L-Histidine-13C6 hydrochloride hydrate
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L-Histidine-13C6 (hydrochloride hydrate) is the 13C-labeled L-Histidine hydrochloride hydrate (HY-W014423). L-Histidine hydrochloride hydrate is an endogenous metabolite. L-Histidine hydrochloride hydrate scavenges hydroxyl radicals and singlet oxygen, regulate the absorption of zinc, copper and iron, exhibits anti-inflammatory and antioxidant activities. L-Histidine hydrochloride hydrate is blood brain barrier penetrable.
For research use only. We do not sell to patients.
- Purity : 98%
- CAS No.: 201740-88-7
- Formula: 13C6H12ClN3O3
- Molecular Weight:215.59
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Storage:
-20°C, sealed storage, away from moisture and light
* In solvent : -80°C, 6 months; -20°C, 1 month (sealed storage, away from moisture and light)
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. 201740-88-7
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Appearance Solid
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Molecular Weight 215.59
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Formula 13C6H12ClN3O3
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Color White to off-white
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SMILES
O[13C]([13C@@H](N)[13CH2][13C]1=[13CH]N=[13CH]N1)=O.Cl.O
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Synonyms
H-His-OH-13C6 hydrochloride hydrate
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Shipping
Room temperature in continental US; may vary elsewhere.
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Storage
-20°C, sealed storage, away from moisture and light
* In solvent : -80°C, 6 months; -20°C, 1 month (sealed storage, away from moisture and light)
Protocols
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Research Protocol for Inflammation-related Diseases
The NLRP3 inflammasome is a cytosolic innate immune signaling platform that integrates priming signals and danger-signal activation to promote caspase-1 activation, maturation of IL-1β and IL-18, and gasdermin D-mediated pyroptotic cell death. The core experimental logic is to determine whether inflammatory disease phenotypes are driven by increased NLRP3 expression, ASC-containing inflammasome assembly, caspase-1 cleavage, GSDMD cleavage, and extracellular release of IL-1β/IL-18 rather than by nonspecific cell injury alone. The pathway is strongly linked to inflammation-related disease phenotypes because monosodium urate crystals activate NALP3/NLRP3 inflammasome signaling in gout-like crystal inflammation, cholesterol crystals activate NLRP3 inflammasomes in atherogenesis models, and DSS-induced intestinal inflammation has been reported to involve NLRP3 inflammasome activity. However, experimental colitis studies also show context-dependent protective effects of NLRP3 inflammasome co
Purity & Documentation
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Data Sheet (272 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]. Palomba L, et al., Low levels of hydrogen peroxide and L-histidine induce DNA double-strand breakage and apoptosis. Eur J Pharmacol. 1996 Dec 27;318(1):167-73. [Content Brief]
[2]. Kawahara M, et al., D-histidine and L-histidine attenuate zinc-induced neuronal death in GT1-7 cells. Metallomics. 2013 May;5(5):453-60. [Content Brief]
Calculators
Concentration (start) × Volume (start) = Concentration (final) × Volume (final)