Coagulation is the formation of insoluble fibrin clots which help to prevent bleeding from damaged blood vessels. Deficiency in various components of the coagulation cascade results in bleeding disorders such as hemophilia and Von Willebrand disease. In contrast, pathological thrombosis is a life threatening complication of myocardial infarction, atherosclerosis, stroke, and vascular thromboembolism (VTE). Fibrinolytic therapy with Tissue Plasminogen Activator (tPA), Urokinase (uPA), or Streptokinase (SK) has shown efficacy at restoring blood flow in these emergencies.

Clot formation is triggered and inhibited by a cascade of coagulation factors, proteases, and regulators. The extrinsic pathway is initiated by contact between blood borne factors and subendothelial Tissue Factor. The intrinsic pathway is triggered by contact of these factors with negatively charged surfaces. Both pathways result in the activation of Coagulation Factor X.

Learn More
Cascade Overview

The backbone of the coagulation cascade is a system of serine proteases (coagulation factors and plasminogen activators) which are held in check by protease inhibitors (Serpins and Protein S). The endpoint of cascade activation is the cleavage of Fibrinogen by Thrombin and the crosslinking of Fibrin into the clot.

Investigate Coagulation Enzymes
Coagulation Cascade Proteases and Inhibitors

The activation of platelets at sites of endothelial damage results in the release of many coagulation cascade factors and regulators. In addition, activated platelets express adhesion proteins which promote platelet aggregation and clot formation.

Multianalyte Immunoassays

These assay platforms let you detect many proteins in one experiment. They cover secreted factors, shed soluble receptors, and intracellular molecules. These assays are optimized for high sensitivity, low background, and minimal cross-reactivity.

Regulate Platelet Activation
Platelet Activation