Thrombosis is the pathology that underlies cardiovascular diseases, including venous thrombosis, heart attack and ischemic stroke.1 Collectively, these diseases are the leading cause of premature death and disability worldwide, superseding cancer.2-3Thrombosis is the abnormal formation of blood clots that restrict blood flow throughout veins and arteries, thereby starving surrounding tissues of life-sustaining oxygen and nutrients. The coagulant and inflammatory activities of contact-system plasma proteases, namely Factor XIIa (FXIIa), are implicated in thrombosis but considered dispensable for haemostasis. Inhibition of FXIIa has proven thrombo-protective in animal models and human deficiencies of the enzyme prolong activated thromboplastin time (aPTT) without inducing a bleeding phenotype.4-8 As such, FXIIa is a promising target for the development of safe anti-thrombotics. We have identified a series of potent and selective cyclic peptide inhibitors of FXIIa by application of Randomised Non-standard Peptide Integrated Discovery (RaPID), a modern form of mRNA display technology.9,10 These inhibitors were evaluated in vitro and two lead peptides demonstrated potent inhibition of intrinsic coagulation and the inflammatory cascade.