TN-783
TN-783 is an orally active, brain-penetrant NLRP3 (IC50 = 19.3 nM) inhibitor. TN-783 enhances the effects of the GLP-1 receptor agonist semaglutide. TN-783 requires sustained targeted action, not permanent metabolic remodeling. TN-783 can be used for the study of obesity.
For research use only. We do not sell to patients.
- Formula: C16H11F4IN4O2
- Molecular Weight:494.18
-
Storage:
Please store the product under the recommended conditions in the Certificate of Analysis.
Biological Activity
Description
IC50 & Target
|
NLRP3 19.3 nM (IC50) |
In Vitro
TN-783 (2 h) can effectively inhibit the secretion of IL-1β (IC50 = 45.9 nM) by THP-1 cells, under Lipopolysaccharides (HY-D1056) (LPS)/Nigericin (HY-127019) stimulation[1].
TN-783 (0.3 nM-6 μM, 1 h) can dose-dependently inhibit the secretion of IL-1β (IC50 = 5.17 nM) and IL-18 (IC50 = 12.3 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.
-
Animal Model:Diet-induced obese (DIO) and Normal chow (NC)-fed lean mice[1].
-
Dosage:50 mg/kg
-
Administration:P.o., twice daily for 15 days
-
Result:Caused a decrease in body weight in DIO mice, but did not affect the body weight of lean mice.
-
Animal Model:Diet-induced obese (DIO) and Normal chow (NC)-fed lean mice[1].
-
Dosage:0.5 mg/kg, 2 mg/kg, 50 mg/kg
-
Administration:P.o., twice daily for 28 days
-
Result:50 mg/kg induced progressive and sustained weight loss in DIO mice; lower doses were ineffective.
The weight loss was due to a significant reduction in fat mass, while lean body mass was preserved. It did not affect lean mice.
The weight loss was driven by sustained inhibition of food intake, without altering weight-corrected energy expenditure or activity levels.
Improved glucose tolerance in DIO mice.
-
Animal Model:Diet-induced obese (DIO) and Normal chow (NC)-fed lean mice[1].
-
Dosage:50 mg/kg
-
Administration:P.o., twice daily for 14-28 days
-
Result:Reversed microglia activation and significantly alleviated the dysregulation of a large number of genes and protein expression.
-
Animal Model:Diet-induced obese (DIO) and Normal chow (NC)-fed lean mice[1].
-
Dosage:50 mg/kg; Smegglutide: 0.0041 mg/kg (1 nmol/kg)
-
Administration:P.o., twice daily for 66 days; s.c., once daily for 66 days
-
Result:Combination therapy produced more significant and sustained weight loss than either drug alone.
Effectively prevented weight rebound.
Chemical Information
-
Molecular Weight 494.18
-
Formula C16H11F4IN4O2
-
SMILES
O=C(NC1=NC=C(C=N1)F)CN2C[C@H](C3=C(C2=O)C=CC(I)=C3)C(F)(F)F
-
Shipping
Room temperature in continental US; may vary elsewhere.
-
Storage
Please store the product under the recommended conditions in the Certificate of Analysis.
Protocols
-
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.
-
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)