Factor VIIa

4YT7, 1BF9, 1CVW, 1DAN, 1DVA, 1F7E, 1F7M, 1FAK, 1FF7, 1FFM, 1J9C, 1JBU, 1KLI, 1KLJ, 1O5D, 1QFK, 1W0Y, 1W2K, 1W7X, 1W8B, 1WQV, 1WSS, 1WTG, 1WUN, 1WV7, 1YGC, 1Z6J, 2A2Q, 2AEI, 2AER, 2B7D, 2B8O, 2BZ6, 2C4F, 2EC9, 2F9B, 2FIR, 2FLB, 2FLR, 2PUQ, 2ZP0, 2ZWL, 2ZZU, 3ELA, 3TH2, 3TH3, 3TH4, 4IBL, 4ISH, 4ISI, 4JYU, 4JYV, 4JZD, 4JZE, 4JZF, 4NA9, 4NG9, 4NGA, 4X8S, 4X8T, 4X8U, 4X8V, 4YT6, 4ZXX, 4ZXY, 4Z6A, 4ZMA, 4YLQ, 5I46215514068ENSG00000057593ENSMUSG00000031443P08709P70375NM_000131NM_001267554NM_019616NM_010172NP_000122NP_001254483NP_062562NP_034302Factor VII (EC 3.4.21.21, blood-coagulation factor VIIa, activated blood coagulation factor VII, formerly known as proconvertin) is one of the proteins that causes blood to clot in the coagulation cascade. It is an enzyme of the serine protease class. A recombinant form of human factor VIIa (eptacog alfa , NovoSeven) has U.S. Food and Drug Administration approval for uncontrolled bleeding in hemophilia patients. It is sometimes used unlicensed in severe uncontrollable bleeding, although there have been safety concerns. A biosimilar form of recombinant activated factor VII (AryoSeven) is also available, but does not play any considerable role in the market.1bf9: N-TERMINAL EGF-LIKE DOMAIN FROM HUMAN FACTOR VII, NMR, 23 STRUCTURES1cvw: CRYSTAL STRUCTURE OF ACTIVE SITE-INHIBITED HUMAN COAGULATION FACTOR VIIA (DES-GLA)1dan: COMPLEX OF ACTIVE SITE INHIBITED HUMAN BLOOD COAGULATION FACTOR VIIA WITH HUMAN RECOMBINANT SOLUBLE TISSUE FACTOR1dva: Crystal Structure of the Complex Between the Peptide Exosite Inhibitor E-76 and Coagulation Factor VIIA1f7e: THE FIRST EGF-LIKE DOMAIN FROM HUMAN BLOOD COAGULATION FVII, NMR, 20 STRUCTURES1f7m: THE FIRST EGF-LIKE DOMAIN FROM HUMAN BLOOD COAGULATION FVII, NMR, MINIMIZED AVERAGE STRUCTURE1fak: HUMAN TISSUE FACTOR COMPLEXED WITH COAGULATION FACTOR VIIA INHIBITED WITH A BPTI-MUTANT1ff7: THE FIRST EGF-LIKE DOMAIN FROM HUMAN BLOOD COAGULATION FVII (FUCOSYLATED AT SER-60), NMR, 20 STRUCTURES1ffm: THE FIRST EGF-LIKE DOMAIN FROM HUMAN BLOOD COAGULATION FVII (FUCOSYLATED AT SER-60), NMR, MINIMIZED AVERAGE STRUCTURE1j9c: Crystal Structure of tissue factor-factor VIIa complex1jbu: Coagulation Factor VII Zymogen (EGF2/Protease) in Complex with Inhibitory Exosite Peptide A-1831kli: Cofactor-and substrate-assisted activation of factor VIIa1klj: Crystal structure of uninhibited factor VIIa1o5d: Dissecting and Designing Inhibitor Selectivity Determinants at the S1 site Using an Artificial Ala190 Protease (Ala190 uPA)1qfk: STRUCTURE OF HUMAN FACTOR VIIA AND ITS IMPLICATIONS FOR THE TRIGGERING OF BLOOD COAGULATION1w0y: TF7A_3771 COMPLEX1w2k: TF7A_4380 COMPLEX1w7x: FACTOR7- 413 COMPLEX1w8b: FACTOR7 - 413 COMPLEX1wqv: Human Factor Viia-Tissue Factor Complexed with propylsulfonamide-D-Thr-Met-p-aminobenzamidine1wss: Human Factor Viia-Tissue Factor in Complex with peprid mimetic inhibitor that has two charge groups in P2 and P41wtg: Human Factor Viia-Tissue Factor Complexed with ethylsulfonamide-D-biphenylalanine-Gln-p-aminobenzamidine1wun: Human Factor Viia-Tissue Factor Complexed with ethylsulfonamide-D-Trp-Gln-p-aminobenzamidine1wv7: Human Factor Viia-Tissue Factor Complexed with ethylsulfonamide-D-5-propoxy-Trp-Gln-p-aminobenzamidine1ygc: Short Factor VIIa with a small molecule inhibitor1z6j: Crystal Structure of a ternary complex of Factor VIIa/Tissue Factor/Pyrazinone Inhibitor2a2q: Complex of Active-site Inhibited Human Coagulation Factor VIIa with Human Soluble Tissue Factor in the Presence of Ca2+, Mg2+, Na+, and Zn2+2aei: Crystal structure of a ternary complex of factor VIIa/tissue factor and 2--3,5-difluro-4--2-pyridinyl]oxy]-benzoic acid2aer: Crystal Structure of Benzamidine-Factor VIIa/Soluble Tissue Factor