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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

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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PubMedGeorgian medical news2026-08-15

EFFICACY OF PERINDOPRIL IN PATIENTS WITH HEART FAILURE AND REDUCED EJECTION FRACTION.

Nazghaidze N N, Petriashvili Sh S, Agladze R R, Kuridze N N et al.

Heart failure with reduced ejection fraction (HFrEF) represents a major global health burden, accounting for approximately half of all heart failure cases and characterized by high mortality, frequent hospitalizations, and progressive cardiac remodeling. Angiotensin-converting enzyme (ACE) inhibitors constitute a foundational cornerstone in the therapeutic management of HFrEF. Perindopril is a long-acting ACE inhibitor with a highly favorable safety profile; however, robust clinical data evaluating its specific efficacy in HFrEF cohorts remain scarce. To evaluate the therapeutic efficacy, reverse cardiac remodeling, and clinical outcomes of perindopril versus sacubitril/valsartan in patients with HFrEF in routine clinical practice. This retrospective cohort study included 214 HFrEF patients (LVEF<40%, mean age 64.8±11.0 years) treated at Tbilisi Heart Center between 2018 and 2025. Patients received GDMT and were divided into two groups: Perindopril (n=118) and Sacubitril/Valsartan (n=96). Clinical, echocardiographic, and biochemical metrics were assessed at baseline (Visit 1), 2-3 weeks (Visit 2), and 3-6 months (Visit 3). Primary endpoints included changes in LVEF and NYHA functional class. • Both treatment strategies significantly improved LVEF, reduced left ventricular dimensions (LVEDD, LVESD), and decreased pulmonary artery systolic pressure (ANOVA p < 0.01), with major reverse remodeling occurring between Visits 1 and 2. • LVEF increased from 34.3±3.9% to 41.3±7.4% in the perindopril group and from 30.8±5.2% to 33.8±8.1% in the sacubitril/valsartan group. • In multivariable linear regression analysis, treatment group (B=-3.170, p=0.004), baseline LVEF (B=0.381, p=0.005), and de novo heart failure (B=2.966, p=0.005) were independent predictors of follow-up LVEF. • Both cohorts showed significant longitudinal optimization in NYHA functional class (p<0.001). No significant changes in serum potassium or renal function were observed. One-year all-cause mortality did not differ significantly between groups (33.1% vs. 22.9%, p=0.103). Perindopril therapy is associated with significant clinical improvement, LVEF recovery, and positive reverse cardiac remodeling in patients with HFrEF. Both perindopril and sacubitril/valsartan demonstrate comparable efficacy in reducing cardiac dimensions and optimizing NYHA functional status. Furthermore, perindopril maintains a favorable safety profile with low nephrotoxicity, confirming its potential as an effective therapeutic option in HFrEF management.

PMID 42603340
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PubMedEuropean heart journal. Case reports2026-08-13

Mitral valve posteromedial papillary muscle head rupture presenting after liposomal doxorubicin chemotherapy for metastatic lung liposarcoma: a case report.

Desai Shivam U SU, Gandham Narayana R NR

Doxorubicin-induced cardiotoxicity classically manifests as dose-dependent left ventricular systolic dysfunction. Herein, we describe an unusual case of acute mitral papillary muscle rupture following cumulative anthracycline therapy, presenting despite a preserved ejection fraction. A 78-year-old woman with metastatic liposarcoma and multiple cardiovascular risk factors developed acute dyspnoea 1 week after completing liposomal doxorubicin (cumulative absolute dose 534 mg). She previously received 5-fraction stereotactic body radiation therapy to the lower lung lobes in September 2024 (9 months prior), targeting fields in close geographic proximity to the diaphragmatic and inferior heart walls. Surveillance echocardiograms from 2022 to 2025 showed a preserved left ventricular ejection fraction (65%-75%). At presentation, cardiac biomarkers showed a normal brain natriuretic peptide and flat, minimally elevated troponins. Transoesophageal echocardiography confirmed an acute rupture of the posteromedial papillary muscle head and associated chordae causing severe (4+) mitral regurgitation. Open surgical intervention was deferred due to advanced malignancy and goals of care. Her acute heart failure was optimized medically with intravenous loop diuretics, low-dose lisinopril for afterload reduction, and metoprolol succinate, while home amlodipine and hydrochlorothiazide were discontinued. She stabilized and is undergoing evaluation for transcatheter edge-to-edge repair. While a direct causal link is unproven, this case highlights a rare structural complication. We present this 'two-hit' model as a hypothesis-generating observation, suggesting that chemotherapy-induced structural changes might compound underlying ischaemic or radiation-induced vulnerabilities. As such, advanced imaging modalities may offer value in future efforts to implement risk-adapted surveillance.

PMID 42592268
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PubMedJournal of psychopharmacology (Oxford, England)2026-08-12

Impact of adjunctive dihydropyridine calcium channel blockers on mental health outcomes in people with severe mental illness: A target trial emulation in English electronic health records.

Launders Naomi N, Richards-Belle Alvin A, Wu Stephanie M SM, Man Kenneth K C KKC et al.

Dihydropyridine calcium channel blockers have been implicated in both symptom improvement and exacerbation in pre-existing severe mental illness (SMI). We aimed to test the hypothesis that blood-brain barrier penetrant dihydropyridines (DHPs) reduce rates of mental health hospitalisation and self-harm compared to non-penetrant DHPs. We used English electronic health records (Clinical Practice Research Datalink) to conduct a target trial emulation study in people with schizophrenia, bipolar disorder or other psychosis. We compared admissions for mental health and self-harm in those prescribed blood-brain barrier penetrant (intervention) and non-penetrant DHPs (control). Our primary endpoint was a 12-month intention-to-treat analysis using covariate adjustment. We additionally completed overlap weighting, per-protocol analyses and negative outcome controls. We included 918 people prescribed blood-brain barrier penetrant DHPs and 3384 prescribed amlodipine (control). In the primary covariate-adjusted intention-to-treat analysis, there was no clear evidence of a difference in rates of combined mental health admissions and self-harm events (adjusted hazard ratio (HR): 1.22; 95% confidence interval (CI): 0.78-1.91 at 12 months). In a pre-specified sensitivity analysis using overlap weighting, self-harm event rates were elevated in the intervention group at 12 months (HR: 2.10; 95% CI: 1.13-3.94); however, the equivalent covariate-adjusted estimate showed no clear difference (HR: 1.81; 95% CI: 0.52-6.26). In people with SMI, blood-brain barrier penetrant DHPs were not associated with reduced mental health hospitalisations or self-harm events compared to those treated with amlodipine, though estimates were imprecise. This active comparator design cannot distinguish between absence of effect or equivalent benefit of both drug classes. There are peripheral pathways through which DHPs may impact psychiatric symptoms and these require further exploration.

PMID 42583847
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