Haemophilia A and B are inherited bleeding diatheses caused by a deficiency of coagulation protein factor VIII (FVIII) and factor IX (FIX), respectively. In vitro clot-based assays are predominantly used to measure plasma FVIII and FIX activity and to describe disease phenotype as severe (<1%), moderate (1–5%) or mild (6–40%).¹ Although the clinical phenotypes of both haemophilia A and B are similarly classified based on FVIII and FIX activity levels, there are significant differences in the biochemical properties of the vitamin-K-dependent FIX protein that differentiates its role in haemostasis.^2, 3 A growing body of evidence suggests that the unique extravascular distribution of FIX may contribute to variations in the pharmacokinetic profile, bleeding phenotypes and response to factor replacement observed clinically in patients with haemophilia B in contrast to FVIII in haemophilia A.⁴