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perindopril + indapamide + amlodipine (Triplixam / Viacorind / S06590)

✓ Approved

Servier · CACNA1C · Small Molecule

What is perindopril + indapamide + amlodipine?

perindopril + indapamide + amlodipine is a small molecule developed by Servier. It is approved for therapeutic indications via oral (po).

Drug Profile

Brand NamesTriplixam, Viacorind, S06590
CompanyServier
Drug ClassSmall Molecule
Molecular TargetCACNA1C, ACE, SLC12A3
RouteOral (PO)
StatusApproved
Sources: ClinicalTrials.gov, Servier

Mechanism of Action

Molecular Targets

perindopril + indapamide + amlodipine acts on 3 molecular targets:

CACNA1Ccalcium voltage-gated channel subunit alpha1 C (CACNL1A1, CACNA1C-IT2)
ACEangiotensin I converting enzyme (DCP1, ACE1)
SLC12A3solute carrier family 12 member 3 (NCCT, NCC)
Want deeper analysis?Noah AI can explain complex mechanisms and compare to similar drugs.

Therapeutic Indications

perindopril + indapamide + amlodipine is developed for 1 unique indication across 1 therapeutic area.

Therapeutic AreaConditionPhase
Vascular disordersHypertension✓ Approved

Related Research Articles

PubMedThe Journal of international medical research2026-08-28

Clinical analyses of angiotensin-converting enzyme inhibitor users presenting with cough to a chest diseases outpatient clinic: A single-center retrospective study.

Bektaş Aksoy Hayriye H, Günaydın Selda S

ObjectiveAngiotensin-converting enzyme inhibitors are widely prescribed for cardiovascular disease and are a well-recognized cause of cough. However, cough in patients treated with angiotensin-converting enzyme inhibitor may also reflect underlying pulmonary disease. This study compared the clinical, laboratory, and medication-related characteristics of angiotensin-converting enzyme inhibitor users presenting with pulmonary and non-pulmonary cough.MethodsThis retrospective single-center study included 199 angiotensin-converting enzyme inhibitor-treated patients who presented with cough to the Chest Diseases Outpatient Clinic of Giresun Training and Research Hospital between October 2021 and January 2025. Patients were classified as having cough with pulmonary or non-pulmonary causes according to available clinical, laboratory, and radiological findings. Non-pulmonary cough was not considered synonymous with confirmed angiotensin-converting enzyme inhibitor-induced cough; however, it indicated the absence of identifiable pulmonary pathology based on retrospective data. Demographic, clinical, laboratory, and angiotensin-converting enzyme inhibitor subtype characteristics were compared.ResultsAmong 199 patients, 153 (76.9%) had pulmonary cough and 46 (23.1%) had non-pulmonary cough. Cough duration was longer (p = 0.044) and dyspnea was more frequent (54.2% vs. 13.0%, p < 0.001) in the pulmonary group. Perindopril use was more common in the non-pulmonary group, whereas ramipril use was more common among patients with pulmonary cough (p = 0.015). In a post hoc analysis limited to patients with documented angiotensin-converting enzyme inhibitor discontinuation and evaluable follow-up notes (n = 78), the overall distribution of cough-response categories differed between the groups (Fisher-Freeman-Halton exact p = 0.039), with complete resolution observed in 33.3% of the patients in the non-pulmonary group and 7.9% patients in the pulmonary group. C-reactive protein levels were higher in the pulmonary group (10.87 vs. 5.67 mg/L, p = 0.010), whereas other hematological parameters did not differ significantly.ConclusionsIn the angiotensin-converting enzyme inhibitor-treated patients presenting with cough, shorter symptom duration, absence of dyspnea, and lower C-reactive protein levels may be more compatible with non-pulmonary or presumed angiotensin-converting enzyme inhibitor-related cough, whereas prolonged cough, dyspnea, and elevated C-reactive protein levels may support the consideration of a pulmonary pathology. These findings are hypothesis-generating and require prospective validation.

PMID 42663438
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PubMedPharmaceuticals (Basel, Switzerland)2026-08-27

Metabolic and Inflammatory Adverse Drug Reactions Associated with Amlodipine: A Descriptive and Disproportionality Analysis of EudraVigilance Reports.

