AM79
AM79 is a PGC-1α1 stabilizer. AM79 promotes the accumulation of endogenous PGC-1α1 protein, thereby activating its target genes. AM79 increases uncoupled mitochondrial respiration in brown adipocytes. AM79 induces the expression of Ucp1 and Cidea in brown adipocytes. AM79 can be used for the research of obesity and related metabolic disorders.
For research use only. We do not sell to patients.
- CAS No.: 949229-08-7
- Formula: C25H24N4O2
- Molecular Weight:412.48
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Storage:
Please store the product under the recommended conditions in the Certificate of Analysis.
Biological Activity
Description
In Vitro
AM79 (10 μM; 8 h) enhances the fluorescence intensity of EGFP-PGC-1α1 in HEK 293-EGFPmPGC-1α1 cells, indicating stabilization of the PGC-1α1 fusion protein, with an activation rate of 57.1% relative to proteasome inhibition[1].
AM79 (10 μM; 8 h) significantly induces the expression of thermogenic and mitochondrial target genes (including the upregulated expression of *Ucp1*) in fully differentiated immortalized mouse brown adipocytes, without altering the total expression level of the *PGC-1α* gene[1].
AM79 (10 μM; 8 h) stabilizes endogenous PGC-1α protein in fully differentiated immortalized mouse brown adipocytes[1].
AM79 (10 μM; 8 h) increases basal mitochondrial respiration and uncoupled mitochondrial respiration (12% increase in proton leak) in fully differentiated immortalized mouse brown adipocytes, with no effect on maximal respiratory capacity[1].
MedChemExpress (MCE) has not independently confirmed the accuracy of these methods. They are for reference only. Further protocols information, click here.
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Cell Line:fully differentiated mouse immortalized brown adipocytes
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Concentration:10 μM
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Incubation Time:8 h
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Result:Induced a >10-fold increase in Ucp1 expression relative to DMSO control.
Induced a ~4-fold increase in Cidea expression relative to DMSO control.
Induced modest increases in Cytc, Tfam, Esrra, Prdm16, and Sod1 expression relative to DMSO control.
Left total Ppargc1a (PGC-1α) expression unchanged relative to control.
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Cell Line:fully differentiated mouse immortalized brown adipocytes
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Concentration:10 μM
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Incubation Time:8 h
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Result:Increased endogenous PGC-1α protein levels in brown adipocytes to levels comparable to isoproterenol treatment and lower than MG132-induced stabilization.
Chemical Information
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CAS No. 949229-08-7
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Molecular Weight 412.48
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Formula C25H24N4O2
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SMILES
O=C(C(CC1)=NN(C2=CC(C)=CC=C2)C1=O)N(CC3)CC=C3C4=CNC5=C4C=CC=C5
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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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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.
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Large-size fat particle sorting
Large-size fat particle sorting is widely used to isolate cells up to 200 μm in diameter. Single-cell flow sorting will allow greater insight into adipocyte heterogeneity by identifying gene expression, protein composition, and metabolic signatures at the single-cell level.
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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
References
Calculators
Concentration (start) × Volume (start) = Concentration (final) × Volume (final)