RI-STAD-2
RI-STAD-2 is a high-affinity interfering peptide that regulates the subunit RI of protein kinase A (PKA). RI-STAD-2 interferes with the binding of AKAPs and PKA-RI by simulating the interaction between AKAPs' α-helix domain and PKA-RI's dimerization/anchoration (D/D) domain, thereby affecting PKA activity and intracellular localization. RI-STAD-2 can be used to study the role of AKAPs interaction with PKA-RI in pathological processes such as cardiovascular disease and cancer.
For research use only. We do not sell to patients.
- Formula: C109H181N25O35
- Molecular Weight:2401.75
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Storage:
Please store the product under the recommended conditions in the Certificate of Analysis.
Biological Activity
Description
Chemical Information
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Molecular Weight 2401.75
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Formula C109H181N25O35
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Sequence
{NH2-PEG3-CH2-CO}-Leu-S5-Gln-Tyr-Ala-S5-Gln-Leu-Ala-Asp-Gln-Ile-Ile-Lys-Glu-Ala-Thr-Glu-Lys
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Sequence Shortening
{NH2-PEG3-CH2-CO}-L-S5-QYA-S5-QLADQIIKEATEK
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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)