Thrombosis and thrombo-inflammatory disorders are underlying pathologies associated with cardiovascular diseases (CVD) such as stroke and ischemic heart disease which collectively are the leading cause of death and disability globally.1 Despite the global burden of CVD, current therapeutic prevention and treatment strategies are inadequate. While the first-generation anticoagulants warfarin and heparin are still used in clinical settings, they are being phased out for many indications in favour of newly discovered direct oral anticoagulants (DOACs) that block the blood coagulation enzymes thrombin or FXa. DOACs have greater efficacy and simpler administration regimens than warfarin and heparin, but they still carry the risk of life-threatening bleeding side effects.2
FXII inhibitors have recently attracted significant attention as safer anticoagulants since their activity has been shown to prevent pathological thrombosis in animal models with a limited effect on haemostasis.3 Herein, we pioneer the use of Random Non-standard Peptide Integrated Discovery (RaPID) to source potent and selective macrocyclic peptide inhibitors of FXIIa.4 that demonstrate potent anticoagulation in a murine electrolytic injury model. Together, these results highlight the power of RaPID in sourcing novel modulators of enzymatic activity that when applied to FXIIa, may offer safer alternatives to anticoagulants in current use.