Find answers about THROMBATE III, hereditary antithrombin deficiency (hATd), risk of venous thromboembolism (VTE), and more:
What is THROMBATE III?1
THROMBATE III is a human antithrombin (AT) indicated in patients with hereditary antithrombin deficiency for:
- Treatment and prevention of thromboembolism
- Prevention of peri-operative and peri-partum thromboembolism
What is hereditary antithrombin deficiency (hATd)?
hATd presents the highest risk of thrombosis among inherited thrombophilias18
- hATd affects 1 in every 500 to 5000 individuals9
- Those with hATd have a 20-fold greater risk of thrombosis than the general population18
When should THROMBATE III be used?
THROMBATE III is an effective choice in high-risk situations.1 Clinical studies have shown that THROMBATE III is an effective choice for patients with hATd and for the treatment and prevention of thromboembolism, including before, during, and after surgery and childbirth.1
How is THROMBATE III used?
THROMBATE III is for intravenous use after reconstitution only. THROMBATE III is a sterile lyophilized powder for reconstitution in single use vials. Each vial of THROMBATE III contains the labeled amount of antithrombin in units per vial, typically 500 units. When reconstituted with 10 mL of Sterile Water for Injection, USP, the final concentration is approximately 50 units per mL.1
What are the implications of low antithrombin levels?
Even modest decreases in AT levels significantly increase VTE risk. Low AT can be the reason why surgical patients do not have the expected response to their anticoagulation.* Each year, more than 250,000 patients are hospitalized for VTE in the United States.26 This emphasizes the importance of assessing VTE risk in patients.
*Heparin and enoxaparin.
What is the mechanism of action for THROMBATE III?1
Antithrombin, an alpha2-glycoprotein of molecular weight 58,000, is normally present in human plasma at a concentration of approximately 12.5 mg/dL and is the major plasma inhibitor of thrombin. Inactivation of thrombin by AT occurs by formation of a covalent bond resulting in an inactive 1:1 stoichiometric complex between the two, involving an interaction of the active serine of thrombin and an arginine reactive site on AT. AT is also capable of inactivating other components of the coagulation cascade including factors IXa, Xa, XIa, and XIIa, as well as plasmin. The neutralization rate of serine proteases by AT proceeds slowly in the absence of heparin, but is greatly accelerated in the presence of heparin. As the therapeutic antithrombotic effect of heparin is mediated by AT, heparin in vivo is ineffective in the absence or near absence of AT.
After administration, THROMBATE III temporarily replaces the missing AT in patients with hereditary antithrombin deficiency.
Do heparin and THROMBATE III work differently?
AT activity inhibits many clotting factors in the coagulation cascade. The inhibition of multiple clotting factors by AT helps prevent the expansion of existing clots and the formation of new clots in 3 stages2-4
- Procoagulation factors bind to AT
- Once bound to AT, procoagulation factors are cleared
- This results in arresting the growth of existing clots and helps prevent new clots
The anticoagulation effects of heparin rely entirely on its interaction with AT.2 The administration of heparin increases the anticlotting effects of AT 1000-fold.4
How is THROMBATE III manufactured?1
THROMBATE III is prepared from pooled units of human plasma from normal donors. The capacity of the THROMBATE III manufacturing process to remove and/or inactivate enveloped and non-enveloped viruses has been validated by laboratory spiking studies on a scaled down process model using a wide range of viruses with diverse physicochemical properties. There are two dedicated virus inactivation/removal steps included in the THROMBATE III manufacturing process: a heat treatment step at 60°C ± 0.5°C for not less than 10 hours for virus inactivation and a nanofiltration step for effective removal of viruses as small as 18 nm.
The THROMBATE III manufacturing process was also investigated for its capacity to decrease the infectivity of an experimental agent of transmissible spongiform encephalopathy (TSE), considered as a model for the variant Creutzfeldt-Jakob disease (vCJD) and Creutzfeldt-Jakob disease (CJD) agents. An individual production step in the THROMBATE III manufacturing process has been shown to decrease TSE infectivity of that experimental model agent. The TSE reduction step is the Effluent I to Effluent II + III fractionation step (6.0 log10). These studies provide reasonable assurance that low levels of vCJD/CJD agent infectivity, if present in the starting material, would be removed.
Learn more about:
CONVENIENCE: THROMBATE III delivers trusted therapy
CAUSES OF HEPARIN RESISTANCE: Hear Dr. Bader talk about inherited clotting disorders
THROMBATE III TOOLS AND RESOURCES: Downloadable resources, and much more