Moexipril 15mg tablets
Moexipril is a non-sulfhydryl containing precursor of the active angiotensin-converting enzyme (ACE) inhibitor moexiprilat.
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Suspected adverse reactions reported for Moexipril
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Suspected adverse reactions reported for Moexipril
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1 branded products available
WHO defined daily dose (DDD)
15 mg
Not a recommended dose. The DDD is the assumed average maintenance dose per day for a drug used for its main indication in adults. It is a statistical measure used for research and comparison purposes only.
Source: WHO Collaborating Centre for Drug Statistics Methodology, distributed via the NHS dm+d supplementary BNF/ATC mapping files (NHSBSA). Contains public sector information licensed under the Open Government Licence v3.0.
Therapeutically similar medicines
Similarity is based on WHO Anatomical Therapeutic Chemical (ATC) classification and on a factual NHS dm+d therapeutic-grouping code prefix. Source data: NHS dm+d via TRUD (OGL v3.0), WHO ATC/DDD Index.
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SNOMED CT and dm+d codes from NHS TRUD (Technology Reference data Update Distribution), licensed under the Open Government Licence v3.0. BNF code shown is the factual mapping value distributed by NHS Business Services Authority (NHSBSA) in the dm+d supplementary file under OGL v3.0; it is not affiliated with, nor licensed from, the publishers of the British National Formulary. ATC codes from the WHO Collaborating Centre for Drug Statistics Methodology (whocc.no).
Active and completed clinical studies from ClinicalTrials.gov
Source: ClinicalTrials.gov, a database of the U.S. National Library of Medicine (NLM), National Institutes of Health (NIH). Data accessed via ClinicalTrials.gov API v2. Trial information is provided for research purposes and does not constitute medical advice.
Academic studies and reviews for this medicine's active substance
Showing all 5 studies.
Reviews & meta-analyses: 1 · 2017–2026
Showing all 5 studies, sorted by most relevant.
Hu Y, Liang L, Liu S, et al.
2023
- Antihypertensive Agents
- Hypertension
- Network Meta-Analysis
Studies have shown that angiotensin converting enzyme inhibitors (ACEIs) are superior in primary and secondary prevention for cardiac mortality and morbidity to angiotensin receptor blocker (ARBs). One of the common side effects from ACEI is dry cough. The aims of this systematic review, and network meta-analysis are to rank the risk of cough induced by different ACEIs and between ACEI and placebo, ARB or calcium channel blockers (CCB). We performed a systematic review, and network meta-analysis of randomized controlled trials to rank the risk of cough induced by each ACEI and between ACEI and placebo, ARB or CCB. A total of 135 RCTs with 45,420 patients treated with eleven ACEIs were included in the analyses. The pooled estimated relative risk (RR) between ACEI and placebo was 2.21 (95% CI: 2.05-2.39). ACEI had more incidences of cough than ARB (RR 3.2; 95% CI: 2.91, 3.51), and pooled estimated of RR between ACEI and CCB was 5.30 (95% CI: 4.32-6.50) Moexipril ranked as number one for inducing cough (SUCRA 80.4%) and spirapril ranked the least (SUCRA 12.3%). The order for the rest of the ACEIs are as follows: ramipril (SUCRA 76.4%), fosinopril (SUCRA 72.5%), lisinopril (SUCRA 64.7%), benazepril (SUCRA 58.6%), quinapril (SUCRA 56.5%), perindopril (SUCRA 54.1%), enalapril (SUCRA 49.7%), trandolapril (SUCRA 44.6%) and, captopril (SUCRA 13.7%). All ACEI has the similar risk of developing a cough. ACEI should be avoided in patients who have risk of developing cough, and an ARB or CCB is an alternative based on the patient's comorbidity.
