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IFM Therapeutics Announces Extension of Collaboration Agreement for cGAS-STING Subsidiary, IFM Due

Continued research and development collaboration is advancing immunotherapies that inhibit the cGAS-STING pathway to treat a range of serious inflammatory and autoimmune diseases

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IFM Therapeutics (IFM), a privately-held biopharmaceutical company focused on developing therapies that modulate novel targets in the innate immune system, today announced that IFM Due, an IFM subsidiary company, has extended its collaboration and exclusive option agreement with Novartis to develop immunotherapies that inhibit the cGAS-STING pathway to treat a range of serious inflammatory and autoimmune diseases.

Under the terms of the agreement that began in September 2019, Novartis will continue to make fixed payments sufficient to fully finance IFM Due’s research and development costs for the cGAS-STING program in exchange for the option to acquire the IFM Due subsidiary. Upon option exercise, IFM Due’s shareholders will be entitled to consideration in aggregate value of up to $840 million, including an upfront payment upon option closing and other contingent consideration.

“At IFM, we believe innate immune biology offers a multitude of genetically-validated, clinically-relevant targets and pathways across several therapeutic areas,” said H. Martin Seidel, Ph.D., CEO of IFM Therapeutics. “The continuation of our collaboration with Novartis underscores the value and relevance of this approach. By advancing novel therapies that selectively target the cGAS-STING pathway, we have the potential to deliver powerful therapeutic options for patients with serious chronic illnesses that, to-date, have not been adequately served by existing treatments.”

The cGAS-STING (cyclic GMP-AMP Synthase, Stimulator of Interferon Genes) pathway functions within the innate immune system to sense cytosolic DNA, which is a signal of cellular danger, and then triggers a STING-dependent inflammatory response. Mutations that activate this pathway can cause a variety of serious autoinflammatory and autoimmune diseases in humans that are characterized by excessive interferon/cytokine signaling, including rare diseases such as Aicardi-Goutières syndrome (AGS), STING-associated vasculopathy with onset in infancy (SAVI) and a subset of systemic lupus erythematosus (SLE). Aberrant cGAS-STING activation, such as in the setting of mitochondrial dysfunction, also underlies more common diseases such as nonalcoholic steatohepatitis (NASH), chronic obstructive pulmonary disease (COPD), age-related macular degeneration (AMD) and Parkinson’s disease.

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