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

✓ Approved

Servier · CACNA1C · 小分子

什么是 perindopril + indapamide + amlodipine？

perindopril + indapamide + amlodipine 是一种小分子，由Servier研发。该药已获批，用于治疗相关适应症，给药途径：Oral (PO)。

药物档案

商品名Triplixam, Viacorind, S06590
公司Servier
药物类别小分子
分子靶点CACNA1C, ACE, SLC12A3
给药途径Oral (PO)
状态Approved
来源： ClinicalTrials.gov, Servier

作用机制

分子靶点

perindopril + indapamide + amlodipine 作用于 3 个分子靶点：

CACNA1Ccalcium voltage-gated channel subunit alpha1 C (CACNL1A1, CACNA1C-IT2)
ACEangiotensin I converting enzyme (DCP1, ACE1)
SLC12A3solute carrier family 12 member 3 (NCCT, NCC)
需要更深入的分析？Noah AI 可解释复杂机制并与同类药物比较。

治疗适应症

perindopril + indapamide + amlodipine 针对 1 个适应症，涉及 1 个治疗领域。

治疗领域疾病/病症分期
Vascular disordersHypertension✓ Approved

相关研究文献

PubMedHigh blood pressure & cardiovascular prevention : the official journal of the Italian Society of Hypertension2026-10-26

A Practical Treatment Platform Version 3.0 for Using Angiotensin Receptor Blocker-Based Single-Pill Combinations in Patients With Hypertension.

Tocci Giuliano G, Burnier Michel M, de la Sierra Alejandro A, Grassi Guido G et al.

Elevated blood pressure (BP) is the leading cause of cardiovascular disease and a major contributor to mortality, affecting almost one third of the adult population worldwide. Despite strong scientific evidence, guidelines and multiple therapeutic options, many patients remain undertreated or uncontrolled, largely due to poor medication adherence and medical inertia. Complexity of multi-pill regimens contributes significantly to non-adherence, whereas single-pill combinations (SPCs) improve adherence and persistence, accelerate BP control, and promote better long-term outcomes than multiple combinations. Appropriate selection of SPC in individual hypertensive patients may be a difficult though very important task for physicians. Thus, development of tools that may facilitate use of SPC in clinical practice is desirable. Among renin-angiotensin system blockers, olmesartan (OM) has demonstrated sustained efficacy, favourable tolerability, both as monotherapy and in SPCs with amlodipine and/or hydrochlorothiazide, which are available in multiple dosages. The present OM-based platform builds on earlier frameworks and incorporates guidelines' updates complemented by a systematic review of available literature. This "3.0" proposal expands patient categorization to include comorbidities or complications often overlooked in clinical practice guidelines, providing a practical, evidence-based approach to support individualized hypertension management complementing guideline recommendations.

PMID 42928416
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PubMedPakistan journal of pharmaceutical sciences2026-10-25

Amlodipine besylate and valsartan combined mucoadhesive buccal patch formulations: In-vitro release and ex-vivo permeation studies.

Anwar Nosheen N, Gul Rahman R, Jan Syed Umer SU, Shahwani Ghulam Razaque GR et al.

