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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

PubMedAmerican journal of hypertension2026-10-19

Amlodipine and Nifedipine Associations with B-Type Natriuretic Peptide in Women with Hypertension and Heart Failure with Preserved Ejection Fraction.

Harada Eisaku E, Yamada Toshihiro T, Mizuno Yuji Y, Arima Yuichiro Y et al.

Calcium channel blockers (CCBs) are frequently prescribed to manage hypertension in patients with heart failure with preserved ejection fraction (HFpEF). However, whether individual dihydropyridine agents exert uniform class effects on myocardial wall stress remains unclear. This retrospective, single-center observational study analyzed 465 consecutive patients with hypertension and HFpEF (354 women and 111 men) evaluated at Kumamoto Kinoh Hospital between May 2012 and July 2018. Multivariable linear regression models assessed associations between individual dihydropyridine CCBs (amlodipine vs. nifedipine) and plasma log-transformed B-type natriuretic peptide (lnBNP) levels. In multiple imputation models among women, adjusted differences in lnBNP relative to no-CCB were 0.236 (95% CI, 0.031 to 0.441) for nifedipine and -0.118 (95% CI, -0.273 to 0.037) for amlodipine. Direct linear contrasts in women confirmed lower lnBNP levels with amlodipine than with nifedipine (adjusted difference, -0.355; 95% CI, -0.562 to - 0.147). In men, the corresponding amlodipine-versus-nifedipine difference was -0.051 (95% CI, -0.697 to 0.595; P=0.876). The formal sex-by-drug interaction contrast in complete-case analysis yielded an adjusted difference of - 0.424 (95% CI, -1.055 to 0.208; P = 0.188), with male precision constrained by sample size (7 male nifedipine users). In women with hypertension and heart failure with preserved ejection fraction, amlodipine use was associated with lower adjusted ln(BNP) levels than nifedipine use. These observational findings challenge the assumption of an interchangeable dihydropyridine class effect on myocardial wall stress, suggesting that individual pharmacological profiles-rather than uniform class-level equivalence-warrant attention in clinical evaluations.

PMID 42895302
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PubMedBMC microbiology2026-10-19

Repurposing amlodipine, fluoxetine, and escitalopram as non-antibiotic adjuvants: in vitro enhancement of ciprofloxacin and fluconazole activity against multidrug-resistant bacterial and candida clinical isolates.

Alkhawlani Mohammed A MA, Al-Madhagi Wafa M WM, Alburyhi Mahmoud Mahyoob MM, Al-Kaf Ali Gamal AG et al.

Multidrug-resistant (MDR) Staphylococcus aureus, Pseudomonas aeruginosa, and Candida albicans threaten treatment success, particularly in resource-limited settings. Repurposing licensed, inexpensive non-antibiotic drugs may provide a strategy for enhancing the activity of established antimicrobial agents. Clinical isolates from Sana'a, Yemen, and American Type Culture Collection (ATCC) reference strains were tested in vitro with amlodipine, fluoxetine, and escitalopram, individually and in dual or triple combinations with ciprofloxacin or fluconazole. Antimicrobial activity was evaluated using agar-well diffusion, broth microdilution minimum inhibitory concentration (MIC), minimum bactericidal or fungicidal concentration (MBC/MFC), and checkerboard fractional inhibitory concentration index (FICI) assays. Molecular docking with AutoDock Vina was used to explore plausible interactions with MurB (PDB 1HSK), LasR (PDB 3IX3), and CYP51 (PDB 5V5Z). Normal mode analysis (NMA) with iMODS was performed for selected fluoxetine-LasR and fluoxetine-MurB complexes as a preliminary structural-dynamics assessment. Fluoxetine produced inhibition zones of at least 27 mm across the tested organisms. Amlodipine produced larger zones against S. aureus and C. albicans than against P. aeruginosa, whereas escitalopram produced smaller zones overall. Checkerboard testing identified synergy (FICI ≤ 0.50) for selected combinations. Selected triple combinations reduced MIC values by 4- to 64-fold. The largest diffusion readouts were observed with ciprofloxacin + fluoxetine + amlodipine against S. aureus (101 mm), ciprofloxacin + fluoxetine + escitalopram against P. aeruginosa (88.5 mm), and ciprofloxacin + amlodipine + fluconazole against C. albicans (138.5 mm). Docking scores and NMA outputs provided hypothesis-generating structural context for the experimental findings. Antimicrobial enhancement was combination- and organism-dependent. Selected combinations showed checkerboard-defined synergy, whereas diffusion assays were interpreted as screening outcomes only. Docking and NMA findings were supportive and hypothesis-generating but did not establish target engagement or mechanism.

