ZymoGenetics Inc announced three agreements with Novo Nordisk A/S. ZymoGenetics licensed to Novo Nordisk exclusive development rights outside North America to patents covering Interleukin 28A (IL-28A), Interleukin 29 (IL-29) and Interleukin 31 (IL-31).

IL-28A and IL-29 show potential in providing immunity to viral infection, and Interleukin 31 (IL-31) is believed to play a role in stimulating cellular infiltration and inflammation.

All three licenses resulted from an existing option and license agreement between Novo Nordisk and ZymoGenetics, which was recently extended to November 2006. Under the terms of the agreements, Novo Nordisk will pay ZymoGenetics initial license fees along with potential milestone and royalty payments. Other financial details of the transactions were not disclosed.

"IL-28A, IL-29 and IL-31 demonstrate our continuing ability to discover novel proteins with the potential to save and transform lives," said Bruce L A Carter, president and CEO of ZymoGenetics. "As our focus has been to develop proteins for North American markets, our strategy is to partner with companies like Novo Nordisk that will commercialize proteins outside North America," he added.

ZymoGenetics identified the novel cytokine family containing Interleukins 28A and 29 from human genomic sequence. These interleukins, distantly related to both type I interferons (IFNs) and the IL-10 family, use a newly identified class II cytokine receptor, IL-28R. ZymoGenetics researchers found that like type I IFNs, IL-28A and IL-29 have antiviral activity and are induced by viral infection. The in vitro and in vivo biological activities of IL-28A and IL-29 suggest that this cytokine family may serve as an alternative to type I IFNs in augmenting the body's defenses against viral infection.

ZymoGenetics researchers discovered Interleukin 31 (IL-31) using the Company's genomics-based discovery platform. Current in vitro and in vivo data suggest that IL-31 may affect cellular infiltration and inflammation. Analysis of IL-31 and IL-31 receptor levels in human and murine disease tissues suggests that expression of IL-31, and/or its receptor, is significantly increased in the settings of inflammatory bowel disease, asthma and psoriasis. Further evidence suggests a potential role of IL-31 in the development of atopic dermatitis.