Antidiabetic agent 5
Antidiabetic agent 5 (compound S1) is a antidiabetic agent. Antidiabetic agent 5 inhibits the activity of α-glucosidase and α-amylase with IC50 values of 3.91,8.89 μM,respectively. Antidiabetic agent 5 decreases sugar levels. Antidiabetic agent 5 has the potential for the research of type-II diabetes.
For research use only. We do not sell to patients.
- CAS No.: 2152667-21-3
- Formula: C17H15N3O4S
- Molecular Weight:357.38
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Storage:
Please store the product under the recommended conditions in the Certificate of Analysis.
Biological Activity
Description
IC50 & Target
IC50: 3.91 µM (α-glucosidase); 8.89 µM (α-amylase)[1]
In Vivo
MedChemExpress (MCE) has not independently confirmed the accuracy of these methods. They are for reference only.
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Animal Model:26-33 g, BALB/c mice (diabetes)[1]
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Dosage:3.9, 7.8 mg/kg
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Administration:
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Result:Exhibited a good biochemical profile with lower sugar level (110–115 mg/dL), increased insulin level (25–30 μM/L), and low level of cholesterol (85 mg/dL) and creatinine (0.6 mg/dL) in blood.
Chemical Information
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CAS No. 2152667-21-3
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Molecular Weight 357.38
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Formula C17H15N3O4S
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SMILES
OC1=C(C(N/N=C(C2=CC=CC=C2)\C)=O)NS(C3=CC=CC=C31)(=O)=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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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
References
Calculators
Concentration (start) × Volume (start) = Concentration (final) × Volume (final)