PMID 42894131
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PubMedBioMed research international2026-10-18

Compound Astragalus Oral Liquid Attenuates Ventricular Remodeling in Heart Failure After Myocardial Infarction via the AMPK/TGF-β/Smad Signaling Pathway.

Yang Zhijun Z, Huang Fengfan F, Xu Ji J, Gu Ning N et al.

Ventricular remodeling following acute myocardial infarction (AMI) is a critical cause of heart failure (HF). Compound Astragalus Oral Liquid (CAOL) is a traditional Chinese medicine formulation with anti-inflammatory, antioxidant, and tonifying properties. However, its effects and underlying mechanisms in post-acute myocardial infarction heart failure (AMI-HF) remain unclear. To evaluate the cardioprotective efficacy of CAOL in a rat model of AMI-HF and elucidate the associated molecular mechanisms. CAOL constituents were identified by UPLC-Q-TOF/MS, and network pharmacology predicted potential targets. A rat model of AMI-induced HF was established by left anterior descending (LAD) coronary ligation. Animals received CAOL at low, medium, and high doses, or perindopril. Cardiac function, histopathology, serum oxidative and inflammatory markers, and myocardial molecular expression were assessed by echocardiography, staining, ELISA, Western blotting, and RT-qPCR. CAOL treatment improved cardiac performance in a dose-dependent manner, as evidenced by increased LVEF and improvements in LVIDd and LVIDs. Histological analyses demonstrated that CAOL reduced myocardial necrosis, inflammatory cell infiltration, and collagen deposition in a dose-dependent fashion. CAOL also ameliorated serum markers of inflammation and oxidative stress. Mechanistically, CAOL modulated AMPK activity and inhibited TGF-β1/Smad-mediated profibrotic signaling, consistent with its antifibrotic and cytoprotective effects. CAOL ameliorates postinfarction ventricular remodeling and preserves cardiac function in a manner associated with AMPK activation and suppression of TGF-β/Smad-mediated fibrosis. These findings provide experimental evidence supporting CAOL as a potential therapeutic agent for AMI-HF.

PMID 42893564
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PubMedJournal of visualized experiments : JoVE2026-10-17

Sacubitril/Valsartan Improves Cardiovascular Outcomes in Elderly Patients with Coronary Artery Disease and Hypertension: A Retrospective Cohort Study.

Feng Miaolian M, Xie Ying Y

Elderly patients with concurrent coronary artery disease (CAD) and hypertension face elevated risks of cardiovascular events and require therapies that balance efficacy, safety, and tolerability. Sacubitril/valsartan has demonstrated benefits in heart failure management, but evidence regarding its long-term cardiovascular outcomes in this specific population remains limited. This retrospective cohort study enrolled 150 elderly patients with CAD and hypertension to compare the effects of sacubitril/valsartan versus amlodipine, both combined with conventional therapy. The primary endpoint was the incidence of major adverse cardiovascular events (MACE) over 12 months. Two MACE definitions were applied in this study. Primary analysis used our predefined composite endpoint, including aggravated heart failure and arrhythmia events. A sensitivity analysis adopted the conventional MACE definition (myocardial infarction, stroke, cardiovascular death, revascularization), excluding isolated ventricular premature beats. Secondary endpoints included blood pressure control, cardiac function parameters, and treatment-related adverse events. Results showed that patients treated with sacubitril/valsartan had a significantly lower incidence of MACE (10.26% vs. 27.14%, P = 0.008), superior blood pressure control, and improved left ventricular ejection fraction (LVEF) compared to the amlodipine group. Cox proportional hazards regression (Cox regression) analysis identified sacubitril/valsartan treatment as an independent protective factor against cardiovascular adverse events (hazard ratio (HR) = 0.38, 95% confidence interval (CI): 0.18-0.80, P = 0.011). Both regimens were well-tolerated, with no severe adverse events reported. These findings indicate that sacubitril/valsartan is an effective and safe therapeutic option for elderly patients with CAD and hypertension, reducing long-term cardiovascular risk while improving blood pressure control and cardiac function.

