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pitavastatin + valsartan (Livalsartan / Livasartan)

✓ Approved

JW Pharmaceutical · AGTR1 · 小分子

什么是 pitavastatin + valsartan？

pitavastatin + valsartan 是一种小分子，由JW Pharmaceutical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Livalsartan, Livasartan
公司JW Pharmaceutical
药物类别小分子
分子靶点AGTR1, HMGCR
给药途径Oral (PO)
状态Approved
来源： ClinicalTrials.gov, JW Pharmaceutical

作用机制

分子靶点

pitavastatin + valsartan 作用于 2 个分子靶点：

AGTR1angiotensin II receptor type 1 (HAT1R, AT1)
HMGCR3-hydroxy-3-methylglutaryl-CoA reductase (LDLCQ3, LGMDR28)
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

pitavastatin + valsartan 针对 2 个适应症，涉及 2 个治疗领域。

治疗领域疾病/病症分期
Metabolism and nutrition disordersHypercholesterolaemia✓ Approved
Vascular disordersHypertension✓ Approved

相关研究文献

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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PubMedLa Clinica terapeutica2026-10-25

Myocardial remodelling during sacubitril/valsartan therapy in patients with chronic heart failure.

Tabukashvili David D, Kapetivadze Vera V, Lazashvili Tamar T, Maglaperidze Zviadi Z

The aim of the study was to identify differences between aliskiren and sacubitril/valsartan in their ability to influence cardiac remodelling, metabolic balance, neurohumoral activation, and clinical symptom severity. A comparative assessment of the clinical effectiveness and impact on the structural and functional state of the myocardium was conducted for two therapeutic strategies in patients with chronic heart failure in Georgia over a 12-month follow-up. The results demonstrated fundamentally different trajectories of therapeutic response. In the sacubitril/valsartan group, early clinical improvement was observed by 6 months, including significant reductions in systolic blood pressure (-6.2%, p<0.001), respiratory rate (-4.5%, p<0.001), and N-terminal pro-B-type natriuretic peptide levels (-10.0%, p<0.05), along with improved oxygen saturation (+3.5%, p<0.001). Left ventricular ejection fraction increased significantly already at 6 months (from 34.2±4.7% to 37.4±4.0%, p<0.001) and further at 12 months (40.5±3.5%, p<0.001), accompanied by rapid improvement in New York Heart Association functional class, with 9.3% of patients achieving New York Heart Association I by study end. In contrast, the aliskiren group exhibited slower but more pronounced structural reverse remodelling. Significant reductions in left ventricular end-systolic volume (-15.8%, p=0.009), end-diastolic volume (-17.6%, p=0.016), and end-systolic diameter (p=0.002) were observed only at 12 months, along with a modest but significant increase in ejection fraction (p=0.030). Regression of functional mitral and tricuspid regurgitation and a significant decrease in pulmonary artery systolic pressure (-19.7%, p<0.05) were more prominent in this group. Both therapies led to significant improvements in carbohydrate and lipid metabolism, including reductions in glycated haemoglobin, low-density lipoprotein cholesterol, and triglycerides (p<0.05 for all), indicating a favourable systemic metabolic effect. Overall, findings suggest that sacubitril/valsartan may be preferable when rapid clinical stabilization is required, whereas aliskiren may represent an effective therapeutic option for patients with advanced structural cardiac remodelling.

PMID 42922211
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PubMedJCEM case reports2026-10-25

Persistent atherogenic lipoprotein changes during lorlatinib therapy.

Shibue Kimitaka K, Kunimasa Kei K, Hamasaki Akihiro A

Lorlatinib, a third-generation anaplastic lymphoma kinase (ALK)/ROS1 tyrosine kinase inhibitor, frequently induces hypercholesterolemia and hypertriglyceridemia, but longitudinal qualitative lipoprotein changes remain incompletely characterized. We describe a 52-year-old woman with ALK-rearranged non-small cell lung cancer who developed persistent dyslipidemia despite lipid-lowering therapy. Before lorlatinib, total cholesterol was 164 mg/dL (SI [International System of Units]: 4.24 mmol/L) (reference range, 148-248 mg/dL [SI: 3.83-6.41 mmol/L]), low-density lipoprotein (LDL) cholesterol was 52 mg/dL (SI: 1.34 mmol/L) (reference range, 65-139 mg/dL [SI: 1.68-3.59 mmol/L]), and triglycerides were 54 mg/dL (SI: 0.61 mmol/L) (reference range, 30-117 mg/dL [SI: 0.34-1.32 mmol/L]). Within 3 weeks after lorlatinib initiation, these increased to 340, 245, and 166 mg/dL, respectively. Longitudinal profiling showed persistent apolipoprotein B (ApoB) elevation, increased oxidized LDL, and a prominent pre-β-lipoprotein fraction. Subclinical hypothyroidism was later detected, and pitavastatin was switched to rosuvastatin. This case highlights the potential value of ApoB and qualitative lipid assessment during prolonged lorlatinib therapy.

PMID 42923625
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PubMedJournal of analytical methods in chemistry2026-10-25

Recent Analytical Methods for N-Nitrosamine Analysis as Impurities in Drug Substances and Drug Products.