Solomon Crina Cristina CC, Butuca Anca A, Frum Adina A, Dobrea Carmen Maximiliana CM et al.

Background/Objectives: The global rise in obesity-related hypertension, metabolic syndrome, and chronic inflammation calls for a precise characterization of the safety profiles of first-line therapies. While amlodipine is considered metabolically neutral, its real-world impact on dysglycemia and inflammatory biomarkers remains incompletely defined. This study aims to characterize the metabolic and inflammatory adverse drug reaction profile of amlodipine, using the EudraVigilance database. Methods: Descriptive and disproportionality analyses were performed on 41,872 Individual Case Safety Reports recorded prior to 17 May 2026. Amlodipine was compared against major antihypertensive classes (beta-blockers, angiotensin-converting enzyme (ACE) inhibitors, sartans, and diuretics), calculating reporting odds ratios (ROR) and 95% confidence intervals. Results: "Hyperglycaemia" could be considered a safety signal for amlodipine, compared to beta-blockers (e.g., bisoprolol-ROR: 2.56), ACE inhibitors (e.g., ramipril-ROR: 2.82), and sartans (e.g., candesartan-ROR: 3.85). "Metabolic syndrome" was reported for amlodipine with a lower probability than for hydrochlorothiazide (ROR: 0.35). Inflammatory signals (e.g., increased C-reactive protein) appeared less frequently for amlodipine than for certain renin-angiotensin-aldosterone system inhibitors (e.g., perindopril-ROR: 0.53). Conclusions: The disproportionality analysis identified relatively lower reporting frequencies for several metabolic and inflammatory adverse drug reactions, compared with selected antihypertensive agents. These findings represent pharmacovigilance signals that warrant further investigation in analytical epidemiological and clinical studies. Although hyperglycemia was reported disproportionally relative to several comparator drugs, reports of T2DM were less frequently reported for amlodipine. However, these observations should not be interpreted as evidence of differences in clinical risk, because disproportionality analyses cannot establish incidence or causality. Reports of inflammation likely reflect patient comorbidities rather than a direct drug effect. These findings demonstrate that post-marketing surveillance remains essential, even when accounting for the methodological limitations of spontaneous reporting.

PMID 42653674
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PubMedAdvances in therapy2026-08-27

A Retrospective, Observational Study of Adherence, Persistence and Clinical Outcomes with Perindopril-Based Single-Pill or Free-Pill Antihypertensive Treatments in Italy.

Vintila Ana Maria AM, Masi Stefano S, Degli Esposti Luca L, Dovizio Melania M et al.

Poor adherence limits the effectiveness of pharmacological treatments. Single-pill combinations (SPCs) improve adherence in short-term observational studies, but whether advantages are sustained long term and translate into clinical benefits remains uncertain. We evaluated long-term improvements in adherence, persistence, and clinical outcomes associated with SPCs. Using patient record linking across Italian administrative healthcare databases, we performed a non-interventional, retrospective, observational, longitudinal analysis of hypertension treated with perindopril (PER)-based combinations. We compared adherence [proportion of days covered (PDC)], treatment discontinuation, all-cause mortality, and cardiovascular (CV) event rates between SPCs and free-pill combinations (FPCs) over 10 years. Being the first introduced in Italy, PER-based SPCs were chosen to allow the longest follow-up. Between 2010 and 2022, 24,121 patients with hypertension were treated with PER-based SPCs (n = 22,663) or FPCs (n = 1458). Throughout the 10-year period, ≥ 73% of SPC users had high adherence (PDC ≥ 80%), compared with ≤ 44% of FPC users. Over a 3-year follow-up, discontinuation rates were lower with SPCs (20%) than FPCs (50%). SPCs were associated with lower risks of all-cause mortality (- 27%), CV events (- 31%), ischaemic heart disease (IHD) (- 22%), cerebrovascular events (- 46%), and a composite of mortality/CV events (- 29%) compared with FPCs. Compared with patients with low adherence, those with high adherence had lower risks of all-cause mortality (- 22%), CV events (- 21%), IHD (- 17%), cerebrovascular events (- 33%), and the composite of mortality/CV events (- 22%). SPCs are associated with sustained, better adherence and persistence to antihypertensive pharmacological treatments compared with FPCs, which may contribute to real-world clinical benefits. Graphical abstract available for this article.

