This literature about this compound(89396-94-1)Name: (S)-3-((S)-2-(((S)-1-Ethoxy-1-oxo-4-phenylbutan-2-yl)amino)propanoyl)-1-methyl-2-oxoimidazolidine-4-carboxylic acid hydrochloridehas given us a lot of inspiration, and I hope that the research on this compound((S)-3-((S)-2-(((S)-1-Ethoxy-1-oxo-4-phenylbutan-2-yl)amino)propanoyl)-1-methyl-2-oxoimidazolidine-4-carboxylic acid hydrochloride) can be further advanced. Maybe we can get more compounds in a similar way.
Name: (S)-3-((S)-2-(((S)-1-Ethoxy-1-oxo-4-phenylbutan-2-yl)amino)propanoyl)-1-methyl-2-oxoimidazolidine-4-carboxylic acid hydrochloride. Aromatic heterocyclic compounds can also be classified according to the number of heteroatoms contained in the heterocycle: single heteroatom, two heteroatoms, three heteroatoms and four heteroatoms. Compound: (S)-3-((S)-2-(((S)-1-Ethoxy-1-oxo-4-phenylbutan-2-yl)amino)propanoyl)-1-methyl-2-oxoimidazolidine-4-carboxylic acid hydrochloride, is researched, Molecular C20H28ClN3O6, CAS is 89396-94-1, about Imidapril: a review of its use in essential hypertension, type 1 diabetic nephropathy and chronic heart failure. Author is Robinson, Dean M.; Curran, Monique P.; Lyseng-Williamson, Katherine A..
A review. Imidapril (Tanatril), through its active metabolite imidaprilat, acts as an ACE inhibitor to suppress the conversion of angiotensin I to angiotensin II and thereby reduce total peripheral resistance and systemic blood pressure (BP). In clin. trials, oral imidapril was an effective antihypertensive agent in the treatment of mild to moderate essential hypertension. Some evidence suggests that imidapril also improves exercise capacity in patients with chronic heart failure (CHF) and reduces urinary albumin excretion rate in patients with type 1 diabetes mellitus. Imidapril was well tolerated, with a lower incidence of dry cough than enalapril or benazepril, and is a first choice ACE inhibitor for the treatment of mild to moderate essential hypertension. Pharmacol. Properties The active metabolite of imidapril is imidaprilat, which inhibits the conversion of angiotensin I to angiotensin II. Lowering of plasma and tissue angiotensin II levels results in peripheral vasodilation, reduced systemic BP, renoprotective effects in patients with type 1 diabetes, and decreased renal sodium and water retention. After multidose oral administration in patients with hypertension, steady-state maximum plasma concentrations of imidapril (≈30 ng/mL) and imidaprilat (≈20 ng/mL) are achieved in a median time of 2 and 5 h. In healthy men 25.5% of a single dose of imidapril 10mg was excreted in the urine within 24 h. Elimination occurs primarily through excretion in the urine (≈40%) and feces (≈50%); after oral administration in healthy volunteers, the terminal elimination half-life of imidaprilat is ≈24 h. Therapeutic Efficacy In randomized controlled trials, oral imidapril was effective in the treatment of adults with mild to moderate essential hypertension. In short-term (2- and 4-wk) dose-finding trials, imidapril dosages of 10-40 mg/day were significantly more effective than placebo, inducing 11-15mm Hg reductions in sitting diastolic BP (sDBP; primary endpoint). In comparative 12- and 24-wk trials, imidapril 5-20 mg/day induced reductions in mean sDBP of 10-15mm Hg that did not differ significantly from those induced by hydrochlorothiazide 12.5-50 mg/day or captopril 50-100 mg/day (primary endpoint), nor those induced by enalapril 5-10 mg/day or nifedipine sustained release (SR) 40-80 mg/day (secondary endpoint). In addition, reductions in sDBP and sitting systolic BP (co-primary endpoints) with imidapril did not differ from those induced by candesartan 4-16 mg/day. Favorable reductions in sDBP were maintained during 6-mo and 52-wk noncomparative trials. In patients with type 1 diabetes, the urinary albumin excretion rate (a marker of nephropathy) increased by 72% in placebo recipients, but declined by 41% in imidapril 5 mg/day and by 6% in captopril 37.5 mg/day recipients during a mean treatment period of 1.5 years. In patients with CHF, mean total exercise time increased from baseline in imidapril 2.5-10 mg/day recipients in a dose-related manner after 12-wk of treatment; a 9.7% increase with imidapril 10 mg/day was significantly greater than the change with placebo (+0.7%). Tolerability Overall, imidapril was relatively well tolerated, with an incidence of adverse events in pooled analyses of data from clin. trials and post-marketing surveillance (n = 6632) of 6.6%. The most commonly reported adverse events were cough, hypotension, dizziness and pharyngeal discomfort. During 2- and 4-wk trials, the overall incidence of adverse events was 26% and 40% in recipients of imidapril 2.5-40 mg/day compared with 35% and 37% in placebo recipients. In comparative trials, the incidence of treatment-related adverse events in imidapril vs. enalapril recipients in two 12-wk trials were 5.6% vs. 12.2% and 12.0% vs. 14.1%; in other 12-wk trials treatment-related adverse events were observed in 24.2% of imidapril vs. 41.7% of nifedipine SR, and 20.7% of imidapril vs. 46.4% of captopril recipients, while the overall incidence of adverse events in imidapril vs. candesartan recipients was 11.7% vs. 16.1%. The incidences of adverse events in a 24-wk trial were 46.0% with imidapril and 52.8% with hydrochlorothiazide. In longer-term trials, adverse events were reported by 61.6% of imidapril recipients in the 52-wk trial; however, only 1.7% of imidapril recipients in a 6-mo field trial experienced adverse events considered related to ACE inhibitor treatment. In prospective investigations in hypertensive patients, switching to imidapril did not reduce the incidence of cough (a class effect of ACE inhibitors) in a small open-label trial in hypertensive patients already experiencing ACE-inhibitor induced cough; however, in a large crossover trial, the incidence of cough with imidapril (15.2%) was less than half that with enalapril (38.6%). In addition, cough disappeared in 52.9% of enalapril recipients switched to imidapril, and in patients without cough during imidapril treatment, switching to enalapril induced cough in 20.9%. In contrast, in patients without cough during initial enalapril treatment, only 0.9% developed cough during subsequent imidapril treatment. In a second large, double-blind crossover trial, the incidence of cough was significantly lower in imidapril than benazepril recipients.
This literature about this compound(89396-94-1)Name: (S)-3-((S)-2-(((S)-1-Ethoxy-1-oxo-4-phenylbutan-2-yl)amino)propanoyl)-1-methyl-2-oxoimidazolidine-4-carboxylic acid hydrochloridehas given us a lot of inspiration, and I hope that the research on this compound((S)-3-((S)-2-(((S)-1-Ethoxy-1-oxo-4-phenylbutan-2-yl)amino)propanoyl)-1-methyl-2-oxoimidazolidine-4-carboxylic acid hydrochloride) can be further advanced. Maybe we can get more compounds in a similar way.
Reference:
Copper catalysis in organic synthesis – NCBI,
Special Issue “Fundamentals and Applications of Copper-Based Catalysts”