Z971169476
Z971169476 is a sulfonamide-based protein-RNA interaction inhibitor targeting the KH34 region of insulin-like growth factor 2 mRNA binding protein 2 (IGF2BP2/IMP2).
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- CAS No.: 1356662-88-8
- 화학식: C18H19Cl2NO6S
- 분자량:448.32
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보관:
Please store the product under the recommended conditions in the Certificate of Analysis.
Biological Activity
제품 설명
In Vitro
Z971169476 (compound 18) exhibits high kinetic solubility (>200 μM in 1% DMSO/PBS), moderate lipophilicity (LogD7.4 1.68), metabolic instability in mouse and human liver microsomes, high stability in mouse and human plasma, >99% plasma protein binding in mouse and human plasma, and very low Caco-2 cell permeability (Papp 0.40×10-6 cm/s)[1].
MedChemExpress (MCE) has not independently confirmed the accuracy of these methods. They are for reference only. Further protocols information, click here.
Chemical Information
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CAS No. 1356662-88-8
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분자량 448.32
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화학식 C18H19Cl2NO6S
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SMILES
ClC1=C(OCC(C)C)C=CC(NS(=O)(C2=CC(Cl)=C(OCC(O)=O)C=C2)=O)=C1
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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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RNA extraction experimental
By lysing cells, releasing RNA, and removing impurities such as proteins and DNA, high-purity RNA products are finally obtained. The commonly used traditional method is the guanidine isothiocyanate/phenol/chloroform method (Trizol), which is suitable for a variety of animal materials including animal tissues, microorganisms, cultured cells, etc., and most plant materials.
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Research Protocol for Endocrine Diseases
Endocrine diseases often arise from disrupted hormone production, hormone signaling, or target-tissue responsiveness; for diabetes-focused endocrine disease models, insulin signaling regulates glucose uptake, hepatic glucose output, lipid metabolism, and β-cell compensation. Type 2 diabetes develops through interacting defects in insulin resistance, β-cell dysfunction, adipose inflammation, hepatic glucose overproduction, altered incretin signaling, and ectopic lipid metabolism. A major unresolved question is whether endocrine dysfunction is driven primarily by target-tissue insulin resistance, intrinsic β-cell failure, immune/inflammatory stress, or combined multi-organ failure that differs by disease stage.
순도&문서
References
Calculators
Concentration (start) × Volume (start) = Concentration (final) × Volume (final)