Tranexamic acid (TXA) is a widely used
antifibrinolytic agent that has been used since the 1960's to reduce blood loss in various conditions. TXA is a
lysine analogue that competes for the
lysine binding sites in
plasminogen and
tissue-type plasminogen activator impairing its interaction with the exposed
lysine residues on the
fibrin surface. The presence of TXA therefore, impairs the
plasminogen and tPA engagement and subsequent
plasmin generation on the
fibrin surface, protecting
fibrin clot from proteolytic degradation. However, critical
lysine binding sites for
plasmin(
ogen) also exist on other
proteins and on various
cell-surface receptors allowing
plasmin to exert potent effects on other targets that are unrelated to classical fibrinolysis, notably in relation to immunity and
inflammation. Indeed, TXA was reported to significantly reduce post-surgical
infection rates in patients after cardiac surgery unrelated to its haemostatic effects. This has provided an impetus to consider TXA in other indications beyond inhibition of fibrinolysis. While there is extensive literature on the optimal dosage of TXA to reduce
bleeding rates and transfusion needs, it remains to be determined if these dosages also apply to blocking the non-canonical effects of
plasmin.