Enalapril sodium

Pretreatment with Enalapril (50 µM; 24 h) sodium significantly reduces AD serum-induced apoptosis in HUVECs, whereas post-treatment with the same concentration and duration does not provide this protective effect^[3].
Enalapril (0.1-100.0 μM; 24 h) sodium dose-dependently inhibits staurosporine-induced apoptosis in primary chick embryo telencephalon neurons, with significant reductions in apoptotic neuron percentages observed at all tested concentrations^[8].
Both pretreatment and post-treatment with Enalapril (50 µM; 24 h) sodium significantly reduces elevated nitrite levels in HUVEC culture supernatants induced by exposure to AD patient sera^[3].
Enalapril sodium when incorporated with 10-20% (w/w) stearic acid into microcrystalline cellulose pellets as Enalapril maleate significantly improves Enalapril sodium stability under accelerated 40°C/75% RH conditions for 91 days, reducing formation of the degradation products Enalapril sodiumate and diketopiperazine more effectively than conventional Enalapril maleate or Enalapril sodium salt pellets, while stearic acid destabilizes Enalapril sodium when combined with Enalapril sodium salt in pellets^[7].
Enalapril sodium as Enalapril maleate shows no significant interaction with stearic acid in 1:1 (w/w) binary mixtures, but as Enalapril sodium salt interacts with stearic acid to reduce its thermal stability, lowering the onset temperature for diketopiperazine formation by ~22°C^[7].
Enalapril sodium when incorporated with 5% (w/w) crospovidone into microcrystalline cellulose pellets containing 10% (w/w) stearic acid enables Enalapril sodium release of 89.51% at 30 min, meeting USP immediate-release criteria^[7].
Enalapril (0.1-100.0 μM; 24 h) sodium dose-dependently protects primary chick embryo telencephalon neurons from glutamate- and Fe²⁺/³⁺-induced damage, with significant reductions in damaged neuron percentages observed at concentrations ≥0.1 μM for glutamate and ≥10.0 μM for Fe²⁺/^3+[8].
Enalapril (0.1-100.0 μM; 3 h (Fe²⁺/³⁺, staurosporine); 1 h (glutamate)) sodium dose-dependently reduces Fe²⁺/³⁺-, glutamate-, and staurosporine-induced mitochondrial reactive oxygen species generation in primary chick embryo telencephalon neurons, with significant reductions observed at concentrations ≥1.0 μM for all treatments^[8].

MedChemExpress (MCE) has not independently confirmed the accuracy of these methods. They are for reference only.