Butylated hydroxytoluene-d21
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Butylated hydroxytoluene-d21 is the deuterium labeled Butylated hydroxytoluene. Butylated hydroxytoluene is an antioxidant widely used in foods and in food-related products. Butylated hydroxytoluene is a Ferroptosis inhibitor.
For research use only. We do not sell to patients.
- Purity : 98.4%
- CAS No.: 64502-99-4
- Formula: C15H3D21O
- Molecular Weight:241.48
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Storage:Powder -20°C, 3 years ; In solvent -80°C, 6 months , -20°C, 1 month
All Endogenous Metabolite Isoforms
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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. 64502-99-4
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Unlabeled CAS 128-37-0
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Appearance Solid
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Molecular Weight 241.48
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Formula C15H3D21O
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Color Off-white to light yellow
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SMILES
[2H]C([2H])([2H])C(C([2H])([2H])[2H])(C1=C(C(C(C([2H])([2H])[2H])(C([2H])([2H])[2H])C([2H])([2H])[2H])=C([2H])C(C)=C1[2H])O[2H])C([2H])([2H])[2H]
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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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Ferroptosis Solutions
Ferroptosis is an iron-dependent, non-apoptotic form of regulated cell death characterized by lethal lipid peroxidation and sensitivity to suppression by iron chelators or lipophilic radical-trapping antioxidants. The core pathway links cystine uptake through system Xc−, glutathione availability, GPX4-dependent detoxification of phospholipid hydroperoxides, iron-dependent oxidative reactions, and polyunsaturated-phospholipid metabolism into a cell-death program that is biochemically and morphologically distinct from apoptosis, necrosis, and autophagy. The ferroptosis pathway is experimentally linked to phenotype through chemical and genetic perturbation. Erastin induces ferroptosis by inhibiting cystine uptake through system Xc− and weakening antioxidant defenses, while GPX4 inhibition or depletion causes lipid peroxide accumulation and ferroptotic cancer-cell death. ACSL4 and oxidizable arachidonoyl- or adrenoyl-containing phosphatidylethanolamines shape ferroptosis sensitivity by con
Purity & Documentation
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Data Sheet (277 KB)
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SDS (394 KB)
- English - EN (394 KB)
- Français - FR (394 KB)
- Deutsch - DE (394 KB)
- Norwegian - NO (394 KB)
- Español - ES (394 KB)
- Swedish - SV (394 KB)
- Italian - IT (394 KB)
- Korean - KR (394 KB)
- Portuguese - PT (394 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 Feb;53(2):211-216. [Content Brief]
[2]. Babich H, et al. Butylated hydroxytoluene (BHT): a review. Environ Res. 1982 Oct;29(1):1-29. [Content Brief]
[3]. Umemura T, et al. Butylhydroxytoluene (BHT) increases susceptibility of transgenic rasH2 mice to lung carcinogenesis. J Cancer Res Clin Oncol. 2001 Oct127(10):583-90. [Content Brief]
[4]. Stockwell BR, et al. Ferroptosis: A Regulated Cell Death Nexus Linking Metabolism, Redox Biology, and Disease. ell. 2017 Oct 5171(2):273-285. [Content Brief]
Calculators
Concentration (start) × Volume (start) = Concentration (final) × Volume (final)