NLRP3-IN-79
Based on 1 Customer Validation
NLRP3-IN-79 is an orally active NLRP3 inhibitor. NLRP3-IN-79 inhibits NLRP3 inflammasome with an IC50 of 10.69 nM. NLRP3-IN-79 blocks NLRP3 inflammasome assembly by directly binding to NLRP3 and disrupting the NEK7-NLRP3 interaction. NLRP3-IN-79 can be used for the study of NLRP3-driven diseases model, including systemic inflammation, peritonitis, and colitis.
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- Pureté : 99.10%
- CAS No.: 3088796-72-6
- Formule: C23H28N4O2
- Masse moléculaire:392.49
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Stockage:Powder -20°C, 3 years , 4°C, 2 years ; In solvent -80°C, 6 months , -20°C, 1 month
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Tel: 609-228-6898 E-mail: [email protected] [email protected]
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Activité biologique
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Chemical Information
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Solvant et solubilité
- Protocole
- Pureté et documentation
- Références
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Help & FAQs
Activité biologique
Description
IC50 & Target
[1]|
NLRP3 inflammasome 10.69 nM (IC50) |
NEK7 |
IL-18 |
IL-1β |
In Vitro
NLRP3-IN-79 (compound B6) (3-30 nM, 5 h 45 min) inhibits activation and assembly of NLRP3 inflammasome in Lipopolysaccharide (LPS) (HY-D1056) (100 ng/mL, 4 h) + Adenosine triphosphate (ATP) (HY-B2176) (5 mM, 45 min) induced human and bone macrophages[1].
NLRP3-IN-79 (3-30 nM, 1 h) blocks NLRP3 inflammasome assembly by disrupting NEK7-NLRP3 interaction in LPS (100 ng/mL, 4 h) + ATP (5 mM, 45 min) induced BMDMs[1].
NLRP3-IN-79 (0-500 μM, 20 h) has no significant hepatocellular toxicity in AML-12 and HL-7702[1].
MedChemExpress (MCE) has not independently confirmed the accuracy of these methods. They are for reference only. Further protocols information, click here.
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Cell Line:LPS + ATP induced HMDMs and BMDMs
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Concentration:3, 10, and 30 nM was applied to LPS-primed (100 ng/mL, 4 h) prior to ATP stimulation (5 mM, 45 min)
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Incubation Time:5 h 45 min
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Result:Markedly reduced the caspase-1 cleavage and IL-1β maturation.
Reduced secretion of IL-1β and IL-18.
Markedly reduced the caspase-1 cleavage and IL-1β maturation triggered by both nigericin and monosodium urate.
Reduced secretion of IL-1β and IL-18.
Inhibited formation of NLRP3/ASC/Pro-caspase-1 complexes.
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Cell Line:LPS + ATP induced BMDMs
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Concentration:3, 10, and 30 nM was applied to LPS-primed (100 ng/mL, 4 h) prior to ATP stimulation (5 mM, 45 min)
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Incubation Time:5 h 45 min
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Result:Attenuated ATP-induced ASC oligomerization.
Disrupted the interaction of NEK7-NLRP3 in a concentration-dependent manner.
In Vivo
NLRP3-IN-79 (5-20 mg/kg, i.p., once) mitigates Monosodium urate (MSU) (HY-B2130A)-induced peritonitis in C57BL/6 mice[1].
NLRP3-IN-79 (5-20 mg/kg, o.p., 10 days) markedly alleviates Dextran sulfate sodium salt (DSS) (HY-116282C)-induced colitis in female C57BL/6 mice[1].
MedChemExpress (MCE) has not independently confirmed the accuracy of these methods. They are for reference only.
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Animal Model:LPS (20 mg/kg, i.p., once) induced inflammatory model in female C57BL/6 mice (6-8 weeks, 18-20 g)[1].
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Dosage:5, 10, 20 mg/kg
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Administration:i.p., 1 h before LPS administration, blood samples were collected for detecting 2 h after LPS administration.
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Result:Reduced IL-1β production in both serum and peritoneal lavage fluid.
Reduced proportion of neutrophils in the peritoneal lavage fluids.
Ameliorated LPS-induced systemic inflammation in mice.
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Animal Model:MSU (30 mg/kg, i.p., once) induced inflammatory mode in female C57BL/6 mice (6-8 weeks, 18-20 g)[1].
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Dosage:5; 10; 20 mg/kg
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Administration:i.p., before MSU induction.
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Result:Inhibited infiltration of neutrophils in the peritoneal lavage fluid.
