VS-IP1
VS-IP1 is an interfering peptide that blocks viperin-mediated STAT1 degradation, thereby preventing coxsackievirus B3 (CVB3)-induced acute heart failure (AHF).
For research use only. We do not sell to patients.
- Formula: C162H273N57O47S2
- Molecular Weight:3835.38
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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 3835.38
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Formula C162H273N57O47S2
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Sequence
Val-Thr-Asn-Met-Met-Ser-Asp-Phe-Glu-Val-Ser-Gly-Val-Ile-Arg-Ser-Val-Glu-Asp-Phe-d{Pro-Pro-Arg-Arg-Arg-Gln-Arg-Arg-Lys-Lys-Arg-Gly}
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Sequence Shortening
VTNMMSDFEVSGVIRSVEDF-d{PPRRRQRRKKRG}
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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)