PMID 42891596
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PubMedEuropean journal of case reports in internal medicine2026-10-15

Isolated Ulnar Artery Occlusion with Concurrent Internal Jugular Vein Thrombosis in Severe Iron-Deficiency Anaemia.

Alhaboobi Zahraa H ZH, Jawish Mohammad Kais A MKA, Alshawi Abdullah Layth AL, Homsi Abdulrahman Jihad AJ et al.

Severe iron deficiency anaemia (IDA) is increasingly recognized as a cause of a reversible hypercoagulable state, although simultaneous arterial and venous thrombosis are rare. Several mechanisms have been proposed, including reactive thrombocytosis, endothelial dysfunction, and changes in erythrocyte rheology, which may be secondary to reduced tissue oxygenation. We report the case of a 41-year-old woman with chronic menorrhagia due to fibroids who developed digital cyanosis and neurologic deficits due to severe microcytic anaemia (Hb 6.7 g/dl), associated with severe iron deficiency and mild thrombocytosis (442 ×109/l). She was discharged after blood transfusion with therapy for Raynaud phenomenon (amlodipine) but returned to the emergency room due to an acute right ulnar artery occlusion complicated by internal jugular vein thrombosis that was managed with embolectomy and anticoagulation. Her digital function fully recovered, and she remained free of thrombophilia. Our case highlights the potential for severe IDA to cause both arterial and venous thrombosis, even in the setting of only modest platelet elevations. Chronic tobacco use may have contributed to her presentation, and clinicians should remain aware of the possibility of thrombosis in patients presenting with severe IDA who do not have other known pro-thrombotic conditions. Severe iron deficiency anaemia can cause both arterial and venous thrombosis even in the setting of only mildly elevated platelet count, so platelet count alone should not be used as a determinant for thrombotic risk.Painless discoloration of the digits with diminished or non-existent pulse on examination in a young patient with no vascular risk factors requires vascular imaging prior to arriving at a diagnosis of Raynaud phenomenon, as the presentation can mimic acute arterial occlusion and require urgent intervention.A negative workup for thrombophilia and autoimmune disease cannot be used to rule out the possibility of a prothrombotic state, as severe iron deficiency anaemia can act as a prothrombotic trigger.

PMID 42877300
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PubMedThe AAPS journal2026-10-13

Physiologically based Biopharmaceutics Modeling (PBBM) Reveals a Low Dissolution-related Bioequivalence Risk for Immediate-Release Amlodipine Tablets.

de la Cruz Cruz Porfirio P, Gomide Larissa Lopes Rodrigues LLR, do Nascimento Gabriela Moraes GM, Urizar José Trinidad Pérez JTP et al.

A conservative BCS class III classification was recently proposed for amlodipine based on inconclusive permeability evidence. However, the scarce in vivo data suggest that amlodipine is slowly, though completely, absorbed. This means that the very rapid dissolution criterion associated with a BCS class III classification may be overly restrictive for immediate-release amlodipine products. The aim of this manuscript was to develop and validate a physiologically based biopharmaceutics model (PBBM) to assess the risk of bioequivalence failure associated with dissolution. Given that amlodipine is a lipophilic weak base, the absorption model incorporated a surrogate representation of intracellular lysosomal trapping through the FuEnt parameter, resulting in an adequate description of oral pharmacokinetics. Dissolution input included in vitro profiles obtained in phosphate buffer pH 6.8 at 50 rpm for different multisource products, fitted to either the Johnson model or the Z-factor approach. Although several products did not meet biowaiver dissolution criteria, virtual bioequivalence simulations conducted with the validated PBBM consistently predicted bioequivalence across tested formulations. Overall, these findings suggest that dissolution differences would have limited impact on the in vivo performance of amlodipine and support a low dissolution-related bioequivalence risk for immediate-release amlodipine tablets.

PMID 42864569
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