Mimosinamine
Mimosinamine is a hydroxylase inhibitor with Fe2+ chelating activity. Mimosinamine inhibits bovine adrenal tyrosine hydroxylase, rat liver phenylalanine hydroxylase, and rat brainstem tryptophan hydroxylase. Mimosinamine can be used in the research of hypertension.
For research use only. We do not sell to patients.
- CAS No.: 37053-15-9
- Formula: C7H10N2O2
- Molecular Weight:154.17
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Storage:
Please store the product under the recommended conditions in the Certificate of Analysis.
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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
Biological Activity
Description
In Vitro
Mimosinamine (Compound 6e) (0-1 mM; 20-60 min) inhibits partially purified rat liver phenylalanine hydroxylase, partially purified bovine adrenal tyrosine hydroxylase, and crude rat brainstem tryptophan hydroxylase in vitro, with maximum inhibition rates of 58.3%, 66.1% and 35.0% at a concentration of 1.0 mM[1].
Mimosinamine chelates 16% of Fe2+ in cell-free polarographic assays at pH 7.0[1].
MedChemExpress (MCE) has not independently confirmed the accuracy of these methods. They are for reference only. Further protocols information, click here.
Chemical Information
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CAS No. 37053-15-9
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Molecular Weight 154.17
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Formula C7H10N2O2
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SMILES
O=C1C=CN(CCN)C=C1O
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Structure Classification
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Initial Source
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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)
Mimosinamine Related Classifications
HY-182578 Related Classifications
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