Pratiwi Rimadani R, Shalima Alifa Dhia AD, Mutakin, Hasanah Aliya Nur AN

N-nitrosamine (hereinafter nitrosamine) is among the organic impurities characterized by high potency as genotoxic and probable human carcinogens found in drug substances and drug products. This type of impurity has become a major concern in pharmaceutical industry, since one of nitrosamine type of impurities, NDMA, was detected in valsartan active pharmaceutical ingredients back in 2018. As a result, the development of sensitive, selective, and reliable analytical methods is essential to maintain regulatory compliance and safeguard of patient health. This review provides an overview of recent analytical strategies in 2020-2025 for detecting nitrosamine impurities in pharmaceutical substances and products, with an emphasis on chromatography-based techniques and groundbreaking analytical approaches. Gas chromatography (GC) and liquid chromatography (LC) coupled with mass spectrometry are the predominant methods, offering high sensitivity and selectivity for quantifying trace levels of these impurities. GC-based techniques are most appropriate for volatile and thermally stable nitrosamines, whereas LC-MS methods are suitable for polar, nonvolatile, thermally unstable, and structurally complex nitrosamines, including nitrosamine drug substance-related impurities (NDSRIs). Additionally, alternative LC-based detectors, such as ultraviolet (UV) and fluorescence detection (FLD), as well as total nitrosamine assays, chemiluminescence, and colorimetric methods, are evaluated as complementary or cost-effective analytical options. Key analytical considerations, including sample preparation, ionization techniques, matrix effects, derivatization strategies, and method validation, are also examined. Furthermore, this review highlights current challenges and future directions in nitrosamine analysis.

PMID 42923503
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PubMedCaspian journal of internal medicine2026-10-25

Angiotensin receptor neprilysin inhibitor (ARNI) in right ventricular failure and preserved LV ejection fraction: A systematic review and meta-analysis.

Safari Mohsen M, Safari Zeinab Z

Right ventricular (RV) failure with preserved left ventricular (LV) ejection fraction (LVEF ≥50%) is a distinct clinical entity often associated with pulmonary hypertension (PH), chronic lung diseases, or congenital heart defects, leading to significant morbidity and mortality. Angiotensin receptor neprilysin inhibitors (ARNI), such as sacubitril/valsartan, have demonstrated efficacy in left-sided heart failure, but their role in isolated RV failure remains understudied. A PRISMA-compliant search of PubMed, Embase, Cochrane Library, Web of Science, and Google Scholar was conducted from 2010 to 2025 for RCTs and prospective cohorts assessing ARNI in patients with RV failure and preserved LVEF. Inclusion: Adults with RV dysfunction (e.g., TAPSE <17 mm or RV S' <9.5 cm/s) and LVEF ≥50%; ARNI vs. standard care or pre-treatment; reporting RV parameters, sPAP, NT-proBNP, 6MWD, or NYHA class. Three studies (1 RCT, 2 prospective cohorts; n=120 patients) were included. ARNI improved TAPSE (WMD 1.2 mm, 95% CI 0.7-1.7; p<0.001; I²=0%), RV S' (WMD 0.5 cm/s, 95% CI 0.2-0.8; P=0.002; I²=0%), and reduced sPAP (WMD -7.5 mmHg, 95% CI -10.2 to -4.8; p<0.001; I²=15%). NT-proBNP decreased (WMD -1200 pg/mL, 95% CI -1700 to -700; p<0.001; I²=0%). 6MWD increased (WMD 30 m, 95% CI 10-50; P=0.003; I²=0%). NYHA class improved (RR 1.65 for ≥1 class improvement, 95% CI 1.15-2.37; P=0.007; I²=0%). ARNI enhances RV function, reduces pulmonary pressures, and improves functional status in RV failure with preserved LVEF.

PMID 42924105
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PubMedJournal of the American Heart Association2026-10-25

Efficacy and Safety of Pharmacologic Therapies in Nonobstructive Hypertrophic Cardiomyopathy: A Systematic Review.

Patel Shivam S, Gandhi Akash A, Pabani Arman A, Shah Richa R et al.

Nonobstructive hypertrophic cardiomyopathy (HCM) affects approximately one-third of all patients with HCM and carries substantial morbidity, yet no approved disease-modifying therapies exist. We conducted a systematic review of prospective interventional studies evaluating pharmacologic therapies in adults with nonobstructive HCM. A systematic search of PubMed, Cochrane Central Register of Controlled Trials, and Clinicaltrials.gov was performed through September 2025. Eligible studies included randomized and nonrandomized prospective interventional trials. A narrative synthesis was performed by pharmacologic class and outcome domain. Twenty-nine clinical trials evaluating 9 pharmacologic classes were identified: cardiac myosin inhibitors, cardiac sarcomere modulators, metabolic modulators, angiotensin II receptor blockers, angiotensin receptor-neprilysin inhibitors, mineralocorticoid receptor antagonists, SGLT2 (sodium-glucose cotransporter 2) inhibitors, beta blockers, and calcium channel blockers. Cardiac myosin inhibitors demonstrated reductions in left ventricular hypertrophy, improvements in diastolic function, and marked reductions in cardiac biomarkers, although improvements in exercise capacity and symptoms were variable. SGLT2 inhibition showed concordant improvements in diastolic function, atrial remodeling, biomarkers, and functional status in patients with symptomatic nonobstructive HCM and comorbid type 2 diabetes. Angiotensin receptor blockade showed signals of structural remodeling with valsartan and candesartan without consistent functional benefit. Mineralocorticoid receptor antagonism and angiotensin receptor-neprilysin inhibition demonstrated largely neutral effects. Among metabolic modulators, ninerafaxstat improved ventilatory efficiency and quality of life in patients with greater baseline symptom burden. Pharmacologic responsiveness in nonobstructive HCM is variable and appears to be mechanism- and disease stage-dependent. Ongoing trials evaluating cardiac myosin inhibitors, SGLT inhibitors, and novel therapeutic agents including ninerafaxstat and EDG-7500 will be critical in further defining the therapeutic landscape.

PMID 42924841
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