complex.2b7d: Factor VIIa Inhibitors: Chemical Optimization, Preclinical Pharmacokinetics, Pharmacodynamics, and Efficacy in a Baboon Thrombosis Model2b8o: Crystal Structure of Glu-Gly-Arg-Chloromethyl Ketone-Factor VIIa/Soluble Tissue Factor Complex2bz6: ORALLY AVAILABLE FACTOR7A INHIBITOR2c4f: CRYSTAL STRUCTURE OF FACTOR VII.STF COMPLEXED WITH PD02971212f9b: Discovery of Novel Heterocyclic Factor VIIa Inhibitors2fir: Crystal structure of DFPR-VIIa/sTF2flb: Discovery of a Novel Hydroxy Pyrazole Based Factor IXa Inhibitor2flr: Novel 5-Azaindole Factor VIIa Inhibitors2puq: Crystal structure of active site inhibited coagulation factor VIIA in complex with soluble tissue factor Factor VII (EC 3.4.21.21, blood-coagulation factor VIIa, activated blood coagulation factor VII, formerly known as proconvertin) is one of the proteins that causes blood to clot in the coagulation cascade. It is an enzyme of the serine protease class. A recombinant form of human factor VIIa (eptacog alfa , NovoSeven) has U.S. Food and Drug Administration approval for uncontrolled bleeding in hemophilia patients. It is sometimes used unlicensed in severe uncontrollable bleeding, although there have been safety concerns. A biosimilar form of recombinant activated factor VII (AryoSeven) is also available, but does not play any considerable role in the market. The main role of factor VII (FVII) is to initiate the process of coagulation in conjunction with tissue factor (TF/factor III). Tissue factor is found on the outside of blood vessels - normally not exposed to the bloodstream. Upon vessel injury, tissue factor is exposed to the blood and circulating factor VII. Once bound to TF, FVII is activated to FVIIa by different proteases, among which are thrombin (factor IIa), factor Xa, IXa, XIIa, and the FVIIa-TF complex itself. The complex of factor VIIa with TF catalyzes the conversion of factor IX and factor X into the active proteases, factor IXa and factor Xa, respectively. The action of the factor is impeded by tissue factor pathway inhibitor (TFPI), which is released almost immediately after initiation of coagulation. Factor VII is vitamin K dependent; it is produced in the liver. Use of warfarin or similar anticoagulants decreases hepatic synthesis of FVII. Factor VII shares a common domain architecture with factors IX and X. The gene for factor VII is located on chromosome 13 (13q34). Factor VII deficiency (congenital proconvertin deficiency) is rare and inherited recessively. It presents as a hemophilia-like bleeding disorder. It is treated with recombinant factor VIIa (NovoSeven or AryoSeven). Gene therapy approaches for treating FVII deficiency are very promising () Recombinant factor VIIa, marketed under the trade names AryoSeven and NovoSeven, is used for people with hemophilia (with Factor VIII or IX deficiency) who have developed antibodies against replacement coagulation factor. It has also been used in the setting of uncontrollable hemorrhage, but its role in this setting is controversial with insufficient evidence to support its use outside of clinical trials. The first report of its use in hemorrhage was in an Israeli soldier with uncontrollable bleeding in 1999. Risks of its use include an increase in arterial thrombosis.However, animal studies have not shown complications as seen in humans, in fact same of the studies show a better prognosis. In the military settings it is used as an off label intervention in complications related to disseminated intravascular coagulation related haemorrhage caused by penetrating trauma. Recombinant human factor VII while initially looking promising in intracerebral hemorrhage failed to show benefit following further study and this is no longer recommended.