Post-Bristol/Myers buyout, the IFM team lines up $31M to tackle a troika of NLRP3 targets
After years of lab work, the NLRP3 inflammasome has emerged as a prominent drug target in the biopharma world.
Just weeks after the UK’s NodThera launched to create new inhibitors for NLRP3, the team at IFM has rounded up $31 million to work on new drugs that could play a range of roles in fibrosis and errant immune responses linked to a medley of ailments, including neurodegenerative diseases.
Bristol-Myers snapped up IFM a year ago in a $2.3 billion deal, taking oncology assets from the deal but leaving CEO Gary Glick and his team free to pursue other assets, with a right to negotiate for anything else they might do with NLRP3. And the IFM team still has plenty of backing from Atlas Venture, Abingworth, Bristol-Myers Squibb and now IFM’s management.
The big idea here is that if you can tackle NLRP3 in the right way, you can also prevent the downstream development of pro-inflammatory cytokines IL-1 and IL-18, which trigger diseases. And the IFM team is developing drugs specifically for delivery to the central nervous system, the gut and the brain.
Their work has been heavily influenced by two key scientists, Eicke Latz and Luigi Franchi, who have spent years studying NLRP3.
“They have probably forgotten more about NLRP3 than the world knows,” says Glick. It’s their scientific work which is being married to the drug discovery activities at IFM in Boston.
IFM kept its staff in the wake of the Bristol-Myers deal, which centered on NLRP3 agonists for cancer. About 35 employees are on the payroll as they dive into this new work.
This is still a translational field for biotech to explore, but there are some interesting late-stage connections to consider regarding the IL-1 pathway. Novartis’ heart drug canakinumab is focused on that IL-1 inflammatory pathway, with Phase III data to prove that it can help at-risk cardio patients. That drug is still in late-stage development, with recent positive gout data of its own.
Glick notes, though, that moving upstream of IL-1 has a number of advantages, going after a specific target with different drugs focused on different points in the anatomy. And that could play well on safety, avoiding any unexpected consequences of IL-1 blockades.
It is worth noting that NLRP3 has been the focus of some limited amount of preclinical work regarding the ketogenic diet. A Yale investigator, Vishwa Deep Dixit, has done mouse work to illustrate a potential connection between the ketone beta-hydroxybuterate — which is produced when you move to a high-fat, low carb diet — and tamping down on NLRP3, seeing how that could influence the course of gout. And more work is underway.
You can expect to hear a lot more about NLRP3 in the coming years.