(±)-WB 4101
(±)-WB 4101 is a highly selective α1-adrenergic receptor antagonist. (±)-WB 4101 blocks norepinephrine-induced vascular smooth muscle contraction to exert antihypertensive and benign prostatic hyperplasia (BPH)-relieving effects. (±)-WB 4101 is promising for research of hypertension and BPH.
For research use only. We do not sell to patients.
- CAS No.: 613-67-2
- Formula: C19H23NO5
- Molecular Weight:345.39
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Storage:
Please store the product under the recommended conditions in the Certificate of Analysis.
To place orders, for customer services and technical support, please contact: MedChemExpress USA
Tel: 609-228-6898 E-mail: [email protected] [email protected]
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Biological Activity
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Chemical Information
- Protocols
- Purity & Documentation
- References
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Help & FAQs
All Adrenergic Receptor Isoforms
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Biological Activity
Description
IC50 & Target
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α1-adrenergic receptor |
Cellular Effect
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Cell Line
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Type | Value | Description | References |
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| CHO-K1 | IC50 |
1 nM
Compound: WB 4101
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Antagonist activity against human recombinant alpha1 receptor expressed in CHOK1 cells assessed as reduction in epinephrine-induced increase in intracellular Ca2+ levels
Antagonist activity against human recombinant alpha1 receptor expressed in CHOK1 cells assessed as reduction in epinephrine-induced increase in intracellular Ca2+ levels
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[PMID: 25557493] |
Chemical Information
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CAS No. 613-67-2
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Molecular Weight 345.39
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Formula C19H23NO5
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SMILES
COC1=C(OCCNCC2OC3=CC=CC=C3OC2)C(OC)=CC=C1
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Shipping
Room temperature in continental US; may vary elsewhere.
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Storage
Please store the product under the recommended conditions in the Certificate of Analysis.
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
References
Calculators
Concentration (start) × Volume (start) = Concentration (final) × Volume (final)
(±)-WB 4101 Related Classifications
HY-12718 Related Classifications
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