Dinoprost-d4
Based on 1 Customer Validation
Dinoprost-d4 is the deuterium labeled Dinoprost. Dinoprost (Prostaglandin F2α) is an orally active, potent prostaglandin F (PGF) receptor (FP receptor) agonist. Dinoprost is a luteolytic hormone produced locally in the endometrial luminal epithelium and corpus luteum (CL). Dinoprost plays a key role in the onset and progression of labour.
Nur für Forschungszwecke. Wir verkaufen nicht an Patienten.
- Reinheit : 99.9%
- CAS. Nr.: 34210-11-2
- Formel: C20H30D4O5
- Molecular Weight:358.51
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Speicherung:
Solution, -20°C, 2 years
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Tel: 609-228-6898 E-mail: [email protected] [email protected]
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Biologische Aktivität
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Chemical Information
- Protokoll
- Reinheit & Dokumentation
- Verweise
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Help & FAQs
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Biologische Aktivität
Beschreibung
IC50 & Target
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FP |
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.
Anwendung
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. Nr. 34210-11-2
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Unlabeled CAS 551-11-1
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Appearance Liquid
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Molecular Weight 358.51
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Formel C20H30D4O5
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Color Colorless to light yellow
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SMILES
OC(CC([2H])([2H])C([2H])([2H])/C=C\C[C@@H]([C@H](C1)O)[C@H]([C@@H]1O)/C=C/[C@@H](O)CCCCC)=O
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Synonyms
Prostaglandin F2a-d4; PGF2α-d4
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Versand
Room temperature in continental US; may vary elsewhere.
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Speicherung
Solution, -20°C, 2 years
Protokoll
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Research Protocol for Endocrine Diseases
Endocrine diseases often arise from disrupted hormone production, hormone signaling, or target-tissue responsiveness; for diabetes-focused endocrine disease models, insulin signaling regulates glucose uptake, hepatic glucose output, lipid metabolism, and β-cell compensation. Type 2 diabetes develops through interacting defects in insulin resistance, β-cell dysfunction, adipose inflammation, hepatic glucose overproduction, altered incretin signaling, and ectopic lipid metabolism. A major unresolved question is whether endocrine dysfunction is driven primarily by target-tissue insulin resistance, intrinsic β-cell failure, immune/inflammatory stress, or combined multi-organ failure that differs by disease stage.
Reinheit & Dokumentation
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Data Sheet (273 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)
Verweise
[1]. Russak EM, et al. Impact of Deuterium Substitution on the Pharmacokinetics of Pharmaceuticals. Ann Pharmacother. 2019;53(2):211-216. [Content Brief]
[2]. Hagen Thieme, et al. Endothelin antagonism: effects of FP receptor agonists prostaglandin F2alpha and fluprostenol on trabecular meshwork contractility. Invest Ophthalmol Vis Sci. 2006 Mar;47(3):938-45. [Content Brief]
[3]. Xin Wen, et al. Prostaglandin F2α Induces Goat Corpus Luteum Regression via Endoplasmic Reticulum Stress and Autophagy. Front Physiol. 2020 Sep 11;11:868. [Content Brief]
Calculators
Konzentration (Stammlösung) × Volumen (Stammlösung) = Konzentration (Ziellösung) × Volumen (Ziellösung)
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