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.
연구목적의 판매만을 진행합니다. 환자를 대상으로 한 판매는 하지 않습니다.
- Purity : 99.9%
- CAS No.: 34210-11-2
- 화학식: C20H30D4O5
- 분자량:358.51
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보관:
Solution, -20°C, 2 years
All Endogenous Metabolite Isoforms
More
Biological Activity
제품 설명
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.
신청
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. 34210-11-2
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Unlabeled CAS 551-11-1
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Appearance Liquid
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분자량 358.51
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화학식 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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선적
Room temperature in continental US; may vary elsewhere.
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보관
Solution, -20°C, 2 years
Protocol
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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.
순도&문서
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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)
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]. 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
Concentration (start) × Volume (start) = Concentration (final) × Volume (final)