Achieve Balance
THROMBATE III® replaces low antithrombin levels7,9
THROMBATE III delivers 50x more antithrombin (AT) than the same amount of fresh frozen plasma (FFP)
- A vial of THROMBATE III contains concentrated AT factor, while a bag of FFP contains AT as well as varying amounts of other plasma components.1,13
Properties of antithrombin (AT) concentrate and fresh frozen plasma (FFP)
| THROMBATE III1 | FFP13 | |
|---|---|---|
| Indication | Indicated in patients with hereditary antithrombin deficiency (hATd) for treatment and prevention of thromboembolism and for prevention of perioperative and peripartum thromboembolism | Indicated in the management of patients with selected coagulation factor deficiencies, congenital or acquired, for which no specific coagulation concentrates are available |
| How supplied/ volume | Single-use 10-mL vial (500-IU potency) | Supplied in 200- to 250-mL bags (on average) |
| Concentration | 50 IU/mL AT concentration (after reconstitution with 10 mL sterile water for injection) | ~1 IU/mL AT concentration |
| Use | Intravenous bolus infusion, regardless of ABO status. Can be readily available at the point of care | Needs to be thawed prior to use. Intravenous infusion. Plasma must be ABO compatible with the recipient's red blood cells |
| Content | THROMBATE III provides predictable amounts of AT | Contains AT plus other plasma components in varying levels |
| Half-life | The long half-life of THROMBATE III—91 hours (3.8 days)— is similar to endogenous AT3 | The components of FFP have varying half-lives |
| Storage | THROMBATE III can be stored at room temperature (up to 77°F) for up to 36 months. Do not freeze | FFP should be stored at −18°C (0°F) or colder. Infuse immediately after thawing or store at 1-6°C (34-43°F) |
| Process | THROMBATE III is produced from human plasma— it is fractionated and purified to yield concentrated antithrombin | Centrifuged, separated, and frozen solid at −18°C (0°F) within 8 hours of collection |
| Dosing |
The loading dose for Thrombate III is calculated with a clear formula:
Units required (IU) =
120% - baseline % x body weight (kg) 1.4%
|
The volume of FFP transfused depends on various factors, including the clinical situation and patient weight, and may be guided by laboratory assays of coagulation function |
- Predictable dosing that directly replaces the missing antithrombin (AT)
- Concentrated amounts of AT to minimize additional volume load
- Rapid preparation at the point of care—no thawing needed
- Convenient vial storage for up to 36 months at room temperature
The half-life of AT has been reported to be shortened following surgery, hemorrhage or acute thrombosis, and during intravenous heparin (or low molecular weight heparin) administration. In such conditions, monitor plasma AT levels more frequently, and administer THROMBATE III as necessary.
THROMBATE III provides a direct approach to managing hereditary AT deficiency in high-risk situations1
- The loading dose volume for THROMBATE III is calculated with a clear formula so each dose is precise and accurate
- Healthcare professionals have been successfully treating hereditary AT deficiency with THROMBATE III for more than 25 years
Learn more about:
THE RISKS OF LOW AT: See how THROMBATE III replaces missing AT
CONVENIENCE: THROMBATE III delivers trusted therapy
THROMBATE III TOOLS AND RESOURCES: Downloadable resources, and much more
IMPORTANT SAFETY INFORMATION
THROMBATE III® (antithrombin III [human]) is indicated in patients with hereditary antithrombin deficiency for treatment and prevention of thromboembolism and for prevention of perioperative and peripartum thromboembolism.
Hypersensitivity reactions may occur. Should evidence of an acute hypersensitivity reaction be observed, promptly interrupt the infusion and begin appropriate treatment.
Because THROMBATE III is made from human blood, it may carry a risk of transmitting infectious agents, eg, viruses, the variant Creutzfeldt-Jakob disease (vCJD) agent, and, theoretically, the Creutzfeldt-Jakob disease (CJD) agent. There is also the possibility that unknown infectious agents may be present in the product.
Perform coagulation tests to avoid excessive or insufficient anticoagulation and monitor for bleeding or thrombosis. Measure functional plasma AT levels with amidolytic or clotting assays; do not use immunoassays.
In clinical studies, the most common adverse reactions (≥ 5% of subjects) were dizziness, chest discomfort, nausea, dysgeusia, and pain (cramps).
The anticoagulant effect of heparin is enhanced by concurrent treatment with THROMBATE III in patients with hereditary AT deficiency. Thus, in order to avoid bleeding, the dosage of heparin (or low molecular weight heparin) may need to be reduced during treatment with THROMBATE III.
Please see full Prescribing Information for THROMBATE III.