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Animal Model:DSS (2.8%, p.o., 10 days) induced inflammatory model in female C57BL/6 mice (6-8 weeks old, 18-20 g)[1].
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Dosage:5, 10, 20 mg/kg
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Administration:i.p., for 10 consecutive days.
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Result:Inhibited infiltration of neutrophils in the peritoneal lavage fluid.
Chemical Information
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CAS No. 3088796-72-6
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Appearance Solid
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Masse moléculaire 392.49
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Formule C23H28N4O2
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Color Light yellow to yellow
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SMILES
CCNC(N(CC1=CN=CC=C1)CC(NC2=C3C(CCC3)=CC4=C2CCC4)=O)=O
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Livraison
Room temperature in continental US; may vary elsewhere.
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Stockage
Powder -20°C 3 years 4°C 2 years In solvent -80°C 6 months -20°C 1 month
Solvant et solubilité
In Vitro:
DMSO : 100 mg/mL (254.78 mM; ultrasonic and warming and heat to 60°C; Hygroscopic DMSO has a significant impact on the solubility of product, please use newly opened DMSO)
Please refer to the solubility information to select the appropriate solvent. Once prepared, please aliquot and store the solution to prevent product inactivation from repeated freeze-thaw cycles.
Storage method and period of stock solution: -80°C, 6 months; -20°C, 1 month. When stored at -80°C, please use it within 6 months. When stored at -20°C, please use it within 1 month.
Please refer to the solubility information to select the appropriate solvent. Once prepared, please aliquot and store the solution to prevent product inactivation from repeated freeze-thaw cycles.
Storage method and period of stock solution: -80°C, 6 months; -20°C, 1 month. When stored at -80°C, please use it within 6 months. When stored at -20°C, please use it within 1 month.
Concentration (start) × Volume (start) = Concentration (final) × Volume (final)
Protocole
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LPS-Induced Endotoxemia/Systemic Inflammation
Lipopolysaccharide (LPS)-induced endotoxemia is a widely used in vivo model of acute systemic inflammation in which LPS, a Gram-negative bacterial endotoxin, activates innate immune signaling primarily through TLR4, leading to rapid and transient induction of pro-inflammatory cytokines such as TNF-α, IL-6, and IL-1β in circulation and tissues. This cytokine surge is commonly used as a measurable readout of systemic inflammatory activation and immune dysregulation, and is typically assessed within hours after intraperitoneal LPS administration in mouse models of endotoxemia. The model captures key features of systemic inflammatory response syndrome, including cytokine release, immune cell activation, and downstream tissue responses, and has been used to evaluate anti-inflammatory interventions such as cytokine modulation, lipid mediators, and immune cell-targeting therapies.
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DSS-Induced Colitis
Dextran sulfate sodium (DSS)-induced colitis is generated by administering DSS in mouse drinking water, producing epithelial injury, barrier disruption, weight loss, diarrhea, fecal blood, colon shortening, histologic mucosal damage, and inflammatory mediator changes; the model is mainly used to study acute or chronic intestinal inflammation resembling selected features of ulcerative colitis. DSS injury is interpreted through clinical and tissue readouts rather than a single molecular endpoint: daily body weight, stool consistency, and bleeding are combined into a disease activity index, while colon length, histology, cytokines, myeloperoxidase activity, intestinal permeability, and tight-junction markers provide complementary measures of inflammation and barrier damage.
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TNBS-Induced Colitis
TNBS-induced colitis is produced by intrarectal delivery of 2,4,6-trinitrobenzene sulfonic acid in ethanol, where ethanol disrupts the mucosal barrier and TNBS haptenates colonic proteins, generating immune-mediated colonic inflammation with weight loss, diarrhea, ulceration, transmural injury, inflammatory-cell infiltration, and cytokine responses. The model is used as an experimental intestinal inflammation model with Crohn’s disease–like features, especially when Th1-type responses, IL-12–dependent inflammation, chronic relapsing inflammation, or fibrosis-related endpoints are studied.
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Zymosan-Induced Peritonitis
Zymosan-induced peritonitis is a sterile acute-inflammation model produced by intraperitoneal injection of zymosan, a yeast cell-wall particle preparation, followed by quantification of leukocyte recruitment and soluble inflammatory mediators in peritoneal lavage fluid. Low-dose zymosan peritonitis is commonly used as a self-resolving acute inflammation model in which neutrophil recruitment occurs early and monocyte/macrophage accumulation follows later. The assay readouts include total peritoneal leukocyte number, differential neutrophil and monocyte/macrophage counts, peritoneal cytokines and chemokines, plasma or peritoneal exudation, and optional lipidomic or metabolomic changes during inflammation and resolution. Early neutrophil recruitment after zymosan depends strongly on complement and mast-cell C5a receptor signaling, whereas later monocyte recruitment is linked to MCP-1/CCL2 production.
