Pharmacokinetic model of

un highly sulfated linear glucosamine-glycans with varying molecular weights (3–30 kD) [1,2]. The anti-coagulation so the anti-FIIa assay may have a smaller lower limit of quantitation (LLOQ) [5]. We measured anti-F activity as Jia et al. Journal of Translational Medicine (2015) 13:45 DOI 10.1186/s12967-015-0404-5verted from the free to the bound state. Moreover, plasmaBeijing 100029, China Full list of author information is available at the end of the articleeffect of heparin is dependent upon binding with the serine protease inhibitor anti-thrombin III (ATIII) [3]. Binding with ATIII increases the inhibitory activity of ATIII against both thrombin (FIIa) and factor Xa (FXa) and other serine proteases in the coagulation cascade by over IIa an index to quantify plasma UFH levels in humans [6]. The UFH half-life is 1–2 h in human plasma, depend-ing on dose [2], as higher doses produce a prolonged half-life due to the mechanism of plasma clearance, which involves rapid distribution via UFH binding to plasma proteins and receptors on endothelial cells and macrophages, followed by slower elimination through the kidneys [5]. Thus, UFH pharmacokinetics may include a “peripheral process ” by which the UFH molecule is con