α-Amylase/α-Glucosidase-IN-27
α-Amylase/α-Glucosidase-IN-27 is a dual-target inhibitor of α-glucosidase and α-amylase, with IC50 values of 18.12 and 37.85 μM, respectively. α-Amylase/α-Glucosidase-IN-27 inhibits the hydrolysis of internal α-1,4-glycosidic bonds in polysaccharides by α-amylase through acting on the amylase active site. α-Amylase/α-Glucosidase-IN-27 can be used in diabetes-related research.
For research use only. We do not sell to patients.
- Formula: C24H16BrClN6O3S
- Molecular Weight:583.84
-
Storage:
Please store the product under the recommended conditions in the Certificate of Analysis.
Biological Activity
Description
IC50 & Target
[1]|
α‑glucosidase 18.12 μM (IC50) |
α-amylase 37.85 μM (IC50) |
In Vitro
α-Amylase/α-Glucosidase-IN-27 (Compound 7g) exhibits potent inhibitory activity against human pancreatic α-amylase, with an IC50 of 37.85 μM[1].
α-Amylase/α-Glucosidase-IN-27 inhibits human lysosomal acid α-glucosidase with an IC50 of 18.12 μM[1].
α-Amylase/α-Glucosidase-IN-27 exhibits a favorable orientation near GLU233, ASP197, TRP59, ILE235, TYR151, HIE201, and GLN63 of α-amylase, with a docking score of -4.050[1].
MedChemExpress (MCE) has not independently confirmed the accuracy of these methods. They are for reference only. Further protocols information, click here.
Chemical Information
-
Molecular Weight 583.84
-
Formula C24H16BrClN6O3S
-
SMILES
S=C(N/N=C/C1=CC=C(C=C1)OC2=CC=NC3=CC(Cl)=CC=C32)N/N=C/C4=C([N+]([O-])=O)C=CC(Br)=C4
-
Shipping
Room temperature in continental US; may vary elsewhere.
-
Storage
Please store the product under the recommended conditions in the Certificate of Analysis.
Protocols
-
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.
-
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)