nlrp3 in 2

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.

NLRP3 AIM2-IN-2 is a novel potent inhibitor with different species-specific effects on NLRP3 and AIM2 inflammasome dependent pyroptosis with IC50 of 0.2392 ± 0.0233 μ M.

NLRP3-IN-NBC6 is a potent, selective NLRP3 inflammasome inhibitor with an IC50 of 574 nM. It acts independently of Ca 2+ and inhibits Nigericin-induced inflammasome activation in THP-1 cells, as well as Imiquimod-induced IL-1β release from LPS-primed bone marrow-derived macrophages (BMDMs) [1].

Lobeglitazone Sulfate(CKD-501 Sulfate) is a novel thiazolidinedione with anti-inflammatory activity that inhibits LPS-induced NLRP3 inflammasome activation and hepatic inflammation, and can be used in the study of type 2 diabetes mellitus (T2DM).

TNKS-2-IN-1 is a TNKS-2 inhibitor.TNKS-2-IN-1 inhibits TNKS-1 and TNKS-2 with IC50s of 259 nM and 1100 nM, respectively.TNKS-2-IN-1 has antimicrobial activity against E. coli and S. aureus.TNKS-2-IN-1 inhibits the release of IL-1β from the NLRP3 inflammasome (IC50: 5 μM) by inhibiting IL-1β release from ATP-stimulated J1A.774 cells.

NLRP3-IN-64 (Compound 2) is an inhibitor of NLRP3, effectively suppressing its activation with an EC50 of 5 nM.

NEK7-IN-2 (compound 23) is a potent inhibitor of the NLRP3-NEK7 interaction. It enhances the thermal stability of NEK7 and modulates the assembly of the NLRP3 inflammasome. Additionally, NEK7-IN-2 inhibits the release of IL-1β.

NLRP3-IN-69 (Compound 23) inhibits the activation of NF-κBp65 and the formation of the NLRP3 inflammasome. It suppresses the overexpression of IL-1β, iNOS, and COX-2 induced by LPS, and inhibits the production of NO (IC50=5.66 μM), thereby demonstrating anti-inflammatory activity.

NLRP3-IN-72 (Compound 2) is a benzimidazole derivative. It exhibits anti-inflammatory and antioxidant properties, with an IC50 of 0.3 μM for NLRP3 IL-1β, a PD50 of 0.4 μM for protection against cell pyroptosis, and an EC50 of 0.6 μM for inducing HO-1.

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].

NLRP3-IN-8 (compound 27), an orally active NLRP3 inflammasome inhibitor, directly binds to its target with an IC50 of 1.23 μM for IL-1β inhibition. It demonstrates robust metabolic stability in liver microsomes (t1 2 = 138.63 min) and exhibits minimal toxicity (against L02: IC50 > 100 μM) [1].

1. Ruscogenin has anti-inflammatory activity, suppressed zymosan A-evoked peritoneal total leukocyte migration in mice in a dose-dependent manner, 2. Ruscogenin inhibited adhesion of leukocytes to a human umbilical vein endothelial cell line (ECV34) injured by tumor necrosis factor-alpha (TNF-alpha) in a concentration-dependent manner. 3. Ruscogenin significantly attenuate LPS-induced acute lung injury via inhibiting expressions of TF and iNOS and NF-kappa B p65 activation.

Peptide5 TFA, a connexin 43 mimetic peptide, mitigates swelling, astrogliosis, and neuronal cell death in animal models of spinal cord injury, and suppresses the NLRP3 inflammasome, functioning as an anti-inflammatory agent (1) (2) (3).

Oxidized ATP trisodium salt (oATP) is a broad-spectrum P2 receptor inhibitor that irreversibly antagonizes P2X7R activation and inhibits CRP-induced NLRP3 inflammasome activation, making it useful in atherosclerosis research [1] [2].

CYP51 PD-L1-IN-1 (compound L11), a quinazoline with antifungal properties, inhibits CYP51 (IC50: 0.884 μM) and PD-L1 (IC50: 0.083 μM), induces early apoptosis in the fungal cell cycle, decreases intracellular IL-2, NLRP3, and NF-κBp65 protein levels, causes mitochondrial damage and ROS accumulation, leading to fungal lysis and cell death [1].

CYP51 PD-L1-IN-2 (compound L20), a quinazoline with antifungal properties, is a potent dual inhibitor targeting both CYP51 (IC50: 0.263 μM) and PD-L1 (IC50: 0.017 μM). The compound promotes early apoptosis in the fungal cell cycle, diminishes intracellular proteins IL-2, NLRP3, and NF-κBp65, causes mitochondrial damage and ROS build-up, leading to fungal cell lysis and death [1].

CYP51 PD-L1-IN-3 (compound L21), a quinazoline with antifungal properties, serves as a dual inhibitor targeting CYP51 (IC50: 0.205 μM) and PD-L1 (IC50: 0.039 μM). This compound promotes early fungal apoptosis, diminishes intracellular concentrations of IL-2, NLRP3, and NF-κBp65 proteins, incites mitochondrial impairment and ROS accumulation, and culminates in fungal cell lysis and death [1].

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