Chemical Properties
White to Off-White Solid
Uses
An angiotensin-converting enzyme (ACE) inhibitor. Antihypertensive.
Uses
Perindoprilat is an angiotensin-converting enzyme (ACE) inhibitor and antihypertensive.
Uses
Perindoprilat is the active metabolite of perindopril, an inhibitor of angiotensin converting enzyme (ACE) that has efficacy against hypertension. Perindoprilat specifically and competitively inhibits ACE in vitro with IC50 values ranging between 1.5 and 3.2 nM. Elimination of perindoprilat is decreased in the elderly and in patients with heart or renal failure.[Cayman Chemical]
Definition
ChEBI: Perindoprilat is a dipeptide obtained by formal condensation of one of the carboxy groups of N-[(1S)-1-carboxyethyl]-L-norvaline with the amino group of (2S,3aS,7aS)-octahydroindole-2-carboxylic acid. The major active metabolite of perindopril. It has a role as an antihypertensive agent, an EC 3.4.15.1 (peptidyl-dipeptidase A) inhibitor and a drug metabolite. It is an organic heterobicyclic compound, a dipeptide, a dicarboxylic acid and a L-alanine derivative.
in vivo
Perindoprilat (oral gavage; 1.5 mg/kg; once daily; 7 d) treatment improves cardiac function in mice with acute myocardial infarction and reduces the number of apoptotic myocardial cells[4].
Perindoprilat (oral gavage; 1.5 mg/kg; once daily; 7 d) treatment reduces the expression levels of myocardial Bax and Bcl-2 in infarction zones of mice with acute myocardial infarction[4].
Perindoprilat (oral gavage; 1.5 mg/kg; once daily; 7 d) treatment lowers the expression of myocardial TLR4/NF-κB in infarction zones in mice with acute myocardial infarction[4].
| Animal Model: | C57BL/6J mice underwent coronary ligation[4] |
| Dosage: | 1.5 mg/kg |
| Administration: | Oral gavage; 1.5 mg/kg; once daily; 7 days |
| Result: | Exhibited markedly lowered the number of apoptotic myocardial cells in comparison with the acute myocardial infarction group (p<0.05). |
| Animal Model: | C57BL/6J mice underwent coronary ligation[4] |
| Dosage: | 1.5 mg/kg |
| Administration: | Oral gavage; 1.5 mg/kg; once daily; 7 days |
| Result: | Reduced the gene and protein expression levels of Bax (a myocardial apoptosis gene) in infarction zones in mice with acute myocardial infarction. |
| Animal Model: | C57BL/6J mice underwent coronary ligation[4] |
| Dosage: | 1.5 mg/kg |
| Administration: | Oral gavage; 1.5 mg/kg; once daily; 7 days |
| Result: | Declined the number of stained NF-κB p50 protein in the nucleus in infarction zones (p<0.05), compared to the acute myocardial infarction group. |
