The 2011 Coagulation Market: New Product Development Opportunities, Market Penetration Strategies, Entry Barriers and Risks17 Feb 2011 • by Natalie Aster
New York - The report “The 2011 Coagulation Market: New Product Development Opportunities, Market Penetration Strategies, Entry Barriers and Risks ” by Venture Planning Group presents a comprehensive worldwide review of the coagulation testing market dynamics and technologies; provides detailed analyses of the world's seven major markets; analyzes leading competitors; and identifies specific business opportunities with potentially significant market appeal during the next ten years.
Published: April 2010
Price: US$ 950
Report Sample Abstract
Recent advances in genetic engineering have made possible the development of specific monoclonal antibodies against Fibrin fragments. The insertion of cross-links between the D domains of Fibrin by Factor XIIIa has generated specific neoantigenic determinants that permit differentiation of its proteolytic cleavage products. A monoclonal antibody directed against the conformational epitope of the plasmin-resistant D-Dimer fragment of cross-linked Fibrin has been developed. The D-Dimers result from Plasmin digestion of cross linked Fibrin monomers, and their presence is a highly specific indicator of in vivo lysis of Fibrin clots. The D-Dimer antibody does not cross-react with Fibrinogen or its derivatives and can be used in plasma.
The monoclonal antibody to Fibrin D-Dimer immobilized on latex particles is a rapid, sensitive and specific test for the diagnosis and management of patients with diseases associated with fibrinolysis. Thus, the D-Dimer test is clinically significant in the diagnosis of DIC, and its use is expected to become more widespread.
The D-Dimer assay is specific for fibrin degradation products, whereas the formation of fibrinolytic degradation products, X, Y, D, and E fragments, may be either fibrinogen or fibrin derived following plasmin digestion.
The presence of D-Dimer implies the generation of both plasmin and thrombin, the generation of thrombin being implied by thrombin-induced activation of Factor XIII studied, Factor V was resistant to Protein C and S. In the initial epidemiologic study, Factor V deficiency appears to be one of the most common defects of thrombosis, more common than AT3, Protein C or Protein S. A modified Factor V assay is a part of the thrombotic panels developed by Diagnostica Stago, Helena and several other companies. The new clotting assay measures the ability for Protein C to inhibit Factor V activity.
The genetic deficiencies of antithrombin, Protein C, and Protein S, as well as dysfibrinogenemia, are fairly rare and have a prevalence of less than 3% in the general populations. Among families with inherited thrombophilia, 4.3% have antithrombin deficiency, 5.7% have Protein C deficiency, and 5.7% have Protein S deficiency. Leiden University Medical Center (Leiden, The Netherlands), has identified the gene that causes activated Protein C (APC) resistance. These protein deficiencies come from heterogenous and highly variable mutations, making DNA-based diagnosis screening difficult. Most labs still rely on functional and immunological tests for diagnosis. People with an inherited antithrombin deficiency have an approximately 20-fold increased risk, people with Protein C deficiency have an approximately eight-fold increased risk, and those with APC resistance have a four-fold increased risk. Although these predisposi-tions seem dramatic, they are not as dangerous as other risk factors, such as a prior thrombosis and aging, that confer a 40- to 60-fold increased risk.
More information can be found in the report “The 2011 Coagulation Market: New Product Development Opportunities, Market Penetration Strategies, Entry Barriers and Risks ” by Venture Planning Group .
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