BIM5078
BIM5078 is a hepatocyte nuclear factor 4α (HNF4α) antagonist that can inhibit the expression of known HNF4α target genes. BIM5078 represses insulin promoter activity through HNF4α antagonism. BIM5078 can be used for the research of cancer and diabetes.
For research use only. We do not sell to patients.
- CAS No.: 337506-43-1
- Formula: C14H10ClN3O4S
- Molecular Weight:351.76
-
Storage:Powder -20°C, 3 years ; In solvent -80°C, 6 months , -20°C, 1 month
All Nuclear Hormone Receptor 4A/NR4A Isoforms
More
Biological Activity
Description
IC50 & Target
hepatocyte nuclear factor 4α (HNF4α)[1]
In Vitro
BIM5078 (0.63-5μM; 48 h) inhibits the expression of endogenous insulin in T6PNE cells with IC50 value of 930 nM[1].
BIM5078 (2.5-10 μM; 5-48 h) inhibits HNF4α gene expression in HepG2 cells[1].
MedChemExpress (MCE) has not independently confirmed the accuracy of these methods. They are for reference only. Further protocols information, click here.
Chemical Information
-
CAS No. 337506-43-1
-
Appearance Solid
-
Molecular Weight 351.76
-
Formula C14H10ClN3O4S
-
Color White to off-white
-
SMILES
[O-][N+](C1=CC=C(C(S(=O)(N2C3=C(N=C2C)C=CC=C3)=O)=C1)Cl)=O
-
Shipping
Room temperature in continental US; may vary elsewhere.
-
Storage
Powder -20°C 3 years In solvent -80°C 6 months -20°C 1 month
Protocols
-
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.
-
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.
-
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.
-
Research Protocol for Metabolic Diseases
AMP-activated protein kinase, AMPK, is a conserved cellular energy sensor that responds to reduced cellular energy status and coordinates metabolism by increasing ATP-generating catabolic pathways while suppressing ATP-consuming anabolic processes. In metabolic disease research, the AMPK pathway is experimentally relevant because it regulates hepatic lipid synthesis, fatty acid oxidation, glucose production, skeletal-muscle glucose disposal, mTORC1-linked biosynthesis, autophagy, mitochondrial homeostasis, and whole-body energy balance. The central pathway logic is that energy stress, metformin, exercise-like stimulation, or direct AMPK activators increase AMPKα Thr172 phosphorylation and downstream substrate phosphorylation, including ACC and RAPTOR. Phosphorylation of ACC suppresses lipogenesis and supports fatty acid oxidation, whereas phosphorylation of RAPTOR suppresses mTORC1 signaling and links cellular energy status to growth and protein synthesis control. The pathway is linked
Purity & Documentation
-
Data Sheet (277 KB)
-
SDS (480 KB)
- English - EN (480 KB)
- Français - FR (480 KB)
- Deutsch - DE (480 KB)
- Norwegian - NO (480 KB)
- Español - ES (480 KB)
- Swedish - SV (480 KB)
- Italian - IT (480 KB)
- Korean - KR (480 KB)
- Portuguese - PT (480 KB)
-
Handling Instructions (2659 KB)
References
Calculators
Concentration (start) × Volume (start) = Concentration (final) × Volume (final)