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Research Protocol for Inflammation-related Diseases
The NLRP3 inflammasome is a cytosolic innate immune signaling platform that integrates priming signals and danger-signal activation to promote caspase-1 activation, maturation of IL-1β and IL-18, and gasdermin D-mediated pyroptotic cell death. The core experimental logic is to determine whether inflammatory disease phenotypes are driven by increased NLRP3 expression, ASC-containing inflammasome assembly, caspase-1 cleavage, GSDMD cleavage, and extracellular release of IL-1β/IL-18 rather than by nonspecific cell injury alone. The pathway is strongly linked to inflammation-related disease phenotypes because monosodium urate crystals activate NALP3/NLRP3 inflammasome signaling in gout-like crystal inflammation, cholesterol crystals activate NLRP3 inflammasomes in atherogenesis models, and DSS-induced intestinal inflammation has been reported to involve NLRP3 inflammasome activity. However, experimental colitis studies also show context-dependent protective effects of NLRP3 inflammasome co
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Pyroptosis Solutions
Pyroptosis is a lytic inflammatory cell-death pathway executed by gasdermin pores, most classically through inflammasome-mediated activation of caspase-1, cleavage of gasdermin D, membrane pore formation, LDH release, and secretion of IL-1β and IL-18. The canonical pathway is commonly modeled by priming cells with an inflammatory signal such as LPS to induce pro-IL-1β and inflammasome components, followed by an activation signal such as ATP or nigericin to activate NLRP3, ASC speck formation, caspase-1 cleavage, GSDMD cleavage, cytokine release, and pyroptotic membrane rupture. The non-canonical pathway is triggered when cytosolic LPS activates mouse caspase-11 or human caspase-4/5, leading to GSDMD cleavage and pyroptosis, and this can secondarily activate NLRP3-dependent IL-1β release. Pyroptosis is linked to inflammatory injury, infection, cancer, liver disease, ocular disease, placental inflammation, and other disease phenotypes, but unresolved questions include which gasdermin fam
Pureté et documentation
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Fiche technique (280 KB)
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SDS (251 KB)
- English - EN (251 KB)
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- Italian - IT (251 KB)
- Korean - KR (251 KB)
- Portuguese - PT (251 KB)
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Instruction de manipulation (2659 KB)
Références
Complete Stock Solution Preparation Table
Please refer to the solubility information to select the appropriate solvent. Once prepared, please aliquot and store the solution to prevent product inactivation from repeated freeze-thaw cycles.
Storage method and period of stock solution: -80°C, 6 months; -20°C, 1 month. When stored at -80°C, please use it within 6 months. When stored at -20°C, please use it within 1 month.
| Optional Solvent | Concentration Solvent Mass | 1 mg | 5 mg | 10 mg | 25 mg |
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| DMSO | 1 mM | 2.5478 mL | 12.7392 mL | 25.4784 mL | 63.6959 mL |
| 5 mM | 0.5096 mL | 2.5478 mL | 5.0957 mL | 12.7392 mL | |
| 10 mM | 0.2548 mL | 1.2739 mL | 2.5478 mL | 6.3696 mL | |
| 15 mM | 0.1699 mL | 0.8493 mL | 1.6986 mL | 4.2464 mL | |
| 20 mM | 0.1274 mL | 0.6370 mL | 1.2739 mL | 3.1848 mL | |
| 25 mM | 0.1019 mL | 0.5096 mL | 1.0191 mL | 2.5478 mL | |
| 30 mM | 0.0849 mL | 0.4246 mL | 0.8493 mL | 2.1232 mL | |
| 40 mM | 0.0637 mL | 0.3185 mL | 0.6370 mL | 1.5924 mL | |
| 50 mM | 0.0510 mL | 0.2548 mL | 0.5096 mL | 1.2739 mL | |
| 60 mM | 0.0425 mL | 0.2123 mL | 0.4246 mL | 1.0616 mL | |
| 80 mM | 0.0318 mL | 0.1592 mL | 0.3185 mL | 0.7962 mL | |
| 100 mM | 0.0255 mL | 0.1274 mL | 0.2548 mL | 0.6370 mL |
NLRP3-IN-79 Related Classifications
HY-174270 Related Classifications
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