InflammX Technology

The NLRP3 inflammasome is a multiprotein innate immune complex that forms inside cells. The inflammasome pathway of inflammation is a relatively new discovery, first described in 2002. Since then it has become a major target for therapeutic intervention since inflammasome mediated inflammation has been shown to be a common pathway of pathology in multiple disease states. The inflammasome once activated results in the activation of multiple pro-inflammatory cytokines and downstream pathology to affected tissues. If not terminated, these dynamic immune responses contribute to long lasting inflammatory disease. Xiflam™ regulates upstream signaling and activation of the inflammasome, breaking the persistent inflammation that is a feature of the disease. 

Connexin43 (Cx43) hemichannels continuously form in the cell membrane of most of the organs of our body. They have one physiological function in life, which is to remain closed in the cell membrane until they dock with another Cx43 hemichannel on an adjoining cell. At this point both open to create the communication portal between cells called the Gap Junction.

In certain disease states, Cx43 hemichannels are over expressed, crowd the cell membrane and open prematurely. Prematurely open Cx43 hemichannels, facilitate the release of ATP into the extracellular space. The extracellular ATP signals the activation of the NLRP3 inflammasome resulting in a perpetuated cycle of inflammation. This cycle precipitates further release of ATP and activation of pro-inflammatory cytokines. This leads to inflammation. resulting in significant tissue damage including ischemia, microvascular leak, edema, microvascular dropout, and if left untreated, fibrosis.

 Xiflam™, breaks the cycle of inflammasome mediated inflammation, by closing prematurely open Cx43 hemichannels, preventing the release of extracellular ATP and the signal for continued inflammasome activation. Xiflam acts specifically to close pathologically open Cx43 hemichannels preventing continued signaling of the inflammasome. Due to this mechanism of upstream inhibition of inflammasome signaling, the inflammation is controlled and at the same time patients remain immunocompetent.