PMID 42649356
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PubMedLuminescence : the journal of biological and chemical luminescence2026-08-24

Micellar Enhanced Second Derivative Spectrofluorimetric Determination of Hydrochlorothiazide, Amlodipine, and Telmisartan in Fixed Dose Combination and Spiked Human Plasma.

Yenduri Suvarna S, H Shashank S, K Naga Prashant NP

A very sensitive and eco-friendly second-derivative spectrofluorimetric method was developed for simultaneous analysis of hydrochlorothiazide (HCTZ), amlodipine besylate (AML), and telmisartan (TEL) in pharmaceutical products and human plasma. Native fluorescence of HCTZ (λex267/λem295 nm), AML (λex362/λem415 nm), and TEL (λex292/λem369 nm) was used together with fluorescence enhancement achieved through sodium lauryl sulfate micelles at optimum excitation/emission wavelengths for all other analytes being analyzed. Overlap of spectroscopic data was able to be resolved through second-derivative spectrofluorimetry without prior separation. Method validation was performed according to ICH Q2(R1) guidelines; results showed excellent linearity (R2 > 0.999) across a concentration range of 3-18, 2-10, and 10-50 ng/mL for HCTZ, AML, and TEL, respectively. Accuracy, precision and robustness were demonstrated with %RSD values below two. Application of the method to pharmaceutical product and spiked plasma samples gave satisfactory recoveries with minimal matrix interference. Assessment of method greenness was conducted using AGREE Prep, MoGAPI, AGSA, SAMI, Ma Tool, CACI, and WECA metrics, all of which indicate superior environmental sustainability. The proposed method is simple, fast, low-cost, ultra-sensitive, and suitable for routine quality control and/or bioanalytical analysis.

PMID 42634090
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PubMedPharmacological reports : PR2026-08-24

preSCRIPT: Large-scale prescription search and annotation engine for pharmacogenomic studies.

Pieczarka Maria M, Pieńkowski Paweł P, Konowalska Paula P, Grubarek Sylwia S et al.

Pharmacogenetics (PGx) has traditionally focused on a small number of high-impact variants affecting drug response due to the fact that PGx studies are labor-intensive and therefore low-throughput. Population biobanks linked to electronic health records (EHRs), including the UK Biobank (UKB) with prescription data for ~ 230,000 individuals offer opportunities to scale PGx research. This, however, comes with a challenge as EHRs do not provide direct treatment response outcomes. One way to overcome this is to draw indirect drug response phenotypes from prescription records. Here, we propose preSCRIPT, a framework to filter and annotate raw prescriptions from the UKB to derive phenotypes for analyses which includes an algorithm to distinguish short prescription gaps from true dose changes. As a proof of concept, we applied preSCRIPT to warfarin, paracetamol, codeine, amitriptyline, simvastatin, aspirin, and amlodipine and derived therapy length and median daily doses. We tested associations for those seven drugs and two phenotypes across single-nucleotide polymorphisms (SNPs), cytochrome P450 (CYP) genes, and human leukocyte antigen (HLA) alleles. We recovered known associations such as CYP2D6 variants with amitriptyline therapy length and dose, CYP2C9/CYP4F2/CYP2C19 with warfarin dose, and CYP2D6 with codeine dose. For drugs without formal PGx guidelines, we identified an association between CYP2D6 enzyme activity and aspirin therapy length and several SNPs, including rs62471929 (CYP3A5), a variant for amlodipine dose, which reached nominal significance in an independent hold-out set. Overall, preSCRIPT provides a scalable framework for prescription-based discovery in pharmacogenomics. As a proof of concept it recovers established PGx associations and nominates novel, hypothesis-generating candidate loci.

