Indolaprilat
Indolaprilat is an ACE inhibitor with an IC50 value of 3.0 nM. Indolaprilat also inhibits aminopeptidase P, with an IC50 of 485 μM for aminopeptidase P. Indolaprilat inhibits the zinc metallopeptidase-mediated cleavage of angiotensin I, Bradykinin (HY-P0206), and proline-containing oligopeptides. Indolaprilat can be used in related research on hypertension and congestive heart failure.
For research use only. We do not sell to patients.
- CAS No.: 80828-34-8
- Formula: C22H30N2O5
- Molecular Weight:402.48
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Storage:
Please store the product under the recommended conditions in the Certificate of Analysis.
Biological Activity
Description
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ACE 3 nM (IC50) |
aminopeptidase P 485 μM (IC50) |
In Vitro
Indolaprilat (1 mM; 5 min) inhibits purified porcine renal cortical aminopeptidase P with an IC50 of 485 μM, and also inhibits purified porcine renal angiotensin-converting enzyme with an IC50 of 3.0 nM[1].
Indolaprilat exhibits potent angiotensin-converting enzyme (ACE) inhibitory activity in vitro[2].
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. 80828-34-8
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Molecular Weight 402.48
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Formula C22H30N2O5
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SMILES
OC([C@H](CCC1=CC=CC=C1)N[C@@H](C)C(N2[C@]3([H])[C@](CCCC3)([H])C[C@H]2C(O)=O)=O)=O
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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)