| Name | Ramipril |
| Description | Ramipril (Altace) is a long-acting angiotensin-converting enzyme inhibitor. It is a prodrug that is transformed in the liver to its active metabolite ramiprilat. |
| Cell Research | The HUVECs are pretreated with the active metabolites of Ramipril for 24 hours. A serum deprivation method is used to induce apoptosis in the presence of Ramipril for an additional 24 hours. The rate of apoptosis is then determined using flow cytometry with two makers annexinV fluorescein isothiocyanate (FITC+) and propidium iodide (PI).(Only for Reference) |
| In vitro | In spontaneously hypertensive rats, Ramipril significantly inhibits both aortic and pulmonary ACE (ACE Angiotensin Converting Enzyme) activity with an IC50 of approximately 5 mg/kg, without affecting cerebral ACE. When administered slowly, Ramipril lowers blood pressure similar to its effect in vitro on HUVECs (Human Umbilical Vein Endothelial Cells), and compared to other ACE inhibitors, it notably reduces the apoptosis rate induced by lipopolysaccharide. In spontaneously hypertensive rats, Ramipril suppresses systolic blood pressure (SBP) with an IC50 of 1.97 mg/kg. When used in conjunction with AT1 receptor blockers, it synergistically enhances the reduction in SBP. Furthermore, in rats treated with bone morphogenetic protein, Ramipril inhibits beta-cell dysfunction by decreasing monocyte/macrophage permeability, apoptosis, and fibrosis, while also reducing the expression of growth factor genes, the Renin-Angiotensin System (RAS), and inflammatory molecules. |
| In vivo | Long-term treatment of primary human endothelial cells with Ramipril increases ACE expression, an effect that is blocked by the JNK inhibitor SP600125. In serum-starved endothelial cells in vitro, Ramipril does not promote apoptosis. When applied to cultured endothelial cells, Ramipril enhances the activity of CK2 associated with ACE and increases phosphorylation at the ACE Ser1270 site. However, in cells lacking ACE or possessing the S1270A ACE mutation, Ramipril fails to stimulate nuclear accumulation of c-Jun or activate JNK. |
| Storage | Powder: -20°C for 3 years | In solvent: -80°C for 1 year | Shipping with blue ice/Shipping at ambient temperature. |
| Solubility Information | DMSO : 50 mg/mL (120.05 mM), Sonication is recommended.
10% DMSO+40% PEG300+5% Tween 80+45% Saline : 2.5 mg/mL (6 mM), Sonication is recommended.
Ethanol : 41.7 mg/mL (100.12 mM), Sonication is recommended.
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| Keywords | Ramipril | Inhibitor | inhibit | HOE498 | HOE 498 | Apoptosis | Angiotensin-converting Enzyme (ACE) | ACE |
| Inhibitors Related | Stavudine | Aceglutamide | Urea | Cysteamine hydrochloride | Diisononyl phthalate | Sodium 4-phenylbutyrate | Metronidazole | Citric Acid Triammonium | L-Methionine | Dimethyl phthalate | Alginic acid | Dextran sulfate sodium salt (MW 5000) |
| Related Compound Libraries | Failed Clinical Trials Compound Library | Bioactive Compound Library | Membrane Protein-targeted Compound Library | ReFRAME Related Library | Anti-Cancer Clinical Compound Library | Drug Repurposing Compound Library | Inhibitor Library | Anti-Cancer Approved Drug Library | FDA-Approved Drug Library | Immunology/Inflammation Compound Library | Bioactive Compounds Library Max | Anti-Cancer Drug Library |
United States
