nlrp3-in-10

NLRP3-IN-10 (ZVN26391) is a potent NLRP3 inhibitor. NLRP3-IN-10 inhibits IL-1β release with an IC50 value of 251.1 nM. NLRP3-IN-10 attenuates ASC speck formation, leading to suppress activation of NLRP3 inflammasome.

YM-I-26 is a selective inhibitor of the NLRP3 inflammasome. This compound enhances the phagocytic activity of β-amyloid in murine microglial BV2 cells and reduces the production of IL-1β and IL-10. YM-I-26 is useful for research into inflammation-related immunomodulatory activities.

NLRP3-IN-58 (Compound DS15) acts as an inhibitor of NLRP3 inflammasome activation, with an IC50 value of 3.85 μM, and is capable of inhibiting 33% of IL-1β release at a concentration of 10 μM.

N4-Acetylcytidine-13C5 is a 13C-labeled version of N4-acetylcytidine (N4A), an endogenous nucleoside metabolite produced from tRNA degradation. It is synthesized by enzymes such as N-acetyltransferase 10. N4-acetylcytidine may play a role in maintaining the activation of the NLRP3 inflammasome by inducing the expression and release of HMGB1. Additionally, it influences the stability and translation efficiency of mRNA, tRNA, and rRNA (e.g., enterovirus71RNA) through modification. This compound is utilized in studies related to cancer, neuroinflammatory diseases, viral infections, and obesity.

JC-171, a selective inhibitor of the NLRP3 inflammasome, effectively inhibits LPS/ATP-induced interleukin-1β (IL-1β) release from J774A.1 macrophages with an IC50 of 8.45 μM[1].

INF200 (compound 5), a sulfonylurea-based inhibitor of NLRP3 and associated pyroptosis, exhibits cardiometabolic benefits in a rat model of high-fat diet (HFD)-induced metaflammation and demonstrates anti-inflammatory effects by reducing IL-1β release in human macrophages at a concentration of 10 μM. Additionally, it enhances glucose and lipid profiles, diminishes systemic inflammation and cardiac dysfunction biomarkers, notably BNP, and ameliorates myocardial damage linked to ischemia/reperfusion injury (IRI) as assessed by hemodynamic parameters [1].

NLRP3-IN-22 (Compound II-4) is an NLRP3 inhibitor with a 67% inhibition rate at 10 μM [1].

NLRP3-IN-41 administered at doses of 40 and 80 mg/kg through intragastric (i.g.) delivery over a span of 10 days, successfully alleviated the symptoms of colitis induced by DSS in both C57BL/6 and ICR mice.

Kushenol I is a bioactive compound exhibiting anti-inflammatory, antioxidant, and ulcerative colitis–ameliorating effects, demonstrated in a DSS-induced UC mouse model where oral administration improved colon length, body weight, and disease scores while reducing pro-inflammatory cytokines including IL-1β, IL-6, IL-17, and TNF-α. Kushenol I increase IL-10 expression, inhibited key inflammatory signaling proteins such as AKT, p38 MAPK, PI3K, NLRP3, FOXO1, and TLR4, enhancing intestinal barrier integrity. Kushenol I positively modulate gut microbiota, and elevated splenic T-cell proportions, supporting therapeutic potential in inflammatory bowel disease.