9-Nitrooleate
Based on 1 Customer Validation
9-Nitrooleate, a nitro fatty acid, is a nitro derivative of Oleic acid (HY-N1446). 9-Nitrooleate has potential for use in vascular disease research.
For research use only. We do not sell to patients.
- Purity : 99.79%
- CAS No.: 875685-44-2
- Formula: C18H33NO4
- Molecular Weight:327.46
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Storage:
Solution, -20°C, 2 years
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Biological Activity
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Chemical Information
- Protocols
- Purity & Documentation
- References
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Help & FAQs
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Biological Activity
Description
Cellular Effect
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Cell Line
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Type | Value | Description | References |
|---|---|---|---|---|
| HEK293 | EC50 |
1 μM
Compound: 42
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Agonist activity at human TRPA1 channel in HEK293 cells assessed as increase in intracellular calcium influx by radiometric Ca2+ imaging
Agonist activity at human TRPA1 channel in HEK293 cells assessed as increase in intracellular calcium influx by radiometric Ca2+ imaging
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[PMID: 20356305] |
In Vitro
9-Nitrooleate is formed by the reaction of NO with unsaturated fatty acids under oxidative stress conditions. 9-Nitrooleate belongs to a type of nitro-fatty acid. Nitro-fatty acids can exert anti-inflammatory and vascular protective effects by activating the PPARγ pathway or non-PPAR pathways. Especially in cardiovascular disease models, they can antagonize angiotensin II receptors and alleviate hypertension[1].
MedChemExpress (MCE) has not independently confirmed the accuracy of these methods. They are for reference only. Further protocols information, click here.
Chemical Information
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CAS No. 875685-44-2
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Appearance Liquid
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Molecular Weight 327.46
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Formula C18H33NO4
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Color Colorless to light yellow
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SMILES
CCCCCCCC/C=C(CCCCCCCC(O)=O)/[N+]([O-])=O
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Shipping
Room temperature in continental US; may vary elsewhere.
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Storage
Solution, -20°C, 2 years
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
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Data Sheet (263 KB)
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SDS (420 KB)
- English - EN (420 KB)
- Français - FR (420 KB)
- Deutsch - DE (420 KB)
- Norwegian - NO (420 KB)
- Español - ES (420 KB)
- Swedish - SV (420 KB)
- Italian - IT (420 KB)
- Korean - KR (420 KB)
- Portuguese - PT (420 KB)
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Handling Instructions (2659 KB)
References
Calculators
Concentration (start) × Volume (start) = Concentration (final) × Volume (final)
9-Nitrooleate Related Classifications
HY-121457 Related Classifications
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