Glipizide-d11
Based on 1 Customer Validation
Glipizide-d11 is the deuterium labeled Glipizide. Glipizide (CP 2872; K 4024)?a potent, orally active and sulfonylurea class anti-diabetic agent and can be used for type 2?diabetes mellitus research but not type 1. Glipizide acts by partially blocking ATP-sensitive potassium?(KATP) channels among β cells of pancreatic islets of Langerhans.
For research use only. We do not sell to patients.
- Purity : 96.36%
- CAS No.: 1189426-07-0
- Formula: C21H16D11N5O4S
- Molecular Weight:456.60
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Storage:Powder -20°C, 3 years ; In solvent -80°C, 6 months , -20°C, 1 month
Biological Activity
Description
In Vitro
Stable heavy isotopes of hydrogen, carbon, and other elements have been incorporated into drug molecules, largely as tracers for quantitation during the drug development process. Deuteration has gained attention because of its potential to affect the pharmacokinetic and metabolic profiles of drugs[1].
MedChemExpress (MCE) has not independently confirmed the accuracy of these methods. They are for reference only. Further protocols information, click here.
Application
1. This compound can be used as a tracer
2. This compound can be used as an internal standard for quantitative analysis by NMR, GC-MS, or LC-MS.
Chemical Information
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CAS No. 1189426-07-0
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Unlabeled CAS 29094-61-9
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Appearance Solid
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Molecular Weight 456.60
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Formula C21H16D11N5O4S
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Color White to off-white
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SMILES
[2H]C1([2H])C([2H])([2H])C([2H])([2H])C([2H])([2H])C([2H])([2H])C1([2H])NC(NS(=O)(C2=CC=C(C=C2)CCNC(C3=NC=C(C)N=C3)=O)=O)=O
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Shipping
Room temperature in continental US; may vary elsewhere.
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Storage
Powder -20°C 3 years In solvent -80°C 6 months -20°C 1 month
Protocols
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Human Islet Cell Culture
The method of preserving islets in vitro, with purified reduced immunogenicity. The steps are islet isolation, islet cell purification, in vitro determination of islet function and islet cell culture.
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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
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Data Sheet (268 KB)
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SDS (393 KB)
- English - EN (393 KB)
- Français - FR (393 KB)
- Deutsch - DE (393 KB)
- Norwegian - NO (393 KB)
- Español - ES (393 KB)
- Swedish - SV (393 KB)
- Italian - IT (393 KB)
- Korean - KR (393 KB)
- Portuguese - PT (393 KB)
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Handling Instructions (2659 KB)
References
[1]. Russak EM, et al. Impact of Deuterium Substitution on the Pharmacokinetics of Pharmaceuticals. Ann Pharmacother. 2019;53(2):211-216. [Content Brief]
[2]. B J Zünkler, et al. Concentration-dependent effects of tolbutamide, meglitinide, glipizide, glibenclamide and diazoxide on ATP-regulated K+ currents in pancreatic B-cells. Naunyn Schmiedebergs Arch Pharmacol. 1988 Feb;337(2):225-30. [Content Brief]
Calculators
Concentration (start) × Volume (start) = Concentration (final) × Volume (final)