Medgenics said today it will team up with Kyowa Hakko Kirin to develop and commercialize the Japanese biopharma’s KHK252067 for severe pediatric-onset inflammatory bowel disease (IBD) in return for an option to license the Phase II–ready candidate.
The value of the collaboration was not disclosed.
Medgenics said it plans to initiate a signal finding study testing the drug in severe pediatric-onset IBD with Robert Baldassano, M.D., director of the Center for Pediatric IBD at The Children's Hospital of Philadelphia (CHOP).
Upon completion of the study, Medgenics will have an option to license rights to develop the program. Should it agree to exercise the option, Medgenics has agreed to make a one-time, upfront payment in the low single-digit millions to Kyowa Hakko Kirin.
Kyowa Hakko Kirin has agreed in return to select one of two potential collaboration structures—a co-development/co-commercialization partnership or a licensing arrangement. Medgenics will have commercialization rights in the U.S. and Canada in both structures and will also add commercialization rights in Europe if Kyowa Hakko Kirin selects the licensing arrangement.
Kyowa Hakko Kirin will have commercialization rights in the rest of the world under both structures, as well as Europe in the co-development/co-commercialization structure. Terms for both structures have been preagreed and include a combination of royalties and profit-sharing.
KHK252067 is an anti-LIGHT monoclonal antibody designed to treat IBD and potentially other autoimmune diseases. The anti-LIGHT monoclonal antibody binds the proinflammatory cytokine LIGHT (ligand for herpesvirus entry mediator), which is believed to be a major contributor to the chronic relapsing inflammation of autoimmune diseases that include IBD.
Normally LIGHT is bound to and downregulated by DcR3. But research by Hakon Hakonarson, M.D., Ph.D., and colleagues at CHOP’s Center for Applied Genomics (CAG) has shown that many children with pediatric IBD and other autoimmune diseases have loss-of-function mutations in a specific immune regulatory protein, decoy receptor 3 (DcR3). That may allow LIGHT and other proinflammatory molecules to intensify inflammation chronically, which can lead to severe illness and complications, the researchers reason.
The anti-LIGHT monoclonal antibody is designed to bind LIGHT and could replace some of the function of DcR3 in these children, Medgenics said.
