nlr

NLRP3-IN-16 is a potent, selective inhibitor of the NLRP3 inflammasome, effectively reducing IL-1β release with an IC50 of 0.065 μM, and is primarily utilized in inflammation research [1].

NLRP3-IN-21 (compound L38) is an inhibitor of the NLRP3 inflammasome with anti-inflammatory properties, suppressing inflammasome activation and pyroptosis by inhibiting gasdermin D cleavage, ASC oligomerization, and NLRP3 inflammasome assembly [1].

NLRP3-IN-17 is a potent, selective, and orally active inhibitor of the NLRP3 inflammasome with an IC50 of 7 nM, effectively inhibiting NLRP3-dependent IL-1β secretion in mice, making it valuable for chronic inflammatory disease research [1].

JT001 (NLRP3-IN-19) is a potent, specific, and orally active NLRP3 inhibitor that impedes the assembly of the NLRP3 inflammasome, suppressing cytokine release and preventing pyroptosis. JT001 is utilized in research on nonalcoholic steatohepatitis and liver fibrosis [1].

NLRP3 agonist 2 (compound 22) is an orally active agent that activates Caspase-1 in THP1 cells [1].

NLRP3-IN-18, also known as compound 13, is a potent inhibitor of NLRP3, demonstrating an IC50 value of ≤1.0 µM [1].

NLRP3-IN-23 (Compound 15C) is an inhibitor that significantly impedes heme-mediated activation of the NLRP3 inflammasome at a concentration of 0.1 μM [1].

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

NLRP3-IN-20 (compound 11) is an orally administered inhibitor targeting the NLRP3 inflammasome, exhibiting potent inhibition with an IC50 of 25 nM against IL-1β secretion. It possesses excellent pharmacokinetic properties and has shown significant efficacy in models of non-alcoholic steatohepatitis, fatal septic shock, and colitis [1].

Nigericin sodium salt is an antibiotic, an NLRP3 activator, and a cationic ion carrier. Nigericin sodium triggers the activation of the NALP3 inflammasome, which inhibits Golgi function and suppresses the growth of Gram-positive bacteria.

Trimethylamine N-oxide (TMAO) is a colorless amine oxide produced from choline, betaine, and carnitine via intestinal microbial metabolism that accumulates in tissues of marine animals and prevents the protein-damaging effects of urea.Trimethylamine N-oxide induces inflammation through activation of ROS NLRP3 inflammasomes, which can induce fibroblast differentiation and cardiac fibrosis.

MCC950 sodium (CP-456773 sodium) is a potent and selective inhibitor of the inflammatory vesicle NLRP3 (IC50=7.5 nM in BMDMs; IC50=8.1 nM in HMDMs). MCC950 sodium has no effect on other inflammatory vesicles such as AIM2, NLRC4 or NLRP1.

TriDAP (L-Ala-γ-D-Glu-meso-diaminopimelic acid), a biologically active peptide, functions as a specific Nod1 activator.

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].

JC2-11 is an inhibitory compound for inflammation.JC2-11 inhibits the recruitment domain-containing proteins NLRC 4, atypical in melanoma 2 (AIM 2) and atypical (NC) inflammatory vesicles by disrupting reactive oxygen species (ROS) production and caspase-1 activity.JC2-11 reduces caspase-1 (p20) secretion, gasdermin D (GSDMD) cleavage, IL-1β and lactate dehydrogenase (LDH) activity in inflammatory vesicles. JC2-11 reduced caspase-1 (p20) secretion, gasdermin D (GSDMD) cleavage, IL-1β and lactate dehydrogenase (LDH) release from inflammatory vesicles.

Selnoflast (potassium) (example 6), is an NLRP3 inhibitor.

JT002 is an orally active NLRP3 inflammasome inhibitor that decreases the production of NLRP3-dependent proinflammatory cytokines (such as IL-1β, IL-1α, IL-18) and pyroptosis, as well as inhibits the formation of the NLRP3 inflammasome complex. Additionally, JT002 mitigates airway hyperresponsiveness and airway neutrophilia in mice [1].

iE-DAP is a biologically active peptide that functions as a NOD1 agonist.

JT001 (NLRP3-IN-19) sodium is a potent, specific, and orally active NLRP3 inhibitor that impedes NLRP3 inflammasome assembly, curbing cytokine release and averting pyroptosis. It is utilized in research focused on nonalcoholic steatohepatitis and liver fibrosis [1].

M-TriDAP (N-Acetylmuramyl-L-Ala-γ-D-Glu-meso-diaminopimelic acid) is a bioactive peptide that functions as a NOD1 2 agonist.

Selnoflast calcium (example 6), an NLRP3 inhibitor[1], is a chemical compound designed to suppress the activity of the NLRP3 inflammasome.

D359-0396, an orally active NLRP3 inflammasome inhibitor, mitigates pyroptosis and reduces IL-1β release in macrophages by inhibiting the oligomerization of NLRP3, ASC, and the cleavage of GSDMD. The compound is effective in alleviating Experimental Autoimmune Encephalomyelitis (EAE) and enhances survival following septic shock in mice [1].

Anti-neuroinflammation Agent 1 effectively modulates BV2 microglia cell polarization, shifting from an M1 to an M2 phenotype [1].

NLRP3 AIM2-IN-3 is a unique molecule that inhibits NLRP3 and AIM2 inflammasome activation in a species-specific manner. It has an IC50 value for cell lysis of 0.077 ± 0.008 μ M. NLRP3 AIM2-IN-3 is a potent inhibitor of NLRP3 and AIM2 inflammasome-dependent cell lysis with an IC50 value for cell lysis of 0.077 ± 0.008 μ M. NLRP3 AIM2-IN-3 inhibits LPS nigericin NLRP3 AIM2-IN-3 inhibits LPS nigericin-stimulated cell lysis in THP-1 macrophages with an IC50 value of 0.077 ± 0.008 μM. NLRP3 AIM2-IN-3 interferes with the interaction of NLRP3 or AIM2 with the bridging protein ASC, inhibiting oligomerization of ASC.