
EMT inhibitor-1
CAS No. 1638526-21-2
EMT inhibitor-1( —— )
Catalog No. M26197 CAS No. 1638526-21-2
EMT inhibitor -1 is an inhibitor of Hippo, Wnt signaling and TGF- macrophages (TGF-) with antitumor activity.
Purity : >98% (HPLC)






Size | Price / USD | Stock | Quantity |
2MG | 176 | Get Quote |
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5MG | 305 | Get Quote |
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10MG | 484 | Get Quote |
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25MG | 781 | Get Quote |
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50MG | 1062 | Get Quote |
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100MG | 1431 | Get Quote |
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500MG | 2907 | Get Quote |
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1G | Get Quote | Get Quote |
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Biological Information
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Product NameEMT inhibitor-1
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NoteResearch use only, not for human use.
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Brief DescriptionEMT inhibitor -1 is an inhibitor of Hippo, Wnt signaling and TGF- macrophages (TGF-) with antitumor activity.
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DescriptionEMT inhibitor -1 is an inhibitor of Hippo, Wnt signaling and TGF- macrophages (TGF-) with antitumor activity.(In Vitro):EMT inhibitor-1 (C19) inhibiting cancer cell migration, proliferation, and resistance to doxorubicin in vitro.EMT inhibitor-1 (C19) (0-10μM; 24 hours) is an inhibitor of of Hippo, TGF-β, and Wnt signaling pathways with antitumor activities.(In Vivo):EMT inhibitor-1 (C19) (intraperitoneal injection;?5-20 mg/kg) exerts strong antitumor activity in a mouse tumor model.?Mechanistically, EMT inhibitor-1 induces GSK3-β–mediated degradation of the Hippo transducer TAZ, through activation of the Hippo kinases Mst/Lats and the tumor suppressor kinase AMPK upstream of the degradation complex.C19 is dissolved in the vehicle solution (100 μL of DMEM containing 5% dimethyl sulfoxide).
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In Vitro——
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In Vivo——
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Synonyms——
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PathwayWnt/Notch/Hedgehog
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TargetWnt/beta/catenin
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RecptorPDE4| PDE5
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Research Area——
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Indication——
Chemical Information
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CAS Number1638526-21-2
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Formula Weight319.2
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Molecular FormulaC12H12Cl2N2O2S
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Purity>98% (HPLC)
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SolubilityIn Vitro:?DMSO : 100 mg/mL (313.27 mM)
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SMILESOCCCCOc1nsnc1-c1ccc(Cl)c(Cl)c1
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Chemical Name——
Shipping & Storage Information
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Storage(-20℃)
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ShippingWith Ice Pack
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Stability≥ 2 years
Reference
1.Nagendran J, et al. Phosphodiesterase type 5 is highly expressed in the hypertrophied human right ventricle, and acute inhibition of phosphodiesterase type 5 improves contractility. Circulation. 2007 Jul 17;116(3):238-48.
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