Misoprostol acid-d5
Misoprostol acid-d5 is deuterium labeled Misoprostol acid. Misoprostol acid is an active metabolite of Misoprostol. Misoprostol is a synthetic analogue of prostaglandin E1 (PGE1), extensively absorbed, and undergoes rapid de-esterification to Misoprostol acid in the gastrointestinal tract after oral administration. Misoprostol can be used for non-steroidal anti-inflammatory drug-induced (NSAID) gastric ulcers. Misoprostol is an oral agent used to induce labor.
For research use only. We do not sell to patients.
- CAS No.: 1337917-44-8
- Formula: C21H31D5O5
- Molecular Weight:373.54
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Storage:
Please store the product under the recommended conditions in the Certificate of Analysis.
Biological Activity
Description
IC50 & Target
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EP |
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. 1337917-44-8
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Unlabeled CAS 112137-89-0
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Molecular Weight 373.54
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Formula C21H31D5O5
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SMILES
O[C@H]1[C@@H]([C@H](C(C1)=O)CCCCCCC(O)=O)/C=C/CC(C([2H])([2H])[2H])(O)C([2H])([2H])CCC
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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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How to Select the Route of Administration for Mammals
Route-of-administration selection in mammals is a pharmacokinetic, pharmacodynamic, formulation, animal-welfare, and translational decision, not a default technical choice. The selected route should match the study goal: intravenous dosing is most useful when complete systemic exposure and rapid onset are required, oral dosing is most translational for orally intended medicines but is affected by absorption and first-pass metabolism, subcutaneous or intramuscular dosing can provide slower systemic exposure, and intraperitoneal dosing can be useful in rodent proof-of-concept studies but may have limited clinical translation. Published route-comparison studies show that the same compound can produce different exposure, onset, bioavailability, tissue distribution, and tolerability depending on route; therefore, route choice should be supported by pilot pharmacokinetic or pharmacodynamic evidence when the literature is insufficient. Unresolved questions include how to standardize route sel
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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]. Vijaya Bharathi D, et al. Development and validation of highly sensitive method for determination of misoprostol free acid in human plasma by liquid chromatography-electrospray ionization tandem mass spectrometry: application to a clinical pharmacokinetic study. J Chromatogr B Analyt Technol Biomed Life Sci. 2011 Sep 15;879(26):2827-33. [Content Brief]
[2]. Schmidt-Hansen M, et al. Simultaneous compared to interval administration of mifepristone and misoprostol for medical abortion up to 10+0 weeks' gestation: a systematic review with meta-analyses. BMJ Sex Reprod Health. 2020 Feb 20. pii: bmjsrh-2019-200448. [Content Brief]
Calculators
Concentration (start) × Volume (start) = Concentration (final) × Volume (final)