Abstract licence: CC BY
Rao AL
Open Access Journal of Pharmaceutical Research, 2017
Esraa H. Alsaaty, Ali M. Janabi
Journal of Contemporary Medical Sciences, 2024
Objective: The goal of this study is to see if moexipril can protect rats against renal ischemia/reperfusion injury. Methods: Overall twenty-eight males of rats were divided randomly into four groups (7 rat each group). Sham group: Except for ischemiainduction, these rats underwent IP anesthesia and surgery. Induced group: This group rats were anesthetized and given a midlinelaparotomy to induce bilateral renal ischemia for 30 min and 2 hours of reperfusion. DMSO group: Rats received DMSO IP injection 30 minbefore ischemia and subjected to 30 min bilateral ischemia and reperfusion for 2 hours, DMSO is a vehicle of moexipril and considered ascontrol. Moexipril group (pretreated group): moexipril was given in a dose 0.3 mg/kg I.P. injection 30 min before ischemia. Results: Renal IRI as indicated by a significant increase (P < 0.05) in urea, creatinine, NF-KB P65, IL-1β, and caspase-3 level, while GSH,SOD, and Bcl-2 levels significantly (P < 0.05) reduced in Renal tissues of rats in the induced group compared to sham group. Moexiprilpretreatment significantly (P < 0.05) ameliorate RIRI as suggested from significant lowering in urea, creatinine, and inflammatory markers(NF-KB P65 and IL-1β). The renal level of oxidative marker (SOD and GSH) and anti-apoptotic marker Bcl-2 were significant decreased(P < 0.05) and also significantly increase (P < 0.05) in caspase-3 level with moexipril group in comparison to induced group. Conclusion: By inhibiting oxidative stress, inflammation, and the apoptotic pathway, moexipril significantly protect from renal ischemiareperfusion in rats.
Abstract licence: CC BY-NC
Neamat T. Barakat, Heba Abd El-Aziz, Manal I. Eid, et al.
Talanta Open, 2025
• Cutting Edge Self-Emissive Fluorescence: Capitalizing Moexipril fluorescence • Ultrafast microwave-assisted synthesis of N, S-CQDs from Arugula leaves • Bio-Inspired Nanomaterial Innovation: Pioneering the use of Arugula leaves N, S-CQDs • Real World Applications: Methods ensure innovative performance in complex matrices • Eco-Conscious Advancement: The method design aligns with green chemistry principles . Monitoring the level of Moexipril is crucial for hypertensive patients, therefore two environmentally friendly, rapid and selective analytical techniques have been established for its sensitive measurement. First method relies on direct measurement of its native fluorescence at λ ex 282 nm / λ em 315 nm. The second method is based on the efficient and quantitative enhancement of N, S-CQDs fluorescence intensity by Moexipril in the presence of 1% Tween. The remarkably fluorescent N and S-CQDs were developed via 8 minutes microwave-aided one-pot synthesis using promising, cheap and widely available precursors (Arugula leaves) for the first time. The sensor is characterized by excellent doping efficiency (N, 13.01% and S, 12.39%), narrow particle size distribution (2.7±0.6 nm), reproducibility and good fluorescence at λ ex 320nm / λ em 430 nm with 68.5% quantum yield. Also, the designed probe selectivity was verified in presence of possible co-existing excipients, various metal ions and co-administered drugs that grants the practical applicability of N, S-CQDs as an environmental probe. Additionally, both methods showed excellent linearity (r = 0.9999) within the specified concentrations range (0.02-0.6 and 0.004-0.7 µg/mL for method I and II, respectively) and they were implemented for the analysis of Moexipril in pharmaceutical tablets and biological fluids, yielding high recovery percentages. The proposed procedures were fully validated in compliance with the ICH Guidelines. Moreover, the greenness, blueness and whiteness profiles of developed methods were evaluated for accomplishment of a complete ecological profile of the designed fluorimetric methodologies and the excellent obtained results confirmed their excellent eco friendless, good applicability and sustainability. .
