NEK7-IN-2
NEK7-IN-2 is a NEK7 inhibitor. NEK7-IN-2 increases the thermal stability of NEK7, disrupts the NEK7-NLRP3 interaction, inhibits NLRP3 inflammasome assembly, and suppresses the release of IL-1β (with an IC50 of 0.048 μM against IL-1β). NEK7-IN-2 can be used for the research of inflammatory diseases.
For research use only. We do not sell to patients.
- CAS No.: 3103731-64-9
- Formula: C27H28F4N6O2
- Molecular Weight:544.54
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Storage:
Please store the product under the recommended conditions in the Certificate of Analysis.
Biological Activity
Description
IC50 & Target
[1]|
IL-1β 0.048 μM (IC50) |
NEK7 |
NLRP3 |
In Vitro
NEK7-IN-2 (Compound 23) (0.1 μM; 2-4 h) potently inhibits IL-1β release in mouse bone marrow-derived macrophages with an IC50 of 0.048 μM and low cytotoxicity, achieving a high selectivity index of 80.32[1].
NEK7-IN-2 (compound 23) binds directly to NEK7 in mouse bone marrow-derived macrophages, increasing the protein's thermal stability[1].
NEK7-IN-2 (compound 23) blocks the interaction between NLRP3 and NEK7 in mouse bone marrow-derived macrophages, inhibiting NLRP3 inflammasome assembly[1].
NEK7-IN-2 (compound 23) binds to NEK7 (PDB: 6s76) via critical interactions with residues including R121, which disrupts the NLRP3-NEK7 interaction interface[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:mouse bone marrow-derived macrophages (BMDMs)
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Concentration:0.1 μM (IL-1β inhibition assay; cytotoxicity assay); dose-dependent concentrations (IC50/CC50 determination)
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Incubation Time:2 h (IL-1β inhibition assay); 4 h (cytotoxicity assay)
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Result:Inhibited IL-1β release by 90.26%.
Maintained 98.33% cell viability.
Exhibited an IL-1β inhibition IC50 of 0.048 μM and a cytotoxicity CC50 of 3.842 μM, resulting in a selectivity index (SI) of 80.32.
Chemical Information
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CAS No. 3103731-64-9
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Molecular Weight 544.54
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Formula C27H28F4N6O2
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SMILES
FC1=C(NC(NC2=CC(C(F)(F)F)=C(CN3CCN(C)CC3)C=C2)=O)C=CC(C4=CC=C(NC(C)=O)N=C4)=C1
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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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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)