NuP-3
NuP-3 is an orally active dual inhibitor of MAPK13 (IC50 < 250 nM), MAPK14 (IC50 = 7 nM), MAPK12 and MAPK11. NuP-3 blocks airway inflammation and mucus production. NuP-3 is used for the research of respiratory system diseases.
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- CAS No.: 2392969-05-8
- 화학식: C24H24ClFN4O3
- 분자량:470.92
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보관:
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
- Protocol
- 순도&문서
- References
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Help & FAQs
Biological Activity
제품 설명
In Vitro
NuP-3 (Compound 396) at 0.1 μM selectively inhibits MAPK13, MAPK14, MAPK11, and MAPK12; in a cell-free kinome screening, only 4% of the 400 tested kinases show an inhibition rate > 90%[1].
NuP-3 (21 days) potently inhibits MUC5AC production in primary human tracheobronchial epithelial cells stimulated by IL-13, with an IC50 of 0.005 nM within 21 days and a cell therapeutic index of 200000, indicating high safety[1].
NuP-3 (21 days) inhibits MUC5AC production in primary porcine tracheobronchial epithelial cells stimulated by IL-13, with an IC50 of 0.420 nM within 21 days and a cellular therapeutic index of 2381, indicating low toxicity[1].
NuP-3 (100 nM; 21 days) reduces IL-13-induced MUC5AC production in primary human tracheobronchial epithelial cells with MAPK gene knockout via CRISPR/Cas9[1].
MedChemExpress (MCE) has not independently confirmed the accuracy of these methods. They are for reference only. Further protocols information, click here.
In Vivo
NuP-3 (2 mg/kg; p.o.; twice daily; 24 days) blocks virus-induced airway mucus production in Yucatan mini-pigs[1].
NuP-3 (2 mg/kg; i.p.; twice daily) blocks virus-induced airway mucus production, epithelial reprogramming, and type 2 immune response in mice[1].
MedChemExpress (MCE) has not independently confirmed the accuracy of these methods. They are for reference only.
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Animal Model:Yucatan mini-pigs (male and female, 7-8 weeks of age, 21-25 kg, IL-13-challenged model)[1]
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Dosage:0.2 mg/kg; 2 mg/kg; 20 mg/kg
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Administration:p.o.; twice daily; 6 days
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Result:Significantly decreased BAL fluid levels of MUC5AC and CLCA1, and significantly reduced eosinophil and neutrophil influx into the airspace at 2 mg/kg compared to vehicle control.
Showed decreased anti-mucus and anti-inflammatory effects at 0.2 mg/kg and preserved effects at 20 mg/kg compared to vehicle control.
Observed no adverse effects (behavior, appetite, body weight, vital signs, gastrointestinal/urinary function, complete blood count) at any dose.
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Animal Model:Yucatan mini-pigs (male and female, 7-8 weeks of age, 21-25 kg, Sendai virus-infected model)[1]
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Dosage:2 mg/kg
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Administration:p.o.; twice daily; 24 days
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Result:Significantly attenuated SeV-induced increases in BAL fluid levels of MUC5AC and CLCA1 compared to vehicle control.
Did not alter viral titer or cause detectable adverse effects.
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Animal Model:Mice[1]
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Dosage:2 mg/kg
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Administration:i.p.; twice daily; 23 days (pre-infection); twice daily; 11 days (delayed post-infection)
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Result:Fully blocked SeV-induced increases in lung tissue Muc5ac, Clca1, Aqp3, Krt5, Trp63, Il33, Il13, and Arg1 mRNA levels compared to vehicle control when administered starting 2 days before infection.
Significantly attenuated the aforementioned mRNA levels compared to vehicle control when treatment was delayed until 10 days post-infection.
Did not affect mouse behavior, body weight, or clinical signs of infection.
Chemical Information
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CAS No. 2392969-05-8
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분자량 470.92
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화학식 C24H24ClFN4O3
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SMILES
O=C(NC1=CC(C(C)(C)C)=CC=C1Cl)NC2=CC=C(C=C2F)OC3=CC(NC(C)=O)=NC=C3
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선적
Room temperature in continental US; may vary elsewhere.
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보관
Please store the product under the recommended conditions in the Certificate of Analysis.
Protocol
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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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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
순도&문서
References
Calculators
Concentration (start) × Volume (start) = Concentration (final) × Volume (final)
NuP-3 Related Classifications
HY-186241 Related Classifications
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