nlrp3 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-57 (compound 5) inhibits the NLRP3 inflammasome, consequently downregulating IL-1β levels in THP-1 macrophages induced by LPS+Nigericin.

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-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.

Carvedilol (SKF 105517) Phosphate is the phosphate salt form of carvedilol, a racemic mixture and adrenergic blocking agent with antihypertensive activity and devoid of intrinsic sympathomimetic activity. The S enantiomer of carvedilol nonselectively binds to and blocks beta-adrenergic receptors, thereby exerting negative inotropic and chronotropic effects, and leading to a reduction in cardiac output. In addition, both enantiomers of carvedilol bind to and block alpha 1-adrenergic receptors, thereby causing vasodilation and reducing peripheral vascular resistance.

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.

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.

NLRP3-IN-78 (compound 21) is an NLRP3 inhibitor with a 46.72% inhibition rate of GSDMD-induced pyroptosis at 5 μM. It binds to the NLRP3 protein and prevents GSDMD-NT oligomerization. Additionally, NLRP3-IN-78 inhibits GSDMD cleavage and upstream NF-κB signaling, demonstrating anti-inflammatory activity.

ADC-5 drug-linker is an ADC drug-linker conjugate (Drug-Linker Conjugates for ADC) known for its potent antitumor activity. Additionally, ADC-5 drug-linker serves a role in the synthesis of NLRP3 agonist3.

Sebrinoflast (Compound 5) is an NLRP3 inhibitor with an IC50 for hNLRP3 of ≤1 μM. It is utilized in the research of inflammatory and cardiovascular conditions (such as NASH and atherosclerosis), as well as neurological disorders (including Alzheimer's disease).

NLRP3-IN-82 (Compound 2b) is an NLRP3 inhibitor that significantly suppresses IL-1β release in HMDM cells with an IC50 of less than 5 nM. This compound is applicable for research into neurological disorders such as Alzheimer's disease, inflammatory conditions like inflammatory bowel disease, and metabolic disorders such as obesity.

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].

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].

NLRP3-IN-37 (Compound 23), an NLRP3 inhibitor (EC50: 5 nM), can be used for research on NLRP3-related conditions, including gout, pseudogout, CAPS, NASH fibrosis, heart failure, idiopathic pericarditis, atopic dermatitis, inflammatory bowel disease, Alzheimer's Disease, Parkinson's Disease, and traumatic brain injury [1].

Carvedilol-d4 is the deuterated form of Carvedilol. Carvedilol (BM 14190) acts as a non-selective β/α-1 receptor blocker and inhibits lipid peroxidation with an IC50 of 5 μM. It serves as a versatile antihypertensive agent with potential applications in research on angina and congestive heart failure. Furthermore, Carvedilol induces autophagy and inhibits the NLRP3 inflammasome.

Carvedilol-d5 is the deuterated form of Carvedilol, a non-selective β/α-1 receptor blocker. It inhibits lipid peroxidation with an IC50 of 5 μM. Carvedilol serves as a versatile antihypertensive agent, holding potential for research in angina and congestive heart failure. Additionally, it induces autophagy and inhibits the NLRP3 inflammasome.