ZyVersa Therapeutics Announces New Peer-Reviewed Publication Reinforcing the Rationale for Inhibiting ASC Specks with IC 100 to Attenuate Spread of Inflammation into Surrounding Tissues

• The paper, published in Pharmaceuticals, demonstrates that pyrin inflammasome-mediated inflammation induced by traumatic brain injury (TBI) contributes to cardiovascular co-morbidities through systemic release of proinflammatory mediators that activate AIM2 inflammasomes in the heart leading to damaging inflammation.
• Marks the third publication in 2023 supporting the potential need to attenuate the spread of inflammation to surrounding tissues to minimize the potential for co-morbidities in certain diseases.
• ZyVersa is developing Inflammasome ASC Inhibitor IC 100 to inhibit multiple types of inflammasomes and their associated ASC specks that trigger damaging inflammation and its spread to surrounding tissues.
  
  

WESTON, Fla., Oct. 04, 2023 (GLOBE NEWSWIRE) -- ZyVersa Therapeutics, Inc. (Nasdaq: ZVSA, or “ZyVersa”), a clinical stage specialty biopharmaceutical company developing first-in-class drugs for treatment of inflammatory and renal diseases, announces that world 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.

In the paper titled, “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.

“A heightened systemic inflammatory response is often induced after TBI, but the underlying pathomechanisms that contribute to co-morbidities remain poorly understood. Here, we investigated whether extracellular vesicles (EVs) containing inflammasome proteins are released after severe controlled cortical impact in C57BL/6 mice and cause activation of inflammasomes in the heart that result in tissue damage,” said Dr. Robert W. Keane, Professor, Physiology and Biophysics, Neurological Surgery and Microbiology, and Immunology, University of Miami Miller School of Medicine. “TBI resulted in the release of EVs into the serum, which contain a cargo of inflammasome-, complement- and cardiovascular-related signaling proteins, and adoptive transfer of EVs from TBI patients resulted in inflammasome activation in cardiovascular cells.”

“Importantly, here, we also found an increase in ASC specks in the brain and the heart of TBI mice, suggesting that these prion-like ASC structures play a significant role in the inflammatory pathogenesis observed after TBI in the brain and systemically. Moreover, this finding emphasizes the potential benefit of therapies targeting ASC specks after CNS injury,” stated Dr. Juan Pablo de Rivero Vaccari, Associate Professor, Department of Neurological Surgery, University of Miami Miller School of Medicine. To review the paper, .

“This research published in the Journal, Pharmaceuticals, along with recent research published in the and reinforces the importance of attenuating extracellular propagation of IL-1β to minimize induction and perpetuation of inflammation in surrounding tissues and organs,” commented Stephen C. Glover, ZyVersa’s Co-founder, Chairman, CEO, and President. “ZyVersa’s Inflammasome ASC inhibitor IC 100 is designed to inhibit formation of multiple types of inflammasomes to attenuate initiation of the inflammatory cascade, and to inhibit their associated ASC specks to reduce perpetuation of damaging inflammation.”

To review a white paper summarizing the mechanism of action and preclinical data for IC 100, .

About Inflammasome ASC Inhibitor IC 100

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-1β early in the inflammatory cascade. IC 100 also binds to ASC in ASC Specks, both intracellularly and extracellularly, further blocking activation of IL-1β 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.

About ZyVersa Therapeutics, Inc.

ZyVersa (Nasdaq: ZVSA) is a clinical stage specialty biopharmaceutical company leveraging advanced, proprietary technologies to develop first-in-class drugs for patients with renal and inflammatory diseases who have significant unmet medical needs. The Company is currently advancing a therapeutic development pipeline with multiple programs built around its two proprietary technologies – Cholesterol Efflux Mediator™ VAR 200 for treatment of kidney diseases, and Inflammasome ASC Inhibitor IC 100, targeting damaging inflammation associated with numerous CNS and other inflammatory diseases. For more information, please visit .

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