SM-350300
SM-350300 is a glucoprotein. SM-350300 stimulates lipolysis in white adipocytes by activating the cyclic AMP (cAMP) pathway, and upregulates the expression of lipolytic enzymes and uncoupling proteins (UCP1, UCP3) in brown adipose tissue (BAT) and white adipose tissue (WAT). SM-350300 reduces body weight by decreasing carcass fat while increasing lean muscle mass in metabolic disorder models. SM-350300 can be used for the study of metabolic disorders including obesity, type 2 diabetes, and cachexia.
For research use only. We do not sell to patients.
- CAS No.: 902750-48-5
- Formula: C22H27N3O4
- Molecular Weight:397.47
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Storage:
Please store the product under the recommended conditions in the Certificate of Analysis.
Biological Activity
Description
Chemical Information
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CAS No. 902750-48-5
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Molecular Weight 397.47
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Formula C22H27N3O4
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SMILES
C[C@H](OC1=CC=CC2=C1NC=C2CCNC[C@H](O)C3=CC=CN=C3)C(OCC)=O
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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)