Oral fixed-dose combinations of Amlodipine Besylate and Valsartan are widely prescribed for hypertension but are associated with first-pass metabolism and variable bioavailability. Buccal drug delivery provides a favorable substitute to improve systemic availability and provide sustained release. This study aimed to develop and assess mucoadhesive buccal patches containing Amlodipine Besylate and Valsartan to enhance bioavailability and achieve controlled drug release over 24 hours. Buccal patches were developed via the solvent-casting method using Hydroxypropyl Methylcellulose, Polyvinylpyrrolidone, Methylcellulose, Sodium Alginate and Metolose as backing membrane polymers. All the prepared films were evaluated for physicochemical parameters by means of X-ray Diffraction (XRD), Fourier transform infrared spectroscopy (FTIR), Scanning electron microscopy (SEM) and in vitro and ex vivo drug release. In-vitro drug release was studied with USP Apparatus II (paddle method) in 500 ml 6.8 pH phosphate buffer at 37 ± 0.5°C and 50 rpm for 24 hours. Ex vivo permeation studies were performed using a Franz diffusion cell fitted with rabbit buccal mucosa under similar conditions. The formulations generally exhibited acceptable physicochemical characteristics within the evaluated parameters. The developed films appeared transparent with a uniform distribution of components. FTIR analysis did not indicate any detectable incompatibility or significant interaction between the drugs and excipients under the study conditions. Among all formulations, F1 contained the highest drug release and permeation. After 24 hours, cumulative release reached 84.45% for amlodipine and 88.03% for valsartan. Ex-vivo permeation was 76.31% and 78.42% for amlodipine and valsartan, respectively. Furthermore, buccal films' histopathological and stability studies were found to be harmless and functioned as an efficient dosage system. The developed mucoadhesive buccal patches successfully delivered both drugs in a sustained manner. Formulation F1 showed superior release and permeation profiles, suggesting its potential as substitute to conventional oral dosage forms for improved hypertension management.

PMID 42924971
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PubMedJournal of pediatric endocrinology & metabolism : JPEM2026-10-23

Apparent mineralocorticoid excess mimicking Bartter syndrome in infancy.

Hatipoğlu Sevcan S, Yıldırım Erkam E, Şalbaş Özge Yıldırım ÖY, Şahin Kadriye Cansu KC et al.

Apparent mineralocorticoid excess (AME) syndrome is a rare monogenic disorder caused by loss-of-function variants in the HSD11B2 gene encoding 11β-hydroxysteroid dehydrogenase type 2 (11β-HSD2). Deficient enzyme activity results in cortisol-mediated activation of the mineralocorticoid receptor, leading to low-renin hypertension. Because affected infants frequently present with polyuria and hypokalemic metabolic alkalosis, AME syndrome is often misdiagnosed as Bartter syndrome, resulting in significant diagnostic delay. A 13-month-old girl presented with polyuria, hypokalemic metabolic alkalosis, hypercalciuria, and failure to thrive and was initially managed as Bartter syndrome. During follow-up, persistent hypertension accompanied by markedly suppressed plasma renin activity and aldosterone levels prompted evaluation for monogenic hypertension. Urinary steroid analysis demonstrated a markedly reduced cortisone-to-cortisol ratio (0.02), consistent with 11β-HSD2 deficiency. Next-generation sequencing of the HSD11B2 gene identified a homozygous likely pathogenic splice-site variant, c.665-1G>A, confirming the diagnosis of AME syndrome. Treatment with spironolactone, amlodipine, potassium supplementation, and dietary salt restriction achieved blood pressure control and improved electrolyte abnormalities. AME syndrome should be included in the differential diagnosis of infants presenting with hypokalemic metabolic alkalosis and polyuria, particularly when hypertension is detected. Systematic blood pressure assessment is essential in this clinical context, as early recognition of this monogenic disorder may prevent long-term cardiovascular and renal complications.

PMID 42912472
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PubMedMolecular pharmaceutics2026-10-22

Sequential Molecular Events in the Solid-State Acid-Base Incompatibility of Amlodipine Besylate and Citric Acid: 2D-COS-PXRD and 2D-COS-FTIR as Orthogonal Probes of Reaction Sequence in Drug-Excipient Solid-State Incompatibility.

Chenkual Laltanpuii L, Lalchandani Dimple S DS, Sathala Pavan Kumar PK, Divate Madhuri M et al.

