It is genomically related to the family of multicopper oxidases, and is homologous to coagulation factor VIII.

The gene spans 70 kb, consists of 25 exons, and the resulting protein has a relative molecular mass of approximately 330kDa.

Factor Va is degraded by activated protein C, one of the principal physiological inhibitors of coagulation.

The most common one of these, factor V Leiden, is due to the replacement of an arginine residue with glutamine at amino acid position 506 (R506Q).

[12] The suggestion that an additional factor might exist was made by Paul Owren [no] (1905–1990), a Norwegian physician, during his investigations into the bleeding tendency of a lady called Mary (1914–2002).

She had suffered from nosebleeds and menorrhagia (excessive menstrual blood loss) for most her life, and was found to have a prolonged prothrombin time, suggesting either vitamin K deficiency or chronic liver disease leading to prothrombin deficiency.

Using Mary's serum as index, he found that the "missing" factor, which he labeled V (I–IV having been used in Morawitz' model), had particular characteristics.

[14] In 1994 factor V Leiden, resistant to inactivation by protein C, was described; this abnormality is the most common genetic cause for thrombosis.