Abstract licence: CC BY-NC
Nehad Jaser Ahmed
Journal of Public Health Research, 2026
Background and objective: Angiotensin-converting enzyme inhibitors are first-line therapies for hypertension and related cardiovascular and renal conditions. The study aimed to characterize the adverse event profile of ACE inhibitors using the U.S. Food and Drug Administration Adverse Event Reporting System. Methods: This retrospective pharmacovigilance study analyzed FAERS reports submitted from January 1, 1979, through March 31, 2025, for nine ACE inhibitors (benazepril, captopril, enalapril, fosinopril, lisinopril, moexipril, quinapril, ramipril, and trandolapril) identified as primary suspect drugs. Extracted variables included patient age, sex, reporter type, and reported adverse events. Descriptive statistics were used to summarize reporting frequencies. Comparisons between subgroups (male vs female, <18 vs ≥18 years, and healthcare professional vs consumer reporters) were conducted using reporting proportions. Reporting proportion ratios (RPRs) were calculated to compare the proportion of specific adverse events between predefined reference categories. As FAERS does not provide denominator data, findings reflect reporting patterns rather than incidence or risk estimates. Results: A total of 124,638 adverse event reports were identified. ADEs were disproportionately higher in adults and elderly patients compared to those <18 years. Males generally reported more ADEs than females, though some drugs showed the opposite trend. Healthcare professionals submitted the majority of reports (pooled RR = 2.22, 95% CI: 2.20-2.25). The most commonly reported ADEs were angioedema, cough, hypotension, and acute kidney injury. Conclusion: ACE inhibitor adverse event profiles vary by drug, patient age, and sex. Adults and elderly patients carry the highest burden of ADEs, though pediatric cases remain clinically relevant for specific agents. These findings support tailored monitoring and risk mitigation strategies in clinical practice.
Abstract licence: CC BY-NC
Sources: aggregated from Europe PMC (EMBL-EBI), OpenAlex, Crossref, PubMed and other open scholarly databases. Retracted articles are excluded. Study information is provided for research purposes and does not constitute medical advice.
Pharmacology and chemical data from DrugBank
Key facts
Drug status
Approved
Major interactions
40 found
Half-life
1 hour
Mechanism
Moexipril is a prodrug for moexiprilat, which inhibits ACE in humans and animals.
Food interactions
4 warnings
Human targets
1 target
Data: DrugBank · CC BY-NC 4.0
Pharmacokinetics at a glance
Absorption
13%
Half-life
1 hour
Protein binding
50%
Volume of distribution
183 L
Metabolism
Elimination
Clearance
441 mL/min
Pharmacokinetic data: DrugBank · CC BY-NC 4.0
Known interactions with other medications. Always consult a healthcare professional.
Showing 50 of 1121 interactions
Rats, however, tolerated single oral doses of up to 3 g/kg. Common adverse effects include cough, dizziness, diarrhea, flu syndrome, fatigue, pharyngitis, flushing, rash, and myalgia
How the body processes this drug — absorption, distribution, metabolism, and elimination
Proteins and enzymes this drug interacts with in the body
PMID:15615692 PMID:20826823 PMID:2558109 PMID:4322742 PMID:7523412 PMID:7683654
Composed of two similar catalytic domains, each possessing a functional active site, with different selectivity for substrates .
PMID:10913258 PMID:1320019 PMID:1851160 PMID:19773553 PMID:7683654 PMID:7876104
Plays a major role in the angiotensin-renin system that regulates blood pressure and sodium retention by the kidney by converting angiotensin I to angiotensin II, resulting in an increase of the vasoconstrictor activity of angiotensin .
PMID:11432860 PMID:1851160 PMID:19773553 PMID:23056909 PMID:4322742
Also able to inactivate bradykinin, a potent vasodilator, and therefore enhance the blood pressure response .
PMID:15615692 PMID:2558109 PMID:4322742 PMID:6055465 PMID:6270633 PMID:7683654
Acts as a regulator of synaptic transmission by mediating cleavage of neuropeptide hormones, such as substance P, neurotensin or enkephalins .
PMID:15615692 PMID:6208535 PMID:6270633 PMID:656131
Catalyzes degradation of different enkephalin neuropeptides (Met-enkephalin, Leu-enkephalin, Met-enkephalin-Arg-Phe and possibly Met-enkephalin-Arg-Gly-Leu) .
PMID:2982830 PMID:6270633 PMID:656131
Acts as a regulator of synaptic plasticity in the nucleus accumbens of the brain by mediating cleavage of Met-enkephalin-Arg-Phe, a strong ligand of Mu-type opioid receptor OPRM1, into Met-enkephalin (By similarity). Met-enkephalin-Arg-Phe cleavage by ACE decreases activation of OPRM1, leading to long-term synaptic potentiation of glutamate release (By similarity). Also acts as a regulator of hematopoietic stem cell differentiation by mediating degradation of hemoregulatory peptide N-acetyl-SDKP (AcSDKP) .
