The acquisition will expand Celgene’s inflammation and immunology pipeline of potential next-generation medicines, including Delinia’s lead program, DEL106.
DEL106 is a potent and highly selective IL-2 mutein Fc fusion protein designed to augment regulatory T-cells (called Tregs), immune cells that are important to maintaining self-tolerance and immune system balance (homeostasis). IL-2 is a key Treg growth factor.
By activating and augmenting Tregs, a natural regulator of multiple arms of the immune response, DEL106 is intended to offer an alternative to immunosuppressive drugs in the treatment of SLE and other autoimmune diseases, like rheumatoid arthritis.
Patients given autologous Tregs infusions in early stage clinical trials showed significant signs that the treatment was effective, Delinia reported on its website, as did trials in which patients were treated with low-dose IL-2.
“Delinia is at the forefront of advancing new approaches to treating patients with severe and debilitating autoimmune diseases,” Rupert Vessey, FRCP, DPhil, president of R&D for Celgene, said in a press release. “We look forward to progressing DEL106 into the clinic next year.”
Under the terms of the agreement, Celgene will make an initial payment of $300 million to Delinia, and its shareholders will be eligible to receive up to $475 million more in contingent payments from Celgene, upon achieving certain milestones regarding the development, regulation and commercialization of potential products. The transaction is anticipated to close by April.
“We are delighted to enter into this transaction with Celgene,” said Saurabh Saha, MD, PhD, chief executive officer of Delinia. “Their expanding Inflammation and Immunology franchise … makes them an ideal company to continue to move DEL106 forward.”
Regulatory T-cells are a relatively small population of T-cells. The IL-2 pathway is critical for the production and function of regulatory T-cells; however, these cells do not produce their own IL-2 and are dependent on the IL-2 produced by other immune cells. This means that regulatory T-cells both interact closely with, and depend on, the immune cells they regulate.
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