ZyVersa Therapeutics announces publication of data on extracellular ASC

ZyVersa Therapeutics announces data published in the peer-reviewed journal, EMBO Molecular Medicine, demonstrating that extracellular ASC has a crucial role in aggregation and deposition of amyloid A fibrils leading to associated chronic inflammatory conditions. “This research highlighting the role of extracellular ASC specks, independent of IL-1beta, in the pathogenesis of chronic conditions associated with amyloid A amyloidosis reinforces our selection of ASC as a target for our inflammasome inhibitor IC 100,” stated Stephen C. Glover, ZyVersa’s Co-founder, Chairman, CEO, and President. “This paper provides one more piece of evidence that inhibiting extracellular ASC specks associated with multiple types of inflammasomes has potential to control damaging inflammation associated with a broad range of inflammatory diseases.” The paper titled, The ASC inflammasome adapter governs SAA-derived protein aggregation in inflammatory amyloidosis, summarizes data from in vitro and in vivo research investigating the role of ASC in inflammation-associated amyloidosis. Following is a summary of key findings: ASC colocalized tightly with SAA in human AA amyloidosis. ASC specks accelerated SAA fibril formation. Splenic amyloid load was decreased in a Pycard knock-out mouse model of AA Amyloidosis which lacks ASC. Treatment with anti-ASCPYD antibodies decreased amyloid loads in wild-type mice suffering from AA amyloidosis.