JC-171 is a selective NLRP3 inflammasome inhibitor, with an IC50 of 8.45 μM for inhibiting LPS ATP-induced interleukin-1β (IL-1β) release from J774A.1 macrophages[1]. JC-171 (0-100 μM) blocks NLRP3 inflammasome activation and IL-1β production in primary macrophages dose dependently[1]. Cell Viability Assay[1] Cell Line: J774A.1 murine macrophage cells JC-171 treatment delays the progression and reduces the severity of experimental autoimmune encephalomyelitis (EAE) in mouse[1]. Animal Model: Mice immunized subcutaneously with 200 μg Myelin oligodendrocyte glycoprotein (MOG) 35-55 peptide emulsified in Complete Freund's Adjuvant (CFA) on day 0 followed by injection of 200 ng of pertussis toxin. [1]. Chunqing Guo, et al. Development and Characterization of a Hydroxyl-Sulfonamide Analogue, 5-Chloro-N-[2-(4-hydroxysulfamoyl-phenyl)-ethyl]-2-methoxy-benzamide, as a Novel NLRP3 Inflammasome Inhibitor for Potential Treatment of Multiple Sclerosis. ACS Chem Neurosci. 2017 Oct 18;8(10):2194-2201.
Pralnacasan inhibits proinflammatory cytokines IL-18, IL-1β , and IFN-γ. Pralnacasan is an effective, non-peptide, and orally active interleukin-1β converting enzyme inhibitor (Ki: 1.4 nM). Pralnacasan has the potential for osteoarthritis and rheumatoid a
17(S)-HDHA is a primary mono-oxygenation product of docosahexaenoic acid in human whole blood, human leukocytes, and mouse brain. 17(S)-HDHA serves as a precursor to 17(S)-resolvins and has intrinsic biological activity, such as the inhibition of TNF-α-induced interleukin-1β expression in human glioma cells and inhibition of TNF-α-induced leukocyte trafficking to the mouse air pouch.