You are encouraged to report negative side effects of prescription drugs to the FDA. Visit http://www.fda.gov/medwatch, or call 1-800-FDA-1088.
References:1. THROMBATE III [Prescribing Information]. Research Triangle Park, NC: Grifols Therapeutics LLC. 2. Maclean PS, Tait RC. Hereditary and acquired antithrombin deficiency: epidemiology, pathogenesis, and treatment options. Drugs. 2007;67(10):1429-1440. 3. Li W, Johnson DJ, Esmon CT, Huntington JA. Nat Struct Mol Biol. 2004;11(9):857-862. 4. James AH, Konkle BA, Bauer KA. Prevention and treatment of venous thromboembolism in pregnancy and patients with hereditary antithrombin deficiency. Int J Womens Health. 2013;5:233-241. 5. Wolberg AS. Blood Rev. 2007;21(3):131-142. 6. Davi G, Patrono C. N Engl J Med. 2007;357(24):2482-2494. 7. Kottke-Marchant K, Duncan A. Antithrombin deficiency: issues in laboratory diagnosis. Arch Pathol Lab Med. 2002;126(11):1326-1336. 8. Mitton BA, Steineck A. Antithrombin deficiency. eMedicine from WebMD. http://emedicine.medscape.com/article/198573-overview. Updated July 22, 2022. Accessed November 28, 2022. 9. Patnaik MM, Moll S. Inherited antithrombin deficiency: a review. Haemophilia. 2008;14(6):1229-1239.10. Pabinger I, Schneider B. Thrombotic risk in hereditary antithrombin III protein C, or protein S deficiency. Arteroscler Thromb Vasc Biol. 1996;16(6):742-748. 11. Ranucci M. Antithrombin III: key factor in extracorporeal circulation. Minerva Anestesiol. 2002;68(5):454-457. 12. Foy P, Moll S. Thrombophilia: 2009 update. Curr Treat Options Cardiovasc Med. 2009;11(2):114-128. 13. AABB, American Red Cross, America's Blood Centers, Armed Services Blood Program. Circular of information for the use of human blood and blood components. https://www.aabb.org/docs/default-source/default-document-library/resources/circular-of-information-watermark.pdf?sfvrsn=7f5d28ab_5
December 2021. Accessed November 28, 2022. 14. Wells PS, Blajchman MA, Henderson P, et al. Am J Hematol. 1994;45:321-324. 15. US Census Bureau, Population Division. US and World Population Clock. http://www.census.gov/ popclock/. Accessed November 28, 2022. 16. Khawar H, Kelley W,Guzman N. Fresh frozen plasma. In: StatPearls. https://www.ncbi.nlm.nih.gov/books/NBK513347/. Updated September 19, 2022. Accessed November 28, 2022. 17. Hellgren M, Tengborn T, Abildgaard U. Pregnancy in women with congenital antithrombin III deficiency: experience of treatment with heparin and antithrombin. Gynecol Obstet Invest. 1982;14:127-141. 18. Franchini M, Veneri D, Salvagno GL, Manzato F, Lippi G. Inherited thrombophilia. Crit Rev Clin Lab Sci. 2006;43(3):249-290. 19. Rodgers GM. Role of antithrombin concentrate in hereditary antithrombin deficiency: an update. Thromb Haemost. 2009;101(5):806-812. 20. Di Minno MND, Dentali F, Lupoli R, Ageno W. Mild antithrombin deficiency and risk of recurrent venous thromboembolism. Circulation. 2014;129(4):497-503. 21. Bucciarelli P, Passamonti SM, Biguzzi E, et al. Low borderline plasma levels of antithrombin, protein C and protein S are risk factors for venous thromboembolism. J Thromb Haemost. 2012;10(9):1783-1791. 22. Centers for Disease Control and Prevention. Venous thromboembolism in adult hospitalizations – United States, 2007-2009. MMWR Morb Mortal Wkly Rep. 2012;61(22):401-404. 23. Finley A, Greenberg C. Review article: heparin sensitivity and resistance: management during cardiopulmonary bypass. Anesth Analg. 2013;116(6):1210-1222. 24. Kovács B, Bereczky Z, Oláh Z, et al. The superiority of anti-FXa assay over anti-FIIa assay in detecting heparin-binding site antithrombin deficiency. Am J Clin Pathol. 2013;140(5):675-679. 25. Olson E, Whitney M, Friedman B et al. In vivo fluorescence imaging of atherosclerotic plaques with activatable cell-penetrating peptides targeting thrombin activity, Integrative Biology, 2012;4(6):595–605. 26. Lloyd-Jones D, Adams RJ, Brown TM, et al; on behalf of the American Heart Association Statistics Committee and Stroke Statistics Subcommittee. Circulation. 2010;121:e46-e215.