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Novartis to acquire IFM Tre
BOSTON—IFM Therapeutics (IFM) announced today that it has reached a definitive agreement with Novartis, under which Novartis will acquire all of the outstanding capital stock of IFM Tre, a subsidiary company of IFM. Upon the closing of the agreement, IFM will receive $310 million in upfront payments and will be eligible for up to $1.265 billion in milestone payments.
“Based on substantial pre-clinical and translational data, we believe NLRP3 inhibition represents a novel approach to preventing the overactive inflammation that drives the onset and progression of numerous metabolic, fibrotic, autoimmune and neurological diseases,” noted Gary D. Glick, Ph.D., chief executive officer and co-founder of IFM Therapeutics. “With Novartis we have identified a partner that shares our conviction in the potential of this approach, and who has deep expertise bringing inflammatory and autoimmune disease therapeutics to market.
The acquisition will give Novartis full rights to IFM Tre’s portfolio of NLPR3 antagonists, which consists of one clinical and two pre-clinical programs: IFM-2427, a first-in-class clinical stage systemic antagonist for an array of chronic inflammatory disorders including atherosclerosis and nonalcoholic steatohepatitis (NASH); a pre-clinical stage gut-directed molecule for the treatment of inflammatory bowel disease; and a pre-clinical stage central nervous system (CNS)-penetrant molecule.
NLRP3 (NOD-, LRR- and pyrin domain-containing 3) is an intracellular innate immune signaling receptor that allows immune cells to detect the presence of pro-inflammatory foreign or endogenous molecules that signal infection, tissue damage or metabolic derangements. These conditions trigger the assembly of a multi-protein complex called an inflammasome, which initiates an immune response.
Abnormal or chronic activation of the NLRP3 inflammasome is known to cause negative downstream effects, and the onset and progression of numerous diseases. IFM Tre’s programs are said to target the innate immune system by suppressing only the inflammation mediated by the NLRP3 pathway, leaving other immune pathways unsuppressed and free to produce inflammatory responses to confront harmful pathogens.
“We look forward to collaborating with Novartis, while continuing to develop programs that target other components of the innate immune system through IFM Due and the broader IFM enterprise,” Glick added.
Novartis and IFM anticipate the transaction will close during the second quarter of 2019.