Factor XII Inhibitor Plasma
Factor XII Inhibitor Plasma is manufactured from normal citrated human plasma depleted of Factor XII using antibodies directed to FXII immobilized on agarose beads. A polyclonal antibody inhibitory to FXII has been added to provide FXII neutralizing activity. The neutralizing antibody activity is determined by Nijmegen-modified Bethesda Inhibitor Assay and has values reported in Bethesda Units. Our Factor XII Inhibitor Plasma is produced with a mild inhibitor titre or neutralizing activity ranging from 1 BU/ml to 10 BU/ml and is available in two different formats – Frozen and Lyophilized
Only the highest quality citrated plasma is used as starting material and in many cases the parent plasma is available as control material. Our Factor XII Inhibitor Plasma can be used for further manufacturing or research use only applications.
Description of Factor XII (FXII)
Factor XII (FXII, Hageman factor) is a 76 kDa, single chain glycoprotein produced in the liver. In plasma, FXII circulates as a protease zymogen at a concentration of approximately 30 μg/ml (400 nM). Upon vascular injury FXII binds to negatively charged extravascular surfaces such as cartilage and skin, which facilitate activation of the zymogen to the active serine protease. Cleavage of F.XII by kallikrein after residue Arg353 produces the enzyme αFXIIa, consisting of a 28 kDa light chain containing the protease domain, and a 52 kDa heavy chain containing the anionic surface-binding domain. Substrates for surface bound FXIIa include the zymogens prekallikrein (PK) and factor XI (FXI) as well as the procofactor high-molecular weight kininogen (HK). The activation of these substrates results in positive feedback activation of FXII. Further cleavage of αFXIIa by kallikrein produces the 28 kDa fragment βFXIIa (Hageman factor fragment). βFXIIa has reduced procoagulant activity as it lacks the anionic surface-binding domain, but is capable of fluid-phase activation of PK, factor VII and complement C1. The activity of F.XIIa in plasma is regulated predominantly by C1-Inhibitor, with relatively minor contributions by α2antiplasmin, α2macroglobulin and antithrombin, even in the presence of therapeutic levels of heparin1-3.