Cilazapril
Based on 1 publication(s) in Google Scholar
Cilazapril is an orally active prodrug of the angiotensin-converting enzyme (ACE) inhibitor Cilazaprilat (HY-A0113). Cilazapril reduces plasma ACE activity. Cilazapril can be used in the research of hypertension (including essential and renal hypertension) and congestive heart failure.
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- CAS No.: 88768-40-5
- Formule: C22H31N3O5
- Masse moléculaire:417.50
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Activité biologique
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Chemical Information
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- Pureté et documentation
- Références
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Help & FAQs
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Publications Citing Use of MedChemExpress (MCE) Cilazapril
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Activité biologique
Description
In Vivo
Cilazapril (0.1-0.3 mg/kg orally) dose-dependently reduces plasma ACE activity and the pressor response to angiotensin in cats[1].
Cilazapril (10 mg/kg orally twice daily for 3.5 days) gradually reduces blood pressure in dogs with volume-depleted renal hypertension.
Cilazapril (10 mg/kg; p.o.; 2 weeks) decreases blood pressure, reduces heart weight to body weight ratio, and improves postischemic myocardial function in hyperthyroid rats[3].
MedChemExpress (MCE) has not independently confirmed the accuracy of these methods. They are for reference only.
Chemical Information
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CAS No. 88768-40-5
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Masse moléculaire 417.50
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Formule C22H31N3O5
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SMILES
O=C([C@@H]1CCCN2N1C([C@@H](N[C@@H](CCC3=CC=CC=C3)C(OCC)=O)CCC2)=O)O
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Synonyms
Ro 31-2848
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Livraison
Room temperature in continental US; may vary elsewhere.
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Stockage
Please store the product under the recommended conditions in the Certificate of Analysis.
Publications (1)
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Journal Impact Factor
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Most Recent
Protocole
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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.
Pureté et documentation
Références
[1]. Waterfall JF. A review of the preclinical cardiovascular pharmacology of cilazapril, a new angiotensin converting enzyme inhibitor. Br J Clin Pharmacol. 1989;27 Suppl 2(Suppl 2):139S-150S. [Content Brief]
[2]. Asahi T, et al. Cilazapril prevents cardiac hypertrophy and postischemic myocardial dysfunction in hyperthyroid rats. Thyroid. 2001 Nov;11(11):1009-15. [Content Brief]
[3]. Bhutto IA, et al. Effects of cilazapril on the retinal vessels in spontaneously hypertensive rats: corrosion cast and scanning electron microscopic study. Life Sci. 1999;64(3):PL27-39. [Content Brief]
[4]. Szucs, T., Cilazapril. A review. Drugs, 1991. 41 Suppl 1: p. 18-24. [Content Brief]
[5]. Nussberger, J., et al., Repeated administration of the converting enzyme inhibitor cilazapril to normal volunteers. J Cardiovasc Pharmacol, 1987. 9(1): p. 39-44. [Content Brief]
Calculators
Concentration (start) × Volume (start) = Concentration (final) × Volume (final)
Cilazapril Related Classifications
HY-A0043 Related Classifications
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