(+)-JJ-450
(+)-JJ-450 is a non-competitive antagonist targeting the androgen receptor (AR) that inhibits AR nuclear localization and transcriptional activity in the absence of androgen. (+)-JJ-450 is less active than (-)-JJ-450 (HY-403733A) in inhibiting prostate-specific antigen (PSA) expression in LN95 cells, possibly because (+)-JJ-450 targets the ligand binding domain (LBD) of AR. (+)-JJ-450 inhibits the transcriptional activity of AR and its splice variants (e.g., ARv7) by promoting the degradation of unliganded AR in the nucleus and reducing the binding of AR to androgen response elements (AREs). (+)-JJ-450 can be used in castration-resistant prostate cancer (CRPC) studies that are resistant to enzalutamide (MDV3100) (HY-70003).
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- CAS. Nr.: 1998094-24-8
- Formel: C21H22ClFN2O
- Molecular Weight:372.86
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Speicherung:
Please store the product under the recommended conditions in the Certificate of Analysis.
Biologische Aktivität
Beschreibung
Chemical Information
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CAS. Nr. 1998094-24-8
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Molecular Weight 372.86
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Formel C21H22ClFN2O
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SMILES
O=C([C@@H]1C[C@@H]1C2=CC=C(C=C2)F)N3CCN(CC3)C4=CC(Cl)=CC=C4C
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Versand
Room temperature in continental US; may vary elsewhere.
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Speicherung
Please store the product under the recommended conditions in the Certificate of Analysis.
Protokoll
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Dual Luciferin reporter gene assay
Luciferin reporter gene assay is a reporting system to detect the activity of Firefly Luciferase using luciferin as a substrate, which is often used in the research of miRNA target gene verification and promoter transcriptive activity regulation. Dual luciferase usually refers to Firefly luciferase and Renilla luciferase.
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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.
Reinheit & Dokumentation
Verweise
Calculators
Konzentration (Stammlösung) × Volumen (Stammlösung) = Konzentration (Ziellösung) × Volumen (Ziellösung)