Fondaparinux Sodium Mechanism of Action

Identification of Specific Binding to Purified and Human Plasma-Derived Proteins

  • Paolucci, Francis
  • Claviés, Marie-Christine
  • Donat, François
  • Necciari, José
Clinical Pharmacokinetics 41:p 11-18, 2002.

Background

Fondaparinux sodium is a novel antithrombotic agent, the first of a new class of selective factor Xa inhibitors. It has favourable pharmacokinetics including 100% bioavailability, low variability and a mean terminal half-life of 17 hours for young and 21 hours for elderly healthy volunteers, enabling once-daily administration. Studies on the prevention of venous thromboembolism (VTE) after orthopaedic surgery demonstrated significantly improved efficacy over the low-molecular-weight heparin enoxaparin, with a >50% reduced risk of VTE and a similar safety profile.

Objective

To investigate the in vitro binding of fondaparinux sodium to purified antithrombin III (ATIII) and other plasma proteins.

Methods

Fondaparinux sodium was incubated with human plasma, antithrombin-depleted plasma or purified human plasma proteins, including antithrombin, α1-acid glycoprotein, serum albumin and immunoglobulin. Non-protein-bound fondaparinux sodium was determined using a validated chromogenic assay method, enabling the calculation of the free fraction of fondaparinux sodium and its binding parameters.

Results

At steady state, fondaparinux sodium at therapeutic concentrations [i.e. those attainable in the prevention (0.14 to 0.50 mg/L) and treatment (up to approximately 2 mg/L) of VTE] was extensively bound (>97%) to plasma proteins and specifically bound (>94%) to purified ATIII. The specific binding parameters Bmax (binding capacity) and KD (dissociation constant) were similar for human plasma (Bmax = 2072 nmol/L, KD = 28 nmol/L) and purified ATIII (Bmax = 1627 nmol/L and KD = 32 nmol/L). There was no specific binding of fondaparinux sodium to other purified plasma proteins.

Conclusion

At clinically relevant concentrations, fondaparinux sodium is highly and specifically bound to ATIII in human plasma, suggesting that potential interaction with drugs via albumin or α1-acid glycoprotein displacement is unlikely.

Copyright © 2002 Adis International