg) Tablets (Sourced from Turkey)
Rivaroxaban
Original branded product (Turkish writing) - comes with English language leaflet. Made in Germany.
Out Of Stock
Coumadin (Warfarin) 1mg Tablets
Coumadin (Warfarin) 1mg Tablets
Warfarin 1mg
From $0.35 per Tablet
Coumadin (Warfarin) 2mg Tablets
Coumadin (Warfarin) 2mg Tablets
Warfarin
From $0.37 per Tablet
Coumadin (Warfarin) 5mg Tablets
Coumadin (Warfarin) 5mg Tablets
Warfarin
From $0.47 per Tablet
Eliquis (Apixaban) 2.5mg (Sourced from Turkey)
Eliquis (Apixaban) 2.5mg (Sourced from Turkey)
Apixaban
Tablets CANNOT be split - must be taken whole. Original branded product (Turkish writing) - comes with English language leaflet.
From $2.10 per Tablet
Plavix 75mg
Plavix 75mg
Clopidogrel
Discontinued
Clopivas 75mg  (Clopidogrel)
Clopivas 75mg (Clopidogrel)
Generic
clopidogrel bisulfate
Also known as Plavix
From $1.15 per Tablet
Eliquis (Apixaban) 5mg (Sourced from Turkey)
Eliquis (Apixaban) 5mg (Sourced from Turkey)
Apixaban
Tablets CANNOT be split - must be taken whole. Original branded product (Turkish writing) - comes with English language leaflet.
From $2.15 per Tablet
Pytazen SR 150mg (Dipyridamole)
Pytazen SR 150mg (Dipyridamole)
On Sale
Generic
Dipyridamole 150mg
Also known as Persantin, Persantine, Curantyl
From $0.38 per Tablet
Xarelto 20mg (rivaroxaban)
Xarelto 20mg (rivaroxaban)
rivaroxaban 20mg
Out Of Stock

Blood clots 

Haemostasis is the process of preventing bleeding from a damaged blood vessel to keep blood flowing through the artery or vein.  Injury or damage to a blood vessel wall initiates the formation of a blood clot or thrombus to block the site of the damage and prevent bleeding, which if severe can cause haemorrhage or severe bleeding from a ruptured blood vessel.  However a thrombus can form even if the vessel wall is not ruptured as a result of damage by cholesterol deposits; smoking; high blood pressure; or from blood pooling due to atrial fibrillation.  If the thrombus grows into the lumen of the blood vessel it can cause a blockage resulting restriction of blood flow to the heart or brain and this can result in stroke or heart attack. 

Platelet aggregation and thrombus formation 

Blood platelets (thrombocytes), which are the smallest cell type of the blood and are not true cells as they lack a nucleus, play an important role in haemostasis by initiating thrombus formation.  Thrombosis formation is a complex process that begins with platelet aggregation (or clumping).  Platelets are normally prevented from aggregating by factors produced by the endothelial cells that line the blood vessel walls.  When the vessel wall is damaged, this exposes collagen in the vessel wall, which triggers platelets to begin clumping and then they release their own aggregating factors to amplify the process.  One of these factors called adenosine diphosphate (ADP) binds to a specific receptor on the platelet surface.  Platelet aggregation is also triggered by thrombin a protein in the blood that forms part of the coagulation cascade.  A common cause of vessel injury in cardiovascular disease is when an artery wall, hardened by build-up of cholesterol, ruptures exposing an atherosclerotic plaque and this triggers platelet aggregation.

Blood coagulation

The coagulation cascade is activated at the same time as platelet aggregation by the exposure of collagen and tissue factor and involves a series of reactions in which inactive blood enzymes are converted to their active form.  The end product of the coagulation cascade is the conversion of the soluble protein fibrinogen to an insoluble fibrous protein called fibrin, which mixes with the clumps of aggregated plates to form the thrombus.  Several of the coagulation proteins are synthesised in the liver and are dependent on Vitamin K as a cofactor for their production.  The anticoagulants that target vitamin K dependent coagulation factors work by depleting the body’s supply of vitamin K and thereby, preventing the synthesis of these coagulation factors.

