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-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-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].

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-25 (compound 32), an orally available NLRP3 inhibitor, exhibits anti-inflammatory properties by attenuating renal injury in a mouse model of doxorubicin-induced glomerulonephritis and inhibiting IL-1β secretion in THP-1 cells, with an IC 50 value of 21 nM [1].

NLRP3-IN-26 (compound 15Z), with an IC50 of 0.13 μM, functions as an inhibitor of NLRP3. It is applicable in studies involving the DSS-induced colitis model [1].

NLRP3-IN-27, a selective NLRP3 inhibitor with an IC50 of 0.55 μM, can be utilized in studies of inflammation and immunity [1].

NLRP3-IN-28 (compound N77) serves as a potent inhibitor of NLRP3, effectively blocking Nigericin-induced pyroptosis with an EC50 of 0.07μM. Additionally, it mitigates inflammatory reactions in vivo [1].

NLRP3-IN-29 (Compound 5M) is an inhibitor of NLR family pyrin domain containing 3 (NLRP3) with potential for blood-brain barrier permeability and inflammation inhibition both in vivo and in vitro. It can be used for research on Alzheimer's disease [1].

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].