Re Action of AT3;;;;;;;;;;;;;
This post is mainly based on material presented in the Wiedermann paper....Fairly technical but great on AT3
The first thing to understand is AT3 (Atryn) is much more than an "anticoagulant" It has many wide ranging effects both intra and extra cellular. It is a major player in both the coag and the immune system; and probably is important in intra uterine development and the body's reaction to ischemia (O2 deprevation) In addition to its better known role as a serine protease inhibitor (it "blocks the action of thrombin and several other members of the coag cascade). This done from it's active site. AT3 also has other sites which bind heparin.
The ability to bind heparin allows AT3 to act in a completely different manner which does not require the presence of thrombin or other serine proteases. Many cells both in the vascular system and the immune system, including edothelial cells,white cells, and lymphocytes possess, cell membranes dotted with surface receptors composed of HSPGs (Heparin-like glycosaminoglycans). Syndecan-4,an HSPG sydecan family member mediates an AT3 cell surface receptor on endothelial cells and leukocytes. This causes the release of prostaclycans which are thought to diminish the effects of endotoxeamia.
As far of the effects of heparin on AT3.... This is a section of the paper. Even the smallest doses of heparin such as those used in thrombosis prophylaxis can have an impact on the beneficial effect of AT3 on the microcirculatory disturbances in endotoxeamia. This might be due to the fact that heparin competitively inhibits the binding of AT3 to syndecan-4 or other HSPGs.
Later in the paper..... re the observation that AT3 inhbits the production of TNF,, This inhibiting activity of AT3 also depends on it's binding to heparin like substances on the endothelial cell.
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