PBI-6DNJ
PBI-6DNJ is an orally active and potent multivalent glycosidase inhibitor. PBI-6DNJ exhibits good inhibition activity against α-glucosidase from mice, with a Ki of 0.14 μM. PBI-6DNJ exhibits good hypoglycemic activity. PBI-6DNJ can be used for type 2 diabetes research.
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- CAS No.: 2857098-72-5
- Formule: C120H146N26O36
- Masse moléculaire:2528.60
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Stockage:
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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Activité biologique
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Chemical Information
- Protocole
- Pureté et documentation
- Références
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Help & FAQs
Activité biologique
Description
IC50 & Target
Ki: 0.02 ± 0.002 μM (α-glucosidase from rice), 0.08 ± 0.03 μM (α-mannosidase from jack bean), 0.14 ± 0.007 μM (α-glucosidase from mice), 18.88 ± 0.30 μM (α-glucosidase from aspergilcus niger)[1]
In Vivo
PBI-6DNJ (2.0 mg/kg, Orally, daily for 7 day) has good biocompatibility and no damage to mice[1].
MedChemExpress (MCE) has not independently confirmed the accuracy of these methods. They are for reference only.
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Animal Model:C57BL-6J mice (twenty-eight, 4-5 weeks old, 18-20 g)[1]
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Dosage:0.5, 1.0 and 2.0 mg/kg
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Administration:Orally, once
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Result:Reduced postprandial blood glucose (PBG) level, resulting in 24.41 ± 3.02%, 34.65 ± 9.66%, and 37.77 ± 4.35% of decreases in PBG levels at the doses of 0.5, 1.0 and 2.0 mg/kg, respectively.
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Animal Model:C57BL-6J mice (twenty-eight, 4-5 weeks old, 18-20 g)[1]
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Dosage:2.0 mg/kg
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Administration:Orally, daily for 7 day
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Result:Resulted in increase of the level of UREA (8.63 ± 0.59 mmol/L) and decrease of the level of UA level (242.06 ± 14.77 μmol/L). No obvious differences in the levels of UREA and UA were observed. Showed a slight decrease of 0.30 mmol/L in the level of LDL. The AST level of PBI-6DNJ group (269.71 ± 39.77 U/L) was higher than that of the control group (221.38 ± 23.03 U/L), and the ALT level (59.14 ± 7.13 U/L) was lower than that of the control group (70.49 ± 8.78U/L).
Chemical Information
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CAS No. 2857098-72-5
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Masse moléculaire 2528.60
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Formule C120H146N26O36
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SMILES
OC[C@H]1[C@@H]([C@H]([C@@H](CN1CCCN2C=C(COC3=CC=C(C=C3)OC4=CC(C(N5CC6=CN(CCCN7[C@@H](CO)[C@@H]([C@H]([C@@H](C7)O)O)O)N=N6)=O)=C8C9=C4C%10=C%11C(C(C%12=O)=CC(OC%13=CC=C(C=C%13)OCC%14=CN(CCCN%15[C@H](CO)[C@H]([C@@H]([C@H](C%15)O)O)O)N=N%14)=C%11C9=C(C=C8C5=O)OC%16=CC=C(C=C%16)OCC%17=CN(CCCN(C[C@H]([C@@H]([C@H]%18O)O)O)[C@H]%18CO)N=N%17)=C(C=C%10OC%19=CC=C(OCC%20=CN(CCCN%21[C@H](CO)[C@H]([C@@H]([C@H](C%21)O)O)O)N=N%20)C=C%19)C(N%12CC%22=CN(CCCN%23[C@H](CO)[C@H]([C@@H]([C@H](C%23)O)O)O)N=N%22)=O)N=N2)O)O)O
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Livraison
Room temperature in continental US; may vary elsewhere.
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Stockage
Please store the product under the recommended conditions in the Certificate of Analysis.
Protocole
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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
Pureté et documentation
Références
Calculators
Concentration (start) × Volume (start) = Concentration (final) × Volume (final)
PBI-6DNJ Related Classifications
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