ZyVersa Therapeutics Announces Article Published in Peer-Reviewed Biomedical Journal Demonstrating That NLRP3 Inflammasome Inhibition Attenuates Inflammatory Bowel Disease Symptoms in Animal Model

• Inflammatory bowel disease (IBD) is a chronic inflammatory disease of the gastrointestinal tract affecting 1 in 100 Americans (around 2.4 million people) that can lead to disabling bowel symptoms and progressive bowel damage.
  
• Study provides direct evidence that NLRP3 signaling is over-activated in IBD, and that its inhibition attenuates intestinal inflammation and tissue damage, leading to significant improvements in IBD symptoms, and restoration of normal intestinal microbial flora.
• ZyVersa is developing Inflammasome ASC Inhibitor IC 100 which can inhibit up to 12 different inflammasomes (including NLRP3 inflammasomes) and their associated ASC specks which perpetuate damaging inflammation.
  

WESTON, Fla., Nov. 09, 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 publication of an article in the peer-reviewed Biomedical Journal demonstrating that inhibiting NLRP3 inflammasomes in an IBD animal model attenuates intestinal inflammation and tissue damage, leading to significant improvements in IBD symptoms, and restoration of normal intestinal microbial flora.

In the paper titled, “Inhibition of NLRP3 attenuates sodium dextran sulfate-induced inflammatory bowel disease through gut microbiota regulation,” the authors evaluated human colon biopsy samples from patients with IBD and healthy controls, and conducted a study in an IBD mouse model. Following are key findings reported in the paper:

• NLRP3 and IL-1β expression is increased in the colon of IBD patients.
• NLRP3 inhibition in the IBD animal model:
  
  • Inhibited NLRP3 inflammasome signaling in the colon, resulting in significantly reduced levels of the pro-inflammatory cytokines IL-1b, IL-6, and TNF-α.
  • Alleviated severe diarrhea and significantly improved IBD symptoms, based on the disease activity index score.
  • Attenuated histopathological changes indicative of tissue damage (goblet cell reduction, crypt destruction, and epithelial barrier disruption).
  • Restored gut microbiota to normal.

The authors stated, “In conclusion, this study provides direct evidence that NLRP3 signaling is over-activated in IBD patients. The inhibition of NLRP3 reverses the IBD-like symptoms in DSS-induced mice, which the regulatory effects on gut microbiota might mediate. Overall, this present study provides a basis for the clinical application of NLRP3 as a target for IBD treatment.” To read the article, Click Here.