We have clinically validated HJV as a novel target for the treatment of anemia of inflammation (Papanikolaou et al., Nature Genetics, 36, 77-82, 2004), and demonstrated that this protein plays an important role in the regulation and availability of iron for efficient red blood cell production.

Xenon discovered HJV as the defective protein underlying the rare genetic disorder juvenile hemochromatosis. Patients with juvenile hemochromatosis are known to have depleted macrophage iron stores and a hyperabsorption of dietary iron; these features are in stark contrast to the pathophysiology of the common disorder of anemia of inflammation (AI). The cardinal features of AI are macrophage iron retention and decreased dietary iron absorption, which result in reduced iron availability for normal red blood cell production leading to anemia.

Anemia of inflammation is the second most common form of anemia and is an acquired disorder associated with a variety of conditions including infections, cancer and chronic inflammation. The current treatment option for AI comprises erythropoietin which serves to promote red blood cell production, but does not address the maldistribution of iron. HJV represents a novel target that when inhibited may reverse the iron disturbances observed in AI and thereby promote red blood cell production with or without erythropoietin.

We have licensed select protein rights to Roche for development and commercialization of protein-based inhibitors of HJV.