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.
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研究用途以外に使用した場合、当社は一切の責任を負いかねます。
- 純度 : 99.79%
- CAS 番号: 875685-44-2
- 分子式: C18H33NO4
- 分子量:327.46
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保管条件:
Solution, -20°C, 2 years
生物活性
製品説明
Cellular Effect
|
Cell Line
|
Type | Value | Description | References |
|---|---|---|---|---|
| HEK293 | EC50 |
1 μM
Compound: 42
|
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
|
[PMID: 20356305] |
体外実験
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.
化学情報
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CAS 番号 875685-44-2
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性状 Liquid
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分子量 327.46
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分子式 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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輸送条件
Room temperature in continental US; may vary elsewhere.
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保管条件
Solution, -20°C, 2 years
プロトコル
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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.
純度とドキュメンテーション
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データシート (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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取扱説明書 (2659 KB)
参考文献
Calculators
濃度 (開始) × 体積 (開始) = 濃度 (終了) × 体積 (終了)