KB-141
KB-141 is a potent and selective TRβ agonist. The IC50 values are 23.9 nM and 3.3 nM for binding affinities from displacement of T3 from hTRα1 and hTRβ1, respectively. KB-141 has anti-obesity, anti-diabetic, and lipid-lowering effects?and can be used as an anti-cholesteremic agent in vivo.
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- CAS No.: 219691-94-8
- 화학식: C17H16Cl2O4
- 분자량:355.21
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보관:
Please store the product under the recommended conditions in the Certificate of Analysis.
Biological Activity
제품 설명
IC50 & Target
219691-94-8
Cellular Effect
|
Cell Line
|
Type | Value | Description | References |
|---|---|---|---|---|
| CHO-K1 | EC50 |
0.78 nM
Compound: 2a
|
Activity against TRAFbeta expressed in CHOK1 cells by alkaline phosphatse reporter gene assay
Activity against TRAFbeta expressed in CHOK1 cells by alkaline phosphatse reporter gene assay
|
[PMID: 17543524] |
| CHO-K1 | EC50 |
1.7 nM
Compound: 2a
|
Activity against TRAF-alpha-1 expressed in CHOK1 cells by alkaline phosphatase reporter gene assay
Activity against TRAF-alpha-1 expressed in CHOK1 cells by alkaline phosphatase reporter gene assay
|
[PMID: 17543524] |
| CHO-K1 | EC50 |
11 nM
Compound: 15
|
Effect on CHO-K1 cells stably transfected with Thyroid hormone receptor alpha (TRalpha1) and an alkaline phosphate reporter gene downstream thyroid response element TRAF-alpha1 was determined
Effect on CHO-K1 cells stably transfected with Thyroid hormone receptor alpha (TRalpha1) and an alkaline phosphate reporter gene downstream thyroid response element TRAF-alpha1 was determined
|
[PMID: 12699376] |
| CHO-K1 | EC50 |
3.5 nM
Compound: 15
|
Effect on CHO-K1 cells stably transfected with Thyroid hormone receptor beta and an alkaline phosphate reporter gene downstream thyroid response element TRAF-beta1 was determined
Effect on CHO-K1 cells stably transfected with Thyroid hormone receptor beta and an alkaline phosphate reporter gene downstream thyroid response element TRAF-beta1 was determined
|
[PMID: 12699376] |
| CHO-K1 | IC50 |
1.1 nM
Compound: 2a
|
Binding affinity at human thyroid hormone receptor beta-1 expressed in CHOK1 cells
Binding affinity at human thyroid hormone receptor beta-1 expressed in CHOK1 cells
|
[PMID: 17543524] |
| CHO-K1 | IC50 |
25 nM
Compound: 2a
|
Binding affinity at human thyroid hormone receptor alpha 1 expressed in CHOK1 cells
Binding affinity at human thyroid hormone receptor alpha 1 expressed in CHOK1 cells
|
[PMID: 17543524] |
| CV-1 | EC50 |
1.12 nM
Compound: 2, KB-141
|
Agonist activity at human thyroid hormone receptor beta expressed in CV1 cells by TRE-luciferase assay
Agonist activity at human thyroid hormone receptor beta expressed in CV1 cells by TRE-luciferase assay
|
[PMID: 18585912] |
| CV-1 | EC50 |
4.5 nM
Compound: 2, KB-141
|
Agonist activity at human thyroid hormone receptor alpha expressed in CV1 cells by TRE-luciferase assay
Agonist activity at human thyroid hormone receptor alpha expressed in CV1 cells by TRE-luciferase assay
|
[PMID: 18585912] |
Chemical Information
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CAS No. 219691-94-8
-
분자량 355.21
-
화학식 C17H16Cl2O4
-
SMILES
O=C(CC1=CC(Cl)=C(C(Cl)=C1)OC2=CC=C(C(C(C)C)=C2)O)O
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선적
Room temperature in continental US; may vary elsewhere.
-
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 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
순도&문서
Calculators
Concentration (start) × Volume (start) = Concentration (final) × Volume (final)