Anti-platelet drugs and anticoagulants

Anti-clotting and anticoagulant medications (antithrombotic) are used to prevent the formation of a blood clot or thrombosis in conditions where it could be life threatening, such as cardiovascular disease, congestive heart failure, atrial fibrillation and reduced blood flow due to immobility. 

Antiplatelet drugs like clopidogrel work by binding to the ADP receptor on the platelet surface and inhibiting the activation of platelet aggregation.

Anticoagulants like warfarin work by inhibiting an enzyme that recycles used vitamin K after it has participated in the coagulation cascade and thereby depletes the supply of vitamin K.  This action inhibits the synthesis of Vitamin K dependent coagulation factors, which blocks the coagulation cascade and prevents the final stage of clot formation.
...Read more

Blood clots 

Haemostasis is the process of preventing bleeding from a damaged blood vessel to keep blood flowing through the artery or vein.  Injury or damage to a blood vessel wall initiates the formation of a blood clot or thrombus to block the site of the damage and prevent bleeding, which if severe can cause haemorrhage or severe bleeding from a ruptured blood vessel.  However a thrombus can form even if the vessel wall is not ruptured as a result of damage by cholesterol deposits; smoking; high blood pressure; or from blood pooling due to atrial fibrillation.  If the thrombus grows into the lumen of the blood vessel it can cause a blockage resulting restriction of blood flow to the heart or brain and this can result in stroke or heart attack. 

Platelet aggregation and thrombus formation 

Blood platelets (thrombocytes), which are the smallest cell type of the blood and are not true cells as they lack a nucleus, play an important role in haemostasis by initiating thrombus formation.  Thrombosis formation is a complex process that begins with platelet aggregation (or clumping).  Platelets are normally prevented from aggregating by factors produced by the endothelial cells that line the blood vessel walls.  When the vessel wall is damaged, this exposes collagen in the vessel wall, which triggers platelets to begin clumping and then they release their own aggregating factors to amplify the process.  One of these factors called adenosine diphosphate (ADP) binds to a specific receptor on the platelet surface.  Platelet aggregation is also triggered by thrombin a protein in the blood that forms part of the coagulation cascade.  A common cause of vessel injury in cardiovascular disease is when an artery wall, hardened by build-up of cholesterol, ruptures exposing an atherosclerotic plaque and this triggers platelet aggregation.

Blood coagulation

The coagulation cascade is activated at the same time as platelet aggregation by the exposure of collagen and tissue factor and involves a series of reactions in which inactive blood enzymes are converted to their active form.  The end product of the coagulation cascade is the conversion of the soluble protein fibrinogen to an insoluble fibrous protein called fibrin, which mixes with the clumps of aggregated plates to form the thrombus.  Several of the coagulation proteins are synthesised in the liver and are dependent on Vitamin K as a cofactor for their production.  The anticoagulants that target vitamin K dependent coagulation factors work by depleting the body’s supply of vitamin K and thereby, preventing the synthesis of these coagulation factors.

Anti-platelet drugs and anticoagulants

Anti-clotting and anticoagulant medications (antithrombotic) are used to prevent the formation of a blood clot or thrombosis in conditions where it could be life threatening, such as cardiovascular disease, congestive heart failure, atrial fibrillation and reduced blood flow due to immobility. 

Antiplatelet drugs like clopidogrel work by binding to the ADP receptor on the platelet surface and inhibiting the activation of platelet aggregation.

Anticoagulants like warfarin work by inhibiting an enzyme that recycles used vitamin K after it has participated in the coagulation cascade and thereby depletes the supply of vitamin K.  This action inhibits the synthesis of Vitamin K dependent coagulation factors, which blocks the coagulation cascade and prevents the final stage of clot formation.
...Read more

All medicines have risks and benefits, and individual results may vary. Only purchase medicines from this site in accordance with the advice you have obtained from an appropriate medical professional.
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