FACTOR7- 413 COMPLEX
[FA7_HUMAN] Defects in F7 are the cause of factor VII deficiency (FA7D) [MIM:227500]. A hemorrhagic disease with variable presentation. The clinical picture can be very severe, with the early occurrence of intracerebral hemorrhages or repeated hemarthroses, or, in contrast, moderate with cutaneous-mucosal hemorrhages (epistaxis, menorrhagia) or hemorrhages provoked by a surgical intervention. Finally, numerous subjects are completely asymptomatic despite very low factor VII levels.                       
[FA7_HUMAN] Initiates the extrinsic pathway of blood coagulation. Serine protease that circulates in the blood in a zymogen form. Factor VII is converted to factor VIIa by factor Xa, factor XIIa, factor IXa, or thrombin by minor proteolysis. In the presence of tissue factor and calcium ions, factor VIIa then converts factor X to factor Xa by limited proteolysis. Factor VIIa will also convert factor IX to factor IXa in the presence of tissue factor and calcium.
Publication Abstract from PubMed
We describe the structure-based design and synthesis of highly potent, orally bioavailable tissue factor/factor VIIa inhibitors which interfere with the coagulation cascade by selective inhibition of the extrinsic pathway.
Selective and orally bioavailable phenylglycine tissue factor/factor VIIa inhibitors.,Zbinden KG, Obst-Sander U, Hilpert K, Kuhne H, Banner DW, Bohm HJ, Stahl M, Ackermann J, Alig L, Weber L, Wessel HP, Riederer MA, Tschopp TB, Lave T Bioorg Med Chem Lett. 2005 Dec 1;15(23):5344-52. Epub 2005 Oct 4. PMID:16213138
From MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine.