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The flip-side of immunotherapy

How immuno-oncology targets are spawning new therapies for inflammation

In the smaller print of last week’s deal between IFM Therapeutics Inc. and Bristol-Myers Squibb Co. was the latest example of a growing trend of companies aiming to draw extra value out of a cancer target by using its opposite activity to treat autoimmunity.

The deal was noted mostly for its dollar value; BMS acquired two preclinical programs from IFM that stimulate the innate immune system targets NLRP3 and STING for cancer, for an upfront payment of $300 million and up to $1 billion in milestones per program.

But the biotech also spun out IFM Therapeutics LLC to develop the remaining assets, which include a preclinical antagonist of NLRP3 for inflammatory disease and fibrosis. That could lead the company not only into autoimmunity, but to non-alcoholic steatohepatitis (NASH) as well.

NLR proteins detect cellular threats by recognizing pathogen-associated molecular patterns (PAMPs) or damage-associated molecular patterns (DAMPs), and can then change shape to form an inflammasome and trigger inflammatory processes. Other members of the family pursued by IFM include NLRP1, NLRP3, NLRP6, NLRP10 and NLRC4.

According to IFM CEO Gary Glick, the advantage of this target is that it has been researched for both diseases. “What’s great about NLRP3 in particular is that

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