THROMBATE III delivers 50x more antithrombin (AT) than the same amount of fresh frozen plasma (FFP)1

  • The amount of AT in a 10-mL vial of THROMBATE III equals the IU of AT in 500 mL of FFP1
  • 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.13

Properties of antithrombin (AT) concentrate and fresh frozen plasma (FFP)

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 
The loading dose for THROMBATE III is calculated with a clear formula, so each dose is precise and accurate: 

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

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
  • 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
  • Healthcare professionals have been successfully treating hereditary AT deficiency with THROMBATE III for more than 25 years
Image of THROMBATE III (Human) and initial dose requirements

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



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, 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. Updated August 22, 2019. Accessed September 4, 2020. 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. October 2017. Accessed September 4, 2020. 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. popclock/. Accessed February 13, 2020. 16. Khawar H, Kelley W,Guzman N. Fresh frozen plasma. In: StatPearls. Updated October 7, 2019. Accessed February 10, 2020. 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.