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Ramipril RAAS inhibitor

Cat.No.S1793

Ramipril (HOE-498) is an angiotensin-converting enzyme (ACE) inhibitor with IC50 of 5 nM.
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Quality Control

Batch: Purity: 99.46%
99.46

Solubility

In vitro
Batch:

DMSO : 83 mg/mL (199.27 mM)
(Moisture-contaminated DMSO may reduce solubility. Use fresh, anhydrous DMSO.)

Ethanol : 83 mg/mL

Water : Insoluble

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In vivo
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Method for preparing DMSO master liquid: mg drug pre-dissolved in μL DMSO ( Master liquid concentration mg/mL, Please contact us first if the concentration exceeds the DMSO solubility of the batch of drug. )

Method for preparing in vivo formulation: Take μL DMSO master liquid, next addμL PEG300, mix and clarify, next addμL Tween 80, mix and clarify, next add μL ddH2O, mix and clarify.

Method for preparing in vivo formulation: Take μL DMSO master liquid, next add μL Corn oil, mix and clarify.

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Chemical Information, Storage & Stability

Molecular Weight 416.51 Formula

C23H32N2O5

Storage (From the date of receipt)
CAS No. 87333-19-5 Download SDF Storage of Stock Solutions

Synonyms HOE-498 SMILES CCOC(=O)C(CCC1=CC=CC=C1)NC(C)C(=O)N2C3CCCC3CC2C(=O)O

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Mechanism of Action

Features
A pro-drug converted to its active metabolite, ramiprilat, by liver esterase enzymes.
Targets/IC50/Ki
ACE
5 nM
In vitro

Ramipril is an angiotensin-converting enzyme (ACE) inhibitor with IC50 of 5 nM. This compound enhances the activity of ACE-associated CK2 and the phosphorylation of ACE Ser1270 in cultured endothelial cells, but is unable to activate JNK or stimulate the nuclear accumulation of c-Jun in endothelial cells expressing a S1270A ACE mutant or in ACE-deficient cells. Prolonged treatment with this chemical increases ACE expression in primary cultures of human endothelial cells and in vivo (mouse lung), which can be prevented by pretreatment with the JNK inhibitor SP600125. It displays little enhanced effect on the rate of in vitro endothelial apoptosis induced by the serum deprivation method.

In vivo

Chronic in vivo administration of Ramipril to rats at a dosage that has similar hypotensive effects in vitro HUVECs significantly reduces the rate of LPS-induced apoptosis compared to the other ACE inhibitors, which contrasts with the apoptosis effect in vitro. This compound inhibits systolic blood pressure (SBP) with IC50 of 1.97 mg/kg in spontaneously hypertensive rats (SHR). When in combination with AT1-receptor blockade by candesartan-cilexetil increases SBP reduction synergistically rather than additively. Administration of this chemical to spontaneously hypertensive rats (SHR) produces significant inhibition of aorta ACE and lung ACE with IC50 ~5 mg/kg, but shows little effect for brain ACE ex vivo. This agent prevents beta cell dysfunction in osteoprotegerin treated mice through decreasing islet monocyte/macrophage infiltration, fibrosis and apoptosis involving decreasing RAS, growth factor genes and inflammatory molecules expressions.

References
  • [4] https://pubmed.ncbi.nlm.nih.gov/15076168/
  • [5] https://pubmed.ncbi.nlm.nih.gov/2557876/
  • [6] https://pubmed.ncbi.nlm.nih.gov/20832449/

Clinical Trial Information

(data from https://clinicaltrials.gov, updated on 2026-07-31)

NCT Number Recruitment Conditions Sponsor/Collaborators Start Date Phases
NCT05508035 RECRUITING
Heart Failure With Moderately Reduced Ejection Fraction
John Paul II Hospital, Krakow
2023-07-13 PHASE3
NCT06562582 RECRUITING
Myocardial Infarct
Vastra Gotaland Region
2025-01-06 PHASE4
NCT03770936 RECRUITING
Liver Fibroses
Sherief Abd-Elsalam
2018-10-01 PHASE3
NCT02842424 RECRUITING
Peripheral Arterial Disease
University of Nebraska
2016-02-25 PHASE4
NCT05030818 RECRUITING
Coronary Artery Disease
Fundación EPIC
2022-10-14 PHASE4
NCT07259512 RECRUITING
Chronic Kidney Disease; Heart Failure With Reduced Ejection Fraction (HFrEF)
Evi Liliek Wulandari
2025-06-30 PHASE4

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