Hemophilia A, characterized by impaired or absent expression of factor VIII, has 
long been managed via direct factor replacement. Functionally, factor VIII acts 
as a cofactor for factor IXa and allows activation of factor X, which, in 
combination with factor V, generates thrombin. Bispecific antibodies such as 
emicizumab are recombinant, monoclonal antibodies capable of recognizing and 
binding to two distinct antigenic targets simultaneously; emicizumab binds 
factors IXa and X, resulting in spatial approximation and activation of factor 
X, thereby mimicking the actions of factor VIII. Critically, the presence of 
antifactor VIII antibodies, for example, inhibitors, impacts neither the 
mechanism nor the efficacy by which emicizumab functions. The results and 
interim analyses of the emicizumab clinical trials, HAVEN 1, 2, 3, and 4, are 
additionally reviewed and discussed.