NOTICE: Citizendium is still being set up on its newer server, treat as a beta for now; please see here for more.
Citizendium - a community developing a quality comprehensive compendium of knowledge, online and free. Click here to join and contribute—free
CZ thanks our previous donors. Donate here. Treasurer's Financial Report -- Thanks to our content contributors. --

Tranexamic acid

From Citizendium, the Citizens' Compendium
Jump to: navigation, search
This article is developing and not approved.
Main Article
Related Articles  [?]
Bibliography  [?]
External Links  [?]
Citable Version  [?]
Catalogs [?]
This editable Main Article is under development and not meant to be cited; by editing it you can help to improve it towards a future approved, citable version. These unapproved articles are subject to a disclaimer.
© Image: David E. Volk
tranexamic acid
tranexamic acid
IUPAC name: 4-(aminomethyl)cyclohexane-1-carboxylic acid
Synonyms: see below
Formula: C8H15NO2

 Uses: antifibrinolytic

 Properties: fibrinogen inhibitor


Mass (g/mol): CAS #:
157.2102 1197-18-8

In medicine, tranexamic acid a hemostatic agent approved for hemorrhaging in hemophilia, and, orally, for heavy mestrual bleeding, with unapproved uses in cyanide poisioning, hereditary angioedema, hyperfibrinolysis induced hemorrhage, postsurgical hemorrhage and prevention of hemorrhage from cardiovascular instability after coronary artery bypass graft. It is an "inhibitor of plasminogen activation, and at much higher concentrations, a noncompetitive inhibitor of plasmin, i.e., actions similar to aminocaproic acid." It is similar to, but more potent than aminocaproic acid.[1] It is also used to treat acquired angioedema due to deficiency of complement C1 inhibitor protein.

Role in trauma medicine

The large multicenter CRASH-2 trial, in 2010, has shown striking mortality reductions after trauma and elective surgery after administration of tranexamic acid. [2] This was reflected in the new European guidelines.[3]

Mechanism of Action

Work in the CRASH trial is prompting reexamination of the broader clinical implications of antifibrinolysis. [4]

At low concentration, tranexamic acid, which binds to the kringle domain of plasminogen, is a competetive inhibitor of plasminogen activation into plasmin (fibrinolysin), an enzyme that degrades fibrin clots, fibrinogen, and procoagulant plasma proteins such as factor V and factor VIII. At higher concentrations it is a noncompetetive inhibitor of plasmin. It binds to the strong and weak receptor sites of plasminogen with affnities about 10 times greater than aminocaproic acid.


  1. Anonymous. cyklokapron (tranexamic acid) injection, solution. U.S. National Library of Medicine. Retrieved on 2009-02-19.
  2. CRASH-2 trial collaborators* (June 15, 2010), "Effects of tranexamic acid on death, vascular occlusive events, and blood transfusion in trauma patients with significant haemorrhage (CRASH-2): a randomised, placebo-controlled trial", Lancet, DOI:10.1016/S0140-6736(10)60835-5
  3. Rolf Rossaint; Bertil Bouillon; Vladimir Cerny; Timothy J Coats; Jacques Duranteau; Enrique Fernández-Mondéjar; Beverley J Hunt; Radko Komadina; Giuseppe Nardi; Edmund Neugebauer; Yves Ozier; Louis Riddez; Arthur Schultz; Philip F Stahel; Jean-Louis Vincent; Donat R Spahn (2010), "Management of Bleeding Following Major Trauma: An Updated European Guideline", Crit Care. 14 (2): R52
  4. Levy, JH (2010), "Antifibrinolytic therapy: new data and new concepts", Lancet