Efaroxan
Efaroxan is a potent, selective and orally active α2-adrenoceptor antagonist, with antidiabetic activity. Efaroxan is a selective I1-Imidazoline receptor antagonist. Efaroxan can be used for the research of cardiovascular disease.
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- CAS No.: 89197-32-0
- Formule: C13H16N2O
- Masse moléculaire:216.28
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Stockage:
Please store the product under the recommended conditions in the Certificate of Analysis.
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Activité biologique
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Chemical Information
- Protocole
- Pureté et documentation
- Références
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Help & FAQs
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Activité biologique
Description
IC50 & Target
Cellular Effect
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Cell Line
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Type | Value | Description | References |
|---|---|---|---|---|
| K562 | IC50 |
>300 μM
Compound: Efaroxan
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Antiproliferative activity against human K562 cells assessed as inhibition of cell survival after 48 hrs by MTT assay
Antiproliferative activity against human K562 cells assessed as inhibition of cell survival after 48 hrs by MTT assay
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[PMID: 27265687] |
| K562 | IC50 |
300 μM
Compound: Efaroxan
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Antiproliferative activity against human K562 cells assessed as inhibition of cell survival after 48 hrs by MTT assay
Antiproliferative activity against human K562 cells assessed as inhibition of cell survival after 48 hrs by MTT assay
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[PMID: 27265687] |
Chemical Information
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CAS No. 89197-32-0
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Masse moléculaire 216.28
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Formule C13H16N2O
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SMILES
CCC1(C2=NCCN2)OC3=CC=CC=C3C1
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Livraison
Room temperature in continental US; may vary elsewhere.
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Stockage
Please store the product under the recommended conditions in the Certificate of Analysis.
Protocole
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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.
Pureté et documentation
Références
[1]. Berridge TL, et al. Selectivity profile of the alpha 2-adrenoceptor antagonist efaroxan in relation to plasma glucose and insulin levels in the rat. Eur J Pharmacol. 1992 Mar 24;213(2):205-12. [Content Brief]
[2]. A O Abdel-Zaher, et al. The potential antidiabetic activity of some alpha-2 adrenoceptor antagonists. Pharmacol Res. 2001 Nov;44(5):397-409. [Content Brief]
[3]. T L Berridge, et al. Comparison of the effects of efaroxan and glibenclamide on plasma glucose and insulin levels in rats. Eur J Pharmacol. 1992 Mar 24;213(2):213-8. [Content Brief]
Calculators
Concentration (start) × Volume (start) = Concentration (final) × Volume (final)
Efaroxan Related Classifications
HY-B1416 Related Classifications
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