What if chronic inflammation could be stopped at the source…

… before it had a chance to cascade into debilitating and deadly diseases like fibrosis, Alzheimer’s and cancer?

We believe it can be.

NLRP3 is the core subunit of an inflammasome platform that allows the immune system to detect “danger signals,” including foreign molecules derived from pathogens and endogenous molecules associated with tissue damage or metabolic imbalances. The NLRP3 inflammasome complex regulates the release of important pro-inflammatory cytokines, which function as key elements of the body’s innate immune response to infections and tissue injury. However, overactivation of the NLRP3 inflammasome can lead to a chronic state of inflammation that underlies a wide range of human diseases.

Inactive NLRP3
Assembly of activated NLRP3 into inflammasome
Inflammasome forms, triggering the release of cytokines

A rapidly growing body of research shows that selectively inhibiting the activation of the NLRP3 inflammasome can significantly attenuate inflammatory processes, without broadly suppressing the immune system. As our understanding of this pathway has grown, NLRP3 has emerged as one of the most promising therapeutic targets in immunobiology today.


Small molecule therapies have the potential to block the formation of inflammasomes, thereby preventing cytokines from being released and addressing chronic inflammation.