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IFM Therapeutics Announces New Publication in Nature Reviews Drug Discovery Examining NLRP3 as a Target in Serious Inflammatory and Immune-Mediated Diseases

IFM Therapeutics
Posted on: 31 Jul 18

BOSTON, July 30, 2018 /PRNewswire/ -- IFM Therapeutics, LLC (IFM), a privately held biopharmaceutical company focused on developing therapies that modulate novel targets in the innate immune system, today announced the publication of a comprehensive review of current knowledge on NLRP3 inflammasome activation, pathogenesis and pharmacological interventions in Nature Reviews Drug Discovery. The work was co-authored by IFM co-founder Eicke Latz, M.D., Ph.D. and Matthew Mangan, Ph.D., both of the Institute of Innate Immunity at the University of Bonn, along with IFM's Gary D. Glick, Ph.D., William Roush, Ph.D., H. Martin Seidel, Ph.D., and Edward Olhava, Ph.D.

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 then initiates an immune response. While this response can be useful for fending off foreign pathogens, abnormal or chronic activation of the NLRP3 inflammasome is known to cause negative downstream effects and the onset and progression of numerous diseases.  

"Research has identified the NLRP3 inflammasome as a central receptor that mediates unrestricted systemic inflammation in many common inflammatory diseases that affect millions of people worldwide," said Eicke Latz, M.D., Ph.D., IFM co-founder and founder and director of the Institute of Innate Immunity, University of Bonn. "The growing body of literature about NLRP3's role in the pathogenesis of diseases validates it as a promising target for new therapies."

NLRP3 as a Drug Target

Abnormal activation of the NLRP3 inflammasome triggers the maturation and release of IL-1 and IL-18 as well as the release of other pro-inflammatory mediators, all of which are known to drive the onset of a range of auto-inflammatory and other serious, immune-mediated diseases ranging from Crohn's to cardiovascular to Alzheimer's disease. NLRP3 antagonists may offer broad therapeutic potential as a safer, more effective option for the treatment of these conditions by inhibiting only the inflammation mediated by the NLRP3 pathway, leaving other immune pathways intact and uninhibited to produce inflammatory responses to confront harmful pathogens.

"Opportunities for pharmacologically targeting NLRP3 with small molecules have recently advanced, thanks in large part to the discoveries of experts like Dr. Eicke Latz, Dr. Luigi Franchi and their colleagues, who have led transformative discoveries on the role of NLRP3 in health, disease and treatment," said Gary D. Glick, Ph.D., CEO and co-founder of IFM Therapeutics, LLC. "Through our subsidiary, IFM Tre, we look forward to advancing a broad pipeline of NLRP3 antagonists, with the goal of improving the lives of patients living with serious inflammatory diseases."

About IFM Therapeutics, LLC

IFM Therapeutics, LLC (IFM) is a privately held biopharmaceutical company based in Boston, Massachusetts. The company was founded by an international group of preeminent scientists and physicians who have spent decades understanding innate immunity and the role it plays in regulating the immune system. IFM's team has discovered and developed small molecules that modulate novel targets in the innate immune system as next-generation therapies for cancer, auto-immunity, and inflammatory disorders. IFM owns and operates IFM Tre, a subsidiary company launched in July of 2018 that is developing a suite of small-molecule antagonists targeting inappropriate inflammatory responses of the innate immune system via the NLRP3 pathway. For more information, please visit www.ifmthera.com.    

Editor's Details

Mike Wood
PharmiWeb.com
www.pharmiweb.com
editor@pharmiweb.com

Last updated on: 31/07/2018

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