Treprostinil palmitil-d4
Treprostinil palmitil-d4 (INS-1009-d4) is the deuterated-labeled Treprostinil palmitil (HY-109163). Treprostinil palmitil is a long-acting inhaled pulmonary vasodilator prodrug of Treprostinil (HY-100441), formulated in a lipid nanoparticle (LNP). Treprostinil palmitil can inhibit pulmonary vascular remodeling induced by Su/Hx challenge in rats. Treprostinil palmitil can induce cough. Treprostinil palmitil demonstrates a sustained presence in the lungs with reduced systemic exposure and prolonged inhibition of hypoxia-induced pulmonary vasoconstriction in vivo. Treprostinil palmitil can be studied in research for pulmonary arterial hypertension and interstitial lung disease.
For research use only. We do not sell to patients.
- Formula: C39H62D4O5
- Molecular Weight:618.96
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Storage:
Please store the product under the recommended conditions in the Certificate of Analysis.
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.
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 1706528-83-7
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Molecular Weight 618.96
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Formula C39H62D4O5
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SMILES
CCCCC([2H])([2H])[C@H](O)C([2H])([2H])C[C@@H]1[C@]2([H])[C@@](C[C@H]1O)([H])CC3=C(OCC(OCCCCCCCCCCCCCCCC)=O)C=CC=C3C2
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Synonyms
INS-1009-d4
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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 Cardiovascular Diseases
Cardiovascular disease can be modeled as maladaptive cardiac remodeling, where ischemic injury or pressure overload activates inflammatory signaling, fibroblast activation, extracellular-matrix deposition, cardiomyocyte hypertrophy, vascular remodeling, and progressive ventricular dysfunction. The TGF-β/SMAD axis is a central profibrotic pathway after myocardial injury and pressure overload, while innate immune and cytokine pathways regulate leukocyte recruitment, scar formation, and adverse remodeling. Key unresolved questions include which inflammatory signals are reparative versus harmful, when fibrosis is protective versus maladaptive, and whether pathway inhibition improves function without weakening necessary infarct healing or compensatory remodeling.
Purity & Documentation
References
[1]. Chapman RW, Corboz MR, Malinin VS, Plaunt AJ, Konicek DM, Li Z, Perkins WR. An overview of the biology of a long-acting inhaled treprostinil prodrug. Pulm Pharmacol Ther. 2020 Dec;65:102002. [Content Brief]
[2]. Corboz, M. R., et al., (2022). Assessment of Inhaled Treprostinil Palmitil, Inhaled and Intravenous Treprostinil, and Oral Selexipag in a Sugen/Hypoxia Rat Model of Pulmonary Arterial Hypertension. The Journal of pharmacology and experimental therapeutics, 383(1), 103–116. [Content Brief]
[3]. Chapman, R. W., et al., (2021). Characterisation of cough evoked by inhaled treprostinil and treprostinil palmitil. ERJ open research, 7(1), 00592-2020. [Content Brief]
[4]. Plaunt, A. J., et al., (2021). Development and Characterization of Treprostinil Palmitil Inhalation Aerosol for the Investigational Treatment of Pulmonary Arterial Hypertension. International journal of molecular sciences, 22(2), 548. [Content Brief]
Calculators
Concentration (start) × Volume (start) = Concentration (final) × Volume (final)