nlrp-3-in-5

NP3-146 (NLRP3-IN-5) is an inflammasome NLRP3 inhibitor with potential anti-inflammatory activity for the study of autoimmune diseases.

NLRP3-IN-53 (compound 1) is an NLRP3 inhibitor with an IC50 of 3.4nM.

NLRP3-IN-51 (Compound 3q) is an effective activator of the cholinergic anti-inflammatory pathway (CAP). This compound demonstrates potential for treating gouty arthritis as it inhibits the production of IL-1β in THP-1 cells induced by monosodium urate (MSU). Furthermore, NLRP3-IN-51 suppresses the phosphorylation of NF-κBp65 triggered by MSU without impacting the self-cleavage and activation of NLRP3, pro-caspase 1, or the second messenger caspase-1. Therefore, the initial stage of NLRP3 inhibition by NLRP3-IN-51 occurs through the activation of CAP.

NLRP3-IN-56 (compound 062) is an inhibitor of NLRP3. It effectively suppresses the secretion of IL-1β in THP-1 cells, demonstrating an IC50 of 9.7 nM. NLRP3-IN-56 is useful for research into NLRP3-mediated symptoms and/or diseases.

NLRP3-IN-55 (Compound 19) is an effective inhibitor of NLRP3, exhibiting an inhibitory concentration (IC50) of 0.34 μM. It targets the NLRP3 protein directly with a dissociation constant (KD) of 0.45 μM, effectively blocking the assembly and activation of the NLRP3 inflammasome. This action results in anti-inflammatory effects and inhibits cell pyroptosis.

NLRP3-IN-54 (Compound C4) is an inhibitor of NLRP3. It effectively reduces the levels of active Caspase-1 and active IL-1β (IC50= 0.805 μM), making it useful for inflammation research.

NLRP3-IN-52 (compund 1) serves as an inhibitor of NLRP3.

NLRP3-IN-50 (compound SN3-1) is a potential inhibitor of NLRP3, offering therapeutic promise for inflammatory diseases.

NLRP3-IN-57 (compound 5) inhibits the NLRP3 inflammasome, consequently downregulating IL-1β levels in THP-1 macrophages induced by LPS+Nigericin.

NLRP3-IN-2 (5-Chloro-N-(p-sulfamoylphenethyl)-o-anisamide), an intermediate capable of synthesizing glibenclamide, exerts an inhibitory effect on the formation of NLRP3 inflammatory vesicles in cardiomyocytes, limiting infarct size after myocardial ischemia/reperfusion in mice and has no effect on metabolism.