DPP-4-IN-17
DPP-4-IN-17 is an orally active and selective dipeptidyl peptidase-4 (DPP-4) inhibitor with an IC50 value of 0.12 nM. DPP-4-IN-17 increases the enzyme's Km value (75.73 μM vs. 27.18 μM of substrate alone) and reduces catalytic efficiency. DPP-4-IN-17 reduces blood glucose levels and reverses weight loss in Streptozotocin (STZ) (HY-13753)/Nicotinamide (NA) (HY-B0150)-induced diabetic rats. DPP-4-IN-17 can be used for the study of type 2 diabetes mellitus (T2DM).
For research use only. We do not sell to patients.
- Formula: C32H53N5O9
- Molecular Weight:651.79
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Storage:
Please store the product under the recommended conditions in the Certificate of Analysis.
To place orders, for customer services and technical support, please contact: MedChemExpress USA
Tel: 609-228-6898 E-mail: [email protected] [email protected]
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Biological Activity
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Chemical Information
- Protocols
- Purity & Documentation
- References
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Help & FAQs
Biological Activity
Description
IC50 & Target
[1]|
DPP-4 0.12 nM (IC50) |
In Vitro
DPP-4-IN-17 (Compound 8) acts as a competitive DPP-4 inhibitor, increasing the Km value from 27.18 μM to 75.73 μM and decreasing the catalytic efficiency[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.
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Animal Model:Wistar rats (6-8 weeks, 200-250 g) were fasted overnight (12 h), ip injected with 110 mg/kg nicotinamide (NA); 15 min later, ip injected with 50 mg/kg streptozotocin[1]
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Dosage:10, 20, 40 mg/kg
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Administration:p.o., once daily, 21 days
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Result:Reduced blood glucose to normal.
Reversed weight loss.
Normalized serum lipids, liver enzymes and renal parameters.
Repaired kidney (glomerulosclerosis reversed, tubule integrity restored) and pancreas (islet β-cells increased, acinar cells/ducts intact).
Chemical Information
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Molecular Weight 651.79
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Formula C32H53N5O9
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SMILES
COC([C@@H]1CCCN1C([C@@H](NC([C@@H]2CCCN2C(OC(C)(C)C)=O)=O)CCCCNC([C@@H]3CCCN3C(OC(C)(C)C)=O)=O)=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)
DPP-4-IN-17 Related Classifications
HY-175590 Related Classifications
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