ZyVersa Therapeutics, Inc. announced that renowned inflammasome researchers from the University of Miami Miller School of Medicine and inventors of Inflammasome ASC Inhibitor IC 100 have published a scientific paper in the peer-reviewed journal, Pharmaceuticals, highlighting how inflammation in the brain mediated by traumatic injury can trigger inflammation in the heart. Neural?Cardiac Inflammasome Axis after Traumatic Brain Injury- the authors conducted a study in animal models of TBI and evaluated serum from patients following TBI and from healthy controls. Data indicate that pyrin inflammasome-mediated inflammation induced by TBI contributes to cardiovascular co-morbidities through systemic release of proinflammatory mediators that activate AIM2 inflammasomes in the heart leading to damaging inflammation.

The role of inflammasome activation in the development of TBI-induced cardiovascular co-morbidities was substantiated by increased ASC speck formation in the brains and hearts of TBI mouse models. IC 100 is a novel humanized IgG4 monoclonal antibody that inhibits the inflammasome adaptor protein ASC. IC 100 was designed to attenuate both initiation and perpetuation of the inflammatory response.

It does so by binding to a specific region of the ASC component of multiple types of inflammasomes, including NLRP1, NLRP2, NLRP3, NLRC4, AIM2, Pyrin. Intracellularly, IC 100 binds to ASC monomers, inhibiting inflammasome formation, thereby blocking activation of IL-1ß early in the inflammatory cascade. IC 100 also binds to ASC in ASC Specks, both intracellularly and extracellularly, further blocking activation of IL-1ß and the perpetuation of the inflammatory response that is pathogenic in inflammatory diseases.

Because active cytokines amplify adaptive immunity through various mechanisms, IC 100, by attenuating cytokine activation, also attenuates the adaptive immune response.