ZyVersa Therapeutics Announces Publication Reinforcing the Rationale for Inhibiting ASC with IC 100 to Potentially Attenuate Cardiac Comorbidities in Patients with Alzheimer’s Disease

• This publication, authored by leading experts in inflammasome-mediated inflammation and neurology at University of Miami Miller School of Medicine, demonstrates that multiple inflammasome triggers (NLRP1 and pyrin) govern the inflammatory response in Alzheimer’s Disease (AD), and that release of inflammasome laden extracellular vesicles (EV) into the blood induce significant inflammation in cardiovascular cells.
• ZyVersa is developing Inflammasome ASC Inhibitor IC 100 to inhibit multiple types of inflammasomes, including NLRP1 and pyrin, and their associated ASC specks that trigger damaging inflammation and its spread to surrounding tissues.
• AD, a progressive neurodegenerative disease affecting 6.7 million people in the US, is associated with many comorbidities, especially heart disease and stroke, resulting in increased morbidity and mortality.
  

WESTON, Fla., April 29, 2024 (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 acclaimed 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, Frontiers in Molecular Neuroscience, highlighting how inflammasome-mediated inflammation in Alzheimer’s disease can trigger inflammation in the heart.

The paper titled, “Extracellular vesicles mediate inflammasome signaling in the brain and heart of Alzheimer’s disease mice,” summarizes research evaluating serum and tissue cultures from an AD mouse model, and experiments of adoptive transfer of EV from AD patients into cardiovascular cells. Following is a summary of key findings:

• NLRP1, pyrin, caspase-1, and ASC were significantly elevated in the cortex of AD mice.
• In AD mice, there was a heightened level of inflammatory proteins circulating in the body via EVs containing an inflammasome protein cargo.
• Inflammasome activation was demonstrated in the heart of AD mice, associated with an increase in ASC oligomerization into specks.
• In adoptive transfer experiments, EVs released from AD patients induced significant inflammation in cardiovascular cells when compared to EVs from healthy individuals.

“Our data provide evidence that there is a neural-cardiac axis mediated by EVs in AD. Therefore, inflammasomes may provide a novel therapeutic target for the treatment of cardiac comorbidities in AD and beyond,” said Juan Pablo de Rivero Vaccari, Associated Professor of Neurological Surgery and The Miami Project to Cure Paralysis at the University of Miami.