LNP 509
LNP 509 is a selective I1 imidazoline receptor ligand with a bovine pKi value of 6.27. LNP 509 exists mainly in the form of a more stable imine tautomer. Intracisternal administration of LNP 509 in anesthetized rabbits induces a dose-dependent decrease in mean arterial blood pressure. LNP 509 can be used in hypertension-related research.
商品は「研究用試薬」です。人や動物の医療用・臨床診断用・食品用の製品ではありません。
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。
- CAS 番号: 773839-36-4
- 分子式: C13H22N2
- 分子量:206.33
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保管条件:
Please store the product under the recommended conditions in the Certificate of Analysis.
生物活性
製品説明
体外実験
LNP 509 (compound 1e) (10-9 to 10-4 M; 40 min) binds to bovine chromaffin cell I1 imidazoline receptors with a pKi of 6.27 and exhibits no detectable affinity for I2 imidazoline binding sites or α2-adrenoceptors[1].
MedChemExpress (MCE) has not independently confirmed the accuracy of these methods. They are for reference only. Further protocols information, click here.
体内実験
MedChemExpress (MCE) has not independently confirmed the accuracy of these methods. They are for reference only.
化学情報
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CAS 番号 773839-36-4
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分子量 206.33
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分子式 C13H22N2
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SMILES
CC1CC(NC(C2CC2)C3CC3)=NC1C
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輸送条件
Room temperature in continental US; may vary elsewhere.
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保管条件
Please store the product under the recommended conditions in the Certificate of Analysis.
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
参考文献
Calculators
濃度 (開始) × 体積 (開始) = 濃度 (終了) × 体積 (終了)