Eletriptan-d5 hydrochloride
Eletriptan-d5 (hydrochloride) is the deuterium labeled Eletriptan hydrochloride. Eletriptan (UK-116044) hydrochloride is a highly selective and orally active serotonin 5-HT1B and 5-HT1D receptor agonist, with pKi values of 8.0 and 8.9, respectively. Eletriptan hydrochloride has inhibitory effects on markers of neurogenic inflammation in rats. Eletriptan hydrochloride can be used for researching migraine.
For research use only. We do not sell to patients.
- Formula: C22H22D5ClN2O2S
- Molecular Weight:424.01
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Storage:
Please store the product under the recommended conditions in the Certificate of Analysis.
All 5-HT Receptor Isoforms
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Biological Activity
Description
IC50 & Target
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5-HT1B Receptor |
5-HT1D Receptor |
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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Unlabeled CAS 143322-58-1
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Molecular Weight 424.01
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Formula C22H22D5ClN2O2S
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SMILES
O=S(C1=CC=CC=C1)(CCC2=CC3=C(C=C2)NC=C3C([C@H]4CCCN4C([2H])([2H])[2H])([2H])[2H])=O.Cl
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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 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
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]. McCormack PL, Keating GM. Eletriptan: a review of its use in the acute treatment of migraine. Drugs. 2006;66(8):1129-49. [Content Brief]
[3]. Willems E, et al. Porcine carotid vascular effects of eletriptan (UK-116,044): a new 5-HT1B/1D receptor agonist with anti-migraine activity. Naunyn Schmiedebergs Arch Pharmacol. 1998 Aug;358(2):212-9. [Content Brief]
Calculators
Concentration (start) × Volume (start) = Concentration (final) × Volume (final)