Thrombosis, the formation of blood clots in arteries or veins, is a major cause of death in the developed world. Arterial thrombosis is a leading cause of heart attacks and strokes, while venous thromboembolism is the third leading cause of cardiovascular death. The mechanisms underlying thrombosis are not fully understood, but they involve changes in the blood vessel wall and blood components. Understanding these processes is crucial for developing safer and more effective antithrombotic drugs. Arterial thrombosis is primarily triggered by the rupture of atherosclerotic plaques, leading to platelet activation and aggregation. Platelets, small anucleate cells, adhere to the vessel wall and form a primary hemostatic plug. Platelet activation is mediated by various receptors, including PAR1, which is activated by thrombin. Antiplatelet drugs target these pathways to prevent thrombosis, but they can cause bleeding as a side effect. New drugs are being developed to target platelet activation more effectively with fewer bleeding risks. Venous thrombosis is often caused by changes in blood flow, blood composition, or endothelial function. It involves the formation of fibrin-rich clots. Anticoagulant drugs, such as vitamin K antagonists and heparins, target the coagulation cascade to prevent clot formation. However, these drugs also carry bleeding risks. New anticoagulants, such as direct factor Xa and thrombin inhibitors, are being developed to improve safety and efficacy. Both arterial and venous thrombosis require different therapeutic approaches. Antiplatelet drugs target platelet activation, while anticoagulants inhibit the coagulation cascade. Recent advances include new drugs like prasugrel and rivaroxaban, which show promise in reducing thrombosis with fewer side effects. Combination therapy using both antiplatelet and anticoagulant drugs may offer better outcomes. Personalized medicine is also emerging as a potential approach to tailor antithrombotic therapy to individual patients. The development of new antithrombotic drugs is ongoing, with a focus on improving safety and efficacy. Research into the molecular mechanisms of thrombosis is helping to identify new therapeutic targets. Despite these advances, a drug that prevents clotting without causing bleeding remains a challenge. However, ongoing research and clinical trials are bringing new options for the treatment of thrombosis.Thrombosis, the formation of blood clots in arteries or veins, is a major cause of death in the developed world. Arterial thrombosis is a leading cause of heart attacks and strokes, while venous thromboembolism is the third leading cause of cardiovascular death. The mechanisms underlying thrombosis are not fully understood, but they involve changes in the blood vessel wall and blood components. Understanding these processes is crucial for developing safer and more effective antithrombotic drugs. Arterial thrombosis is primarily triggered by the rupture of atherosclerotic plaques, leading to platelet activation and aggregation. Platelets, small anucleate cells, adhere to the vessel wall and form a primary hemostatic plug. Platelet activation is mediated by various receptors, including PAR1, which is activated by thrombin. Antiplatelet drugs target these pathways to prevent thrombosis, but they can cause bleeding as a side effect. New drugs are being developed to target platelet activation more effectively with fewer bleeding risks. Venous thrombosis is often caused by changes in blood flow, blood composition, or endothelial function. It involves the formation of fibrin-rich clots. Anticoagulant drugs, such as vitamin K antagonists and heparins, target the coagulation cascade to prevent clot formation. However, these drugs also carry bleeding risks. New anticoagulants, such as direct factor Xa and thrombin inhibitors, are being developed to improve safety and efficacy. Both arterial and venous thrombosis require different therapeutic approaches. Antiplatelet drugs target platelet activation, while anticoagulants inhibit the coagulation cascade. Recent advances include new drugs like prasugrel and rivaroxaban, which show promise in reducing thrombosis with fewer side effects. Combination therapy using both antiplatelet and anticoagulant drugs may offer better outcomes. Personalized medicine is also emerging as a potential approach to tailor antithrombotic therapy to individual patients. The development of new antithrombotic drugs is ongoing, with a focus on improving safety and efficacy. Research into the molecular mechanisms of thrombosis is helping to identify new therapeutic targets. Despite these advances, a drug that prevents clotting without causing bleeding remains a challenge. However, ongoing research and clinical trials are bringing new options for the treatment of thrombosis.