Flavodilol
Flavodilol is an orally active antihypertensive agent. Flavodilol extensively depletes catecholamines and serotonin in heart tissue of normotensive and spontaneously hypertensive rats (SHR). Flavodilol can be used for hypertension research.
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- CAS No.: 79619-31-1
- Formule: C21H23NO4
- Masse moléculaire:353.41
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Stockage:
Please store the product under the recommended conditions in the Certificate of Analysis.
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Activité biologique
Description
Cellular Effect
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Cell Line
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Type | Value | Description | References |
|---|---|---|---|---|
| DU-145 | IC50 |
17.1 μM
Compound: 11
|
Antiproliferative activity against human DU-145 cells assessed as inhibition of cell proliferation incubated for 72 hrs by WST assay
Antiproliferative activity against human DU-145 cells assessed as inhibition of cell proliferation incubated for 72 hrs by WST assay
|
[PMID: 36493620] |
| HCT-15 | IC50 |
21.38 μM
Compound: 11
|
Antiproliferative activity against human HCT-15 cells assessed as inhibition of cell proliferation incubated for 72 hrs by WST assay
Antiproliferative activity against human HCT-15 cells assessed as inhibition of cell proliferation incubated for 72 hrs by WST assay
|
[PMID: 36493620] |
| T47D | IC50 |
4.85 μM
Compound: 11
|
Antiproliferative activity against human T47D cells assessed as inhibition of cell proliferation incubated for 72 hrs by WST assay
Antiproliferative activity against human T47D cells assessed as inhibition of cell proliferation incubated for 72 hrs by WST assay
|
[PMID: 36493620] |
Chemical Information
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CAS No. 79619-31-1
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Masse moléculaire 353.41
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Formule C21H23NO4
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SMILES
O=C1C2=CC=C(OCC(O)CNCCC)C=C2OC(C3=CC=CC=C3)=C1
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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
Calculators
Concentration (start) × Volume (start) = Concentration (final) × Volume (final)