NLRP3-IN-12
NLRP3-IN-12 is a specific NLRP3 inflammasome inhibitor. NLRP3-IN-12 reduces the release of IL-1β by targeting the NLRP3 protein, with an IC50 of 0.45 μM. NLRP3-IN-12 can be used for the research of inflammatory bowel disease.
For research use only. We do not sell to patients.
- Formula: C27H32ClNO7
- Molecular Weight:518.00
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Storage:
Please store the product under the recommended conditions in the Certificate of Analysis.
To place orders, for customer services and technical support, please contact: MedChemExpress USA
Tel: 609-228-6898 E-mail: [email protected] [email protected]
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Biological Activity
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Chemical Information
- Protocols
- Purity & Documentation
- References
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Help & FAQs
Biological Activity
Description
IC50 & Target
NLRP3 inflammasome[1]
In Vitro
NLRP3-IN-12 (compound 6E) (0.5-2 μM; pretreated for 1 h) inhibits LPS/ATP-stimulated expression of cleaved caspase-1 and IL-1β in THP-M cells[1].
NLRP3-IN-12 (2 μM) inhibits GSDMD-mediated pyroptosis in THP-M cells[1].
NLRP3-IN-12 (1 μM) exhibits the half-life (T1/2) are 53.4 min and 31.8 min in human and rat liver microsomes, respectively[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:THP-M cells
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Concentration:0.5, 1, 2 μM
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Incubation Time:Pretreated for 1 h, then stimulated with LPS (1 μg/mL) for 4.5 h, and ATP (5 mM) for 0.5 h.
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Result:Reduced the secretion of IL-1β and caspase-1.
Had no effect on the levels of NLRP3, pro-IL-1β, ASC, pro-caspase 1, p65, p-p65, IκBα, and p-IκBα.
In Vivo
NLRP3-IN-12 (20 mg/kg; i.v.) exhibits the half-life (T1/2) is 6.64 h, elimination rate constant (Kel) is 0.107 h, clearance rate (CL) is 105 mL/kg/min and steady-state apparent volume of distribution (Vdss) is 23.1 L/kg in rats[1].
MedChemExpress (MCE) has not independently confirmed the accuracy of these methods. They are for reference only.
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Animal Model:C57BL/6 mice were induced acute colitis by drinking 3% DSS (dextran sulfate sodium)[1]
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Dosage:5, 10 mg/kg
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Administration:Intraperitoneal injection daily for 10 days in aqueous solution containing DMSO/0.5% CMC-Na/normal saline
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Result:Attenuated DSS-induced weight loss, loose stools, bloody stools, shortened colons, increased disease activity index score, and lower survival rate.
Chemical Information
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Molecular Weight 518.00
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Formula C27H32ClNO7
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SMILES
O[C@@H]1[C@]2(CO3)[C@@]([C@H](O)[C@]3(O)[C@]45[C@@]2([H])CC[C@](C(C5=O)=C)([H])[C@@]4([H])OC(NC6=CC=CC(Cl)=C6)=O)([H])C(C)(C)CC1
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Shipping
Room temperature in continental US; may vary elsewhere.
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Storage
Please store the product under the recommended conditions in the Certificate of Analysis.
Protocols
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Cell Cytotoxicity Assay
Cytotoxicity assays are usually based on the assessment of cell membrane damage, which can also be indirectly detected by measuring cell viability. Detection methods include MTT assay, CKK-8 assay, LDH assay and ATP assay, etc.
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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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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
Purity & Documentation
References
Calculators
Concentration (start) × Volume (start) = Concentration (final) × Volume (final)
NLRP3-IN-12 Related Classifications
HY-151952 Related Classifications
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