PMID 42635959
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PubMedNaunyn-Schmiedeberg's archives of pharmacology2026-08-22

A mechanism investigation on the effective strategy for alleviating acute myocardial infarction associated with sleep deprivation.

Chen Haiyang H, Zhang Lijun L, Liu Meiyan M, Li Yanwei Y et al.

Acute myocardial infarction (AMI) and insomnia are mutually causal. However, therapeutic strategies for AMI combined with insomnia remain limited. Mechanistically, parachlorophenylalanine (PCPA)-induced sleep deprivation (SD) exacerbates AMI by activating the sympathetic nervous system and triggering systemic inflammatory responses. However, the specific cascade through which PCPA-induced SD-mediated systemic inflammation aggravates myocardial injury remains unclear. Bisoprolol amlodipine tablet (BAT), containing bisoprolol and amlodipine, exerts cardiovascular protective effects, in which bisoprolol mitigates sympathetic overactivation, while amlodipine alleviates AMI-related inflammatory responses. Shumian capsule (SMC) improves sleep quality with potential anti-inflammatory and neuroprotective properties. Given the complementary mechanisms of BAT and SMC, and the unmet clinical need for safe, effective therapies targeting AMI-insomnia comorbidity, this study aims to explore the therapeutic mechanisms of BAT combined with SMC on myocardial injury induced by AMI and PCPA-induced SD, providing novel insights for clinical practice. Male Sprague Dawley rats were randomly divided into five groups: sham, MI, MI + SD, BAT, and BAT + SMC. The MI model was established by ligating the left anterior descending coronary artery, and the SD model was induced by intraperitoneal injection of parachlorophenylalanine. After model establishment, rats in the BAT group received BAT (1.05 mg/kg, i.g.), and those in the BAT + SMC group received BAT combined with SMC (252 mg/kg, i.g.) for one week. Behavioral tests, echocardiography, heart rate, heart weight (HW)/body weight (BW), HW/tibia length (TL), histopathological staining, immunofluorescence co-localization, ELISA, qRT-PCR, and Western blot were used to evaluate anxiety- and depression-like behaviors, cardiac function, tissue injuries, inflammatory responses, and related gene and protein expression. PCPA-induced SD mediated the aggravation of MI-induced anxiety and depression-like behaviors, hippocampal and myocardial pathological injuries, myocardial fibrosis, apoptosis, and cardiac dysfunction in rats. It also increased the levels of myocardial injury biomarkers and inflammatory cytokines, and was accompanied by elevated activation status of the Panx1/P2X7 pathway, which may correlate with promoted neutrophil recruitment and changes in NETosis-related markers. Compared with monotherapy with BAT, the BAT combined with the SMC group showed more favorable alterations across all measured parameters. Compared with monotherapy with BAT, the combination of BAT and SMC showed more favorable alterations in all measured parameters. BAT combined with SMC improved the sucrose preference index and locomotor activity, ameliorated neuronal and dendritic injuries in the hippocampus, increased left ventricular ejection fraction and shortening fraction, reduced left ventricular end-diastolic and end-systolic diameters, HR, HW/BW, and HW/TL, alleviated myocardial fibrosis and apoptosis, decreased the levels of CK-MB, cTnI, TNF-α, and IL-1β, was correlated with suppressed expression of Panx1 and P2X7, and presented lower levels of NETosis-related markers (MPO, NE, and Cit-H3). BAT combined with SMC may alleviate myocardial injuries in rats with AMI and PCPA-induced SD via alterations to the Panx1/P2X7 pathway-associated changes in NETosis-related markers. This combined intervention integrates the cardiovascular-protective actions of BAT with the sleep-improving and neuroprotective properties of SMC, which may help relieve the vicious cycle of PCPA-induced SD-triggered inflammation and myocardial damage. Our findings reveal a molecular link between the Panx1/P2X7-associated changes in NETosis-related markers and the therapeutic benefits of BAT and SMC combination therapy, and provide preclinical evidence for its potential translation into clinical practice. This innovative treatment strategy offers a safe and effective alternative for managing AMI patients with concurrent insomnia, addressing a critical unmet medical need.

PMID 42629421
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