TN-101
TN-101 is an orally active NLRP3 inhibitor (IC50 = 29.8 nM). TN-101 can be used for the study of obesity.
For research use only. We do not sell to patients.
- Formula: C18H20FIN2O3
- Molecular Weight:458.27
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Storage:
Please store the product under the recommended conditions in the Certificate of Analysis.
Biological Activity
Description
IC50 & Target
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NLRP3 29.8 nM (IC50) |
In Vitro
TN-101 (2 h) can effectively inhibit the secretion of IL-1β (IC50 = 5.58 nM) by THP-1 cells, under Lipopolysaccharides (HY-D1056) (LPS)/Nigericin (HY-127019) stimulation[1].
TN-101 (0.3 nM-6 μM, 1 h) can dose-dependently inhibit the secretion of IL-1β (IC50 = 5.97 nM) and IL-18 (IC50 = 12.2 nM) in THP-1 cells induced by Palmitic acid (HY-N0830)-BSA complex[1].
MedChemExpress (MCE) has not independently confirmed the accuracy of these methods. They are for reference only. Further protocols information, click here.
In Vivo
MedChemExpress (MCE) has not independently confirmed the accuracy of these methods. They are for reference only.
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Animal Model:Diet-induced obese (DIO) and Normal chow (NC)-fed lean mice[1].
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Dosage:1 mg/kg, 3 mg/kg, 10 mg/kg
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Administration:P.o., twice daily for 15 days
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Result:Showed no effect on the weight of DIO and NC lean mice.
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Animal Model:Diet-induced obese (DIO) and Normal chow (NC)-fed lean mice[1].
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Dosage:1 mg/kg
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Administration:P.o., twice daily for 28 days
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Result:Showed no effect on the weight of DIO and NC lean mice.
Chemical Information
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Molecular Weight 458.27
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Formula C18H20FIN2O3
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SMILES
O[C@]1(C[C@H](C1)NC(CN2C[C@@]3(C4=C(C2=O)C=CC(I)=C4)C[C@H]3F)=O)C
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Shipping
Room temperature in continental US; may vary elsewhere.
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Storage
Please store the product under the recommended conditions in the Certificate of Analysis.
Protocols
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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
Purity & Documentation
Calculators
Concentration (start) × Volume (start) = Concentration (final) × Volume (final)