Minalrestat
Minalrestat (ARI-509) is a potent and orally active aldose reductase inhibitor. Minalrestat can be used in the research of diabetes.
For research use only. We do not sell to patients.
- CAS No.: 129688-50-2
- Formula: C19H11BrF2N2O4
- Molecular Weight:449.20
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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
In Vitro
Minalrestat (100 μM) decreased intracellular sorbitol without affecting intracellular glucose in primary cultured rat mesangial cells[3].
Minalrestat (100 μM, 48 h) causes accumulation of PKC-α and -β2 in primary cultured rat mesangial cells[3].
MedChemExpress (MCE) has not independently confirmed the accuracy of these methods. They are for reference only. Further protocols information, click here.
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Cell Line:Primary cultured rat mesangial cells
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Concentration:100 μM
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Incubation Time:48 h
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Result:Increased accumulation of PKC-α and -β2.
In Vivo
Minalrestat (Oral gavage, 10 mg/kg) restores the reduced number of leukocytes adhered and migrated leukocytes in postcapillary venules in diabetic rats[2].
MedChemExpress (MCE) has not independently confirmed the accuracy of these methods. They are for reference only.
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Animal Model:Alloxan (40 mg/kg i.v.)-induced diabetic rats[1]
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Dosage:10 mg/kg/day
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Administration:Oral gavage, for 30 days.
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Result:Restored the decreased microvascular reactivity.
Chemical Information
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CAS No. 129688-50-2
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Molecular Weight 449.20
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Formula C19H11BrF2N2O4
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SMILES
O=C(N1CC2=C(C=C(Br)C=C2)F)C3(CC(NC3=O)=O)C4=C(C=CC(F)=C4)C1=O
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Synonyms
ARI-509; WAY-ARI 509
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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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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
[1]. Akamine EH, et al. Minalrestat, an aldose reductase inhibitor, corrects the impaired microvascular reactivity in diabetes. J Pharmacol Exp Ther. 2003 Mar;304(3):1236-42. [Content Brief]
[2]. Cruz JW, et al. Minalrestat and leukocyte migration in diabetes mellitus. Diabetes Metab Res Rev. 2003 May-Jun;19(3):223-31. [Content Brief]
[3]. Kapor-Drezgic J, et al. Effect of high glucose on mesangial cell protein kinase C-delta and -epsilon is polyol pathway-dependent. J Am Soc Nephrol. 1999 Jun;10(6):1193-203. [Content Brief]
Calculators
Concentration (start) × Volume (start) = Concentration (final) × Volume (final)
Minalrestat Related Classifications
HY-106877 Related Classifications
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