Anticoagulant/antithrombotic agents

Heparin is biosynthesized in mast cells as a PG with approximately 10 GAG side chains (5). When mast cells degranulate, PG heparin is enzymatically degraded to GAG heparin (Fig. 1). Exogenous heparin is used primarily as an anticoagulant/antithrombotic agent. Heparin is produced from mast-cell-rich tissues, such as lung and intestinal mucosa, in metric ton quantities yearly for use as a pharmaceutical agent. 

The clinical failure of other synthetic non-heparin anticoagulant/ antithrombotic agents and 3) The concern, particularly in Europe, about difficulties in establishing that heparin is prion-ffee. ... 

Mourao, P. A. (2004). Use of sulfated fucans as anticoagulant and antithrombotic agents Future perspectives. Curr. Pharm. Design 10, 967-981. 

Over the years. Jawed Fareed, Ph.D, FACB, and his colleagues have made highly significant contributions to the development of newer therapeutic anticoagulant and antithrombotic agents. Dr. Fareed s group has published extensively in this area. 

De ite differmces in their mechanisms of action and in vitro activities, pentasaccharide, DX-9065a and TAP have been shown to be effective antithrombotic agents in experimental models of venous thrombosis, coronary artery occlusion, arterial thrombolysis and acute reocclusion, restenosis after angioplasty, dialysis, and DIG. Pentasaccharide has also demonstrated measurable antithrombotic effects in human trials. Both TAP and DX-9065a produce measurable in vitro anticoagulant effects. In contrast, pentasaccharide does not produce an anticoagulant effect by the typical clot based assays. Thus, with fector Xa inhibitors there is not necessarily a correlation between current lab assays and antithrombotic efficacy as there is with heparin. 

It may be noted that some medical databases refer to antithrombotic agents as ANTITHROMBINS. This is not an exact use of the term as antithrombins, mechanistically, are a subtype of anticoagulants. 

Anti thrombin III, an anticoagulant and antithrombotic agent (50 to 100 lU/min IV), is indicated for prophylaxis and adjunct treatment of thromboembolism associated with hereditary antithrombin III deficiency (see also Tables 17 and 18). 

Anticoagulants inhibit blood coagulation, antithrombotic agents prevent platelet aggregation. 

Venous thromboembolism (VTE) is a complicating condition responsible for high morbidity and mortality in North America and Europe. This disease commonly is linked to advanced age but has both hereditary and acquired risk factors, such as surgery, any form of trauma, and childbirth, associated with it. It encompasses the conditions of deep vein thrombosis (DVT) and pulmonary embolism. In excess of 60,000 deaths annually are attributed to pulmonary embolism. Preventative therapy consists of the use of two different classes of antithrombotic agents, namely anticoagulants and antiplatelet drugs (1,2). 

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