PMID:26403559 PMID:7876104 PMID:8257427 PMID:8609242
Acts as a regulator of cannabinoid signaling pathway by mediating degradation of hemopressin, an antagonist peptide of the cannabinoid receptor CNR1 .
PMID:18077343
Involved in amyloid-beta metabolism by catalyzing degradation of Amyloid-beta protein 40 and Amyloid-beta protein 42 peptides, thereby preventing plaque formation .
PMID:11604391 PMID:16154999 PMID:19773553
Catalyzes cleavage of cholecystokinin (maturation of Cholecystokinin-8 and Cholecystokinin-5) and Gonadoliberin-1 (both maturation and degradation) hormones .
PMID:10336644 PMID:2983326 PMID:7683654 PMID:9371719
Degradation of hemoregulatory peptide N-acetyl-SDKP (AcSDKP) and amyloid-beta proteins is mediated by the N-terminal catalytic domain, while angiotensin I and cholecystokinin cleavage is mediated by the C-terminal catalytic region PMID:10336644 PMID:19773553 PMID:7876104
Proteins that transport this drug across cell membranes
PMID:15521010 PMID:18367661 PMID:19685173 PMID:26320580 PMID:7896779 PMID:8914574 PMID:9835627
Primarily responsible for the absorption of dietary di- and tripeptides from the small intestinal lumen (By similarity). Mediates transepithelial transport of muramyl and N-formylated bacterial dipeptides contributing to recognition of pathogenic bacteria by the mucosal immune system PMID:15521010 PMID:9835627
PMID:16434549 PMID:18367661 PMID:7756356
Transports neutral and anionic dipeptides with a proton to peptide stoichiometry of 2:1 or 3:1 (By similarity). In kidney, involved in the absorption of circulating di- and tripeptides from the glomerular filtrate .
PMID:7756356
Can also transport beta-lactam antibiotics, such as the aminocephalosporin cefadroxil, and other antiviral and anticancer drugs .
PMID:16434549
Transports the dipeptide-like aminopeptidase inhibitor bestatin (By similarity). Also able to transport carnosine .
PMID:31073693
Involved in innate immunity by promoting the detection of microbial pathogens by NOD-like receptors (NLRs) (By similarity).
Mediates transport of bacterial peptidoglycans across the plasma membrane or, in macrophages, the phagosome membrane: catalyzes the transport of certain bacterial peptidoglycans, such as muramyl dipeptide (MDP), the NOD2 ligand PMID:20406817
Involved compounds
Involved compounds
ATC C09AA13
ATC C09BA13
Chemical identifiers
CAS, UNII, InChI Key and database cross-references
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Chemical identifiers
CAS, UNII, InChI Key and database cross-references
Linked compound data from DrugBank Open Data (CC BY-NC 4.0)
Moexipril
Additional database identifiers
ChemSpider
82418
BindingDB
50084673
ZINC
ZINC000003812306
HUGO Gene Nomenclature Committee (HGNC)
HGNC:2707
GenAtlas
ACE
GeneCards
ACE
GenBank Gene Database
J04144
GenBank Protein Database
178286
Guide to Pharmacology
1613
UniProt Accession
ACE_HUMAN
HUGO Gene Nomenclature Committee (HGNC)
HGNC:10920
GenAtlas
SLC15A1
GeneCards
SLC15A1
GenBank Gene Database
U13173
GenBank Protein Database
773588
Guide to Pharmacology
984
UniProt Accession
S15A1_HUMAN
HUGO Gene Nomenclature Committee (HGNC)
HGNC:10921
GenAtlas
SLC15A2
GeneCards
SLC15A2
GenBank Gene Database
S78203
GenBank Protein Database
999213
Guide to Pharmacology
985
UniProt Accession
S15A2_HUMAN
DrugBank citations
If you use DrugBank data in your research, please cite the following publications:
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Structured knowledge from the free knowledge base
ATC classifications (Wikidata)
Linked open data from Wikidata (Q2291605), a free and open knowledge base operated by the Wikimedia Foundation. Data is available under the Creative Commons CC0 1.0 Public Domain Dedication. WHO INN from the World Health Organization.