Drug-excipient incompatibility in solid oral dosage forms can generate toxic degradants and compromise potency without producing a visible macroscopic signal in early development. We reported, for the first time, a mechanistically resolved, temperature-sequenced characterization of the solid-state acid-base incompatibility between amlodipine besylate (AMLO; pKa ≈ 9.4) and citric acid (CA; pKa1 3.13; ΔpKa = 6.27) using six orthogonal techniques: DSC, TGA, isothermal titration calorimetry (ITC), powder X-ray diffractometry with two-dimensional correlation spectroscopy (2D-COS-PXR), FTIR with 2D-COS (2D-COS-FTIR), and stability-indicating HPLC coupled to LC-QToF HRMS. Binary mixtures were thermally stressed at 40-90 °C (7 day isothermal, closed-vial). ITC confirmed a spontaneous, entropy-dominated interaction (ΔG = -5.14 kcal/mol; -TΔS = -3.78 kcal/mol; N ≈ 1:1; KD = 197 μM) driven by proton transfer to the AMLO dihydropyridine nitrogen with concurrent besylate displacement. DSC showed complete loss of the AMLO Form-I endotherm (onset 201.01 °C), replaced by a single event at 155.57 °C with super-additive enthalpy (+19.50 J/g), consistent with amlodipine citrate salt formation. Application of Noda's 2D-COS algorithm to temperature-resolved PXRD and FTIR datasets independently resolved a four-stage mechanism, viz., CA surface proton mobilization (40 °C) → amlodipine citrate nucleation (50-60 °C) → besylate counter-ion displacement and d-spacing contraction (∼70 °C) and → partial amorphization and acid-catalyzed covalent degradation (80-90 °C). Three sequential-order reversals in the 2D-COS-FTIR asynchronous map independently corroborated the Stage-3 crystallographic sequence. HPLC revealed a 4.48-fold enhancement of AMLO loss in the mixture (7.97%) versus pure drug (1.78%), with LC-QToF HRMS identifying four mixture-unique degradants consistent with the four-stage model. This is also the first pharmaceutical application of 2D-COS-PXRD as a mechanistic probe of sequential crystallographic events in drug-excipient incompatibility.

PMID 42906161
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PubMedAmerican journal of cardiovascular drugs : drugs, devices, and other interventions2026-10-22

Beyond Conventional Antihypertensives: RNA Interference, Endothelin Antagonism, and Aldosterone-Synthase Inhibition in the Current Therapeutic Landscape.

Gaudio Giovanni Vincenzo GV, Derosa Giuseppe G, De Angelis Giuseppe G, Tremamondo John J et al.

Hypertension is the leading modifiable cardiovascular risk factor, yet long-term adherence to antihypertensive therapy remains suboptimal. RNA-based approaches targeting hepatic angiotensinogen (AGT) have emerged as an attractive strategy for upstream renin-angiotensin-aldosterone system suppression and warrant a timely, focused review of the field. PubMed/MEDLINE, ClinicalTrials.gov and the most relevant scientific and academic databases were searched up to February 2026 to draft a narrative review of peer-reviewed clinical trials, pivotal translational studies, contemporary hypertension guidelines, and official regulatory documents relevant to innovative antihypertensive treatments, such as antisense AGT suppression (zilebesiran), endothelin antagonism (aprocitentan), and aldosterone-synthase inhibition (baxdrostat). Zilebesiran demonstrated durable blood-pressure lowering in monotherapy (KARDIA-1: placebo-adjusted ambulatory systolic blood pressure (BP) - 16.7 mmHg at month 3) and as add-on therapy (KARDIA-2: greatest effect with indapamide background). KARDIA-3 extended evaluation to a higher-risk, heavily medicated population, in which the primary endpoint was not met. The ongoing ZENITH outcomes trial will determine whether AGT silencing reduces hard cardiovascular end-points. Aprocitentan reduced office and ambulatory systolic BP in resistant hypertension (PRECISION trial) and has received regulatory approval in the USA, EU, and UK, with specific monitoring requirements for fluid retention and hematological effects. Baxdrostat demonstrated selective aldosterone-synthase inhibition with meaningful BP reductions across two phase II trials. RNA interference targeting AGT represents one of the most advanced disease-modifying platforms in hypertension, alongside the already-approved endothelin antagonism and the emerging aldosterone synthase inhibition strategy. The available evidence supports cautious optimism and continued translational investment, but not premature adoption into routine practice.

PMID 42907726
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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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