Phe-Tyr
Based on 1 Customer Validation
Phe-Tyr is an ACE inhibitor. Phe-Tyr can be isolated from wakame. Phe-Tyr exhibits mild concentration-dependent toxicity to fibroblasts. Phe-Tyr can be used in studies related to hypertension and cardiovascular diseases.
For research use only. We do not sell to patients.
- CAS No.: 17355-18-9
- Formula: C18H20N2O4
- Molecular Weight:328.36
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Storage:
Sealed storage, away from moisture.
Powder -80°C, 2 years , -20°C, 1 year* In solvent : -80°C, 6 months; -20°C, 1 month (sealed storage, away from moisture)
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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
Cellular Effect
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Cell Line
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Type | Value | Description | References |
|---|---|---|---|---|
| CHO | Inhibition |
68.5985 %
Compound: PHENYLALANYLTYROSINE
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Inhibition of sodium fluorescein uptake in OATP1B3-transfected CHO cells at an equimolar substrate-inhibitor concentration of 10 uM
Inhibition of sodium fluorescein uptake in OATP1B3-transfected CHO cells at an equimolar substrate-inhibitor concentration of 10 uM
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[PMID: 23571415] |
| CHO | Inhibition |
78.5874 %
Compound: PHENYLALANYLTYROSINE
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Inhibition of sodium fluorescein uptake in OATP1B1-transfected CHO cells at an equimolar substrate-inhibitor concentration of 10 uM
Inhibition of sodium fluorescein uptake in OATP1B1-transfected CHO cells at an equimolar substrate-inhibitor concentration of 10 uM
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[PMID: 23571415] |
In Vitro
Phe-Tyr (24 h) shows slight cytotoxicity to L929 fibroblast cells, while encapsulation in PLGA nanoparticles eliminates this toxic effect[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. 17355-18-9
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Appearance Solid
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Molecular Weight 328.36
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Formula C18H20N2O4
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Sequence
Phe-Tyr
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Sequence Shortening
FY
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Shipping
Room temperature in continental US; may vary elsewhere.
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Storage
Sealed storage, away from moisture
Powder -80°C 2 years -20°C 1 year * In solvent : -80°C, 6 months; -20°C, 1 month (sealed storage, away from moisture)
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)
Phe-Tyr Related Classifications
HY-W092110 Related Classifications
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