CP-69799
CP-69799 is an azahomostatine-containing oligopeptide transition-state analogue inhibitor with a hog renin IC50 of 6e-9 M, human plasma renin IC50 of 3e-7 M and Ki of 0.310 μM, and endothiapepsin Ki of 0.27 μM. CP-69799 binds endothiapepsin’s active site cleft in extended conformation, fills S4 to S3' pockets, displaces native solvent molecules, induces domain rotation, and reduces thermal mobility of endothiapepsin’s flap and helix regions. CP-69799 acts as a transition-state analogue inhibitor of hog renin and human plasma renin. CP-69799 contains a polar lysine residue at the P2' position, with a nitrogen atom replacing the P1' Cα atom of the hydroxyethylene dipeptide isostere. CP-69799 can be used for the research of hypertension.
For research use only. We do not sell to patients.
- CAS No.: 105116-61-8
- Formula: C49H73N9O9
- Molecular Weight:932.16
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Storage:
Please store the product under the recommended conditions in the Certificate of Analysis.
Biological Activity
Description
In Vitro
CP-69799 (10-fold molar excess; several weeks), a transition-state analogue renin inhibitor with a nitrogen-containing dipeptide isostere, binds tightly to endothiapepsin with a Ki of 0.27 μM, forming extensive hydrogen bonds and van der Waals contacts, and induces subtle domain rearrangements and reduced flap mobility in the enzyme[1].
CP-69799 inhibits human plasma renin with an IC50 of 0.310 μM 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. 105116-61-8
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Molecular Weight 932.16
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Formula C49H73N9O9
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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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Cell Cytotoxicity Assay
Cytotoxicity assays are usually based on the assessment of cell membrane damage, which can also be indirectly detected by measuring cell viability. Detection methods include MTT assay, CKK-8 assay, LDH assay and ATP assay, etc.
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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)