MGAT2-IN-7
MGAT2-IN-7 is an orally active monoacylglycerol acyltransferase 2 (MGAT2) inhibitor. MGAT2-IN-7 is used for research on obesity and metabolic dysfunction-associated steatotic liver disease (MASLD).
Nur für Forschungszwecke. Wir verkaufen nicht an Patienten.
- CAS. Nr.: 3115123-06-0
- Formel: C31H30F3N3O6S
- Molecular Weight:629.65
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Speicherung:
Please store the product under the recommended conditions in the Certificate of Analysis.
Biologische Aktivität
Beschreibung
In Vitro
MGAT2-IN-7 (compound 27Q) potently inhibits human monacylglycerol acyltransferase 2 with an IC50 of <1 μM in an in vitro thiol-fluorescence enzyme assay[1].
MedChemExpress (MCE) has not independently confirmed the accuracy of these methods. They are for reference only. Further protocols information, click here.
In Vivo
MGAT2-IN-7 (50 mg/kg; p.o.; daily; 22 days) synergistically enhances weight loss and food intake reduction when combined with GLP-1 receptor agonists in diet-induced obese mice[1].
MedChemExpress (MCE) has not independently confirmed the accuracy of these methods. They are for reference only.
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Animal Model:C57BL/6J mice (male, 16 weeks old, diet-induced obese)[1]
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Dosage:15 mg/kg; 50 mg/kg
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Administration:p.o.; daily; 7 days
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Result:Reduced average body weight by 1.39 g (3.6%) over 7 days, with 10% less 24-hour food intake and 9% less 7-day cumulative food.
Reduced average body weight by 2.5 g (6.8%) over 7 days, with 17% less 24-hour food intake and 20% less 7-day cumulative food.
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Animal Model:C57BL/6J mice (male, diet-induced obese)[1]
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Dosage:50 mg/kg
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Administration:p.o.; daily; 22 days
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Result:Increased body weight reduction from -17.8% (tirzepatide alone) to -38% at 17 days and reduced cumulative food intake by 84% relative to vehicle controls (a 4-fold additional reduction over tirzepatide alone) when combined with maximum dose tirzepatide.
Increased body weight reduction from -32% (semaglutide alone) to -74.3% at 17 days and reduced cumulative food intake by 77% relative to vehicle controls (a 3.3-fold additional reduction over semaglutide alone) when combined with maximum dose semaglutide.
All differences were statistically significant.
Chemical Information
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CAS. Nr. 3115123-06-0
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Molecular Weight 629.65
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Formel C31H30F3N3O6S
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SMILES
CC1=CC=C(C(C2=CC=C(C=N2)COC3CCN(CC3)C4=CC=C(C=C4)OC(F)(F)F)=C1)S(=O)(NC(C5=CC=C(O5)C)=O)=O
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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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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
Reinheit & Dokumentation
Verweise
Calculators
Konzentration (Stammlösung) × Volumen (Stammlösung) = Konzentration (Ziellösung) × Volumen (Ziellösung)