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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

PubMedJournal of clinical medicine2026-06-12

Sacubitril/Valsartan Improves Functional Capacity and Reverses LV Remodeling in Obese Patients with Hypertrophic HFpEF: A Randomized Open-Label Study.

Ovchinnikov Artem A, Potekhina Alexandra A, Shchendrygina Anastasiya A, Svirida Olga O et al.

Background: Heart failure with preserved ejection fraction (HFpEF) has multiple phenotypic manifestations with heterogeneous treatment responses. Objective: To evaluate the effect of sacubitril/valsartan (Sac/Val) on functional capacity and cardiac remodeling in overweight/obese HFpEF patients with concentric left ventricular hypertrophy (LVH). Methods: Sixty-one overweight/obese HFpEF patients (body mass index ≥ 25 kg/m2) with hypertensive LVH (LV mass index ≥ 115 g/m2 for men or ≥94 g/m2 for women) were randomized to Sac/Val (100-400 mg a day; n = 30) versus the usual care group (n = 31) for 6 months. Changes in six-minute walk test distance (6MWTD) were the primary outcomes. Secondary outcomes included changes in echocardiographic parameters of cardiac structure and function, and N-terminal pro-brain natriuretic peptide (NT-proBNP). Results: After 6 months of Sac/Val therapy, 6MWTD increased, and E/e' ratio, LV mass index, LA volume index, and NT-proBNP levels decreased compared with the usual care group (p < 0.05 for all). Conclusions: In overweight/obese patients with HFpEF and LVH, Sac/Val significantly improved functional capacity and reduced LV mass and filling pressure compared with standard medical therapy.

PMID 42279146
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PubMedJournal of separation science2026-06-12

A Robust and Universal LC-MS/MS Method for Determination of N-Nitrosodimethylamine in Pharmaceuticals Using a C30 Column.

An Byungchan B, Kim Unyong U, Seo Sumin S, Kim Jiyu J et al.

Since the 2018 valsartan recall, the genotoxic impurity N-nitrosodimethylamine (NDMA) has been frequently detected in various pharmaceuticals. Matrix variability often complicates routine testing, requiring customized analyses. We developed a universal LC-MS/MS method enabling consistent NDMA detection across diverse pharmaceuticals. Separation utilized a C30 column (150 mm × 4.6 mm I.D., 5 µm), offering superior retention and shape selectivity for polar nitrosamines compared to conventional reversed phases. Unlike C18 or pentafluorophenyl phases, which often exhibit limited retention for NDMA, the C30 phase provides exceptional shape selectivity and enhanced hydrophobic interactions. This structural advantage, supplemented by its resistance to phase dewetting under highly aqueous conditions further ensures robust resolution between NDMA and complex drug matrices. The mobile phase consisted of 0.1% v/v formic acid in water and methanol under gradient elution at 1.0 mL/min. Detection used atmospheric pressure chemical ionization in positive ion mode. The method demonstrated a linear range of 2.0-100.0 ng/mL (r2 > 0.999), with a limit of detection of 1.0 ng/mL and a limit of quantification of 2.0 ng/mL. Validation per International Council for Harmonisation (ICH) guidelines confirmed accuracy (87.7%-115.5%) and precision (coefficient of variation, CV ≤ 10.7%). Application to 30 diverse pharmaceutical products, including sartans and ranitidine, showed robust resolution (> 2.0) between the analyte and active pharmaceutical ingredients (APIs). Notably, NDMA was quantified in historical batches of ranitidine (164.83 ± 5.68 ng/mL), nizatidine (10.25 ± 0.52 ng/mL), and amitriptyline (2.28 ± 0.19 ng/mL). While the histamine type 2 receptor antagonists significantly exceeded the acceptable daily intake limit, the remaining 27 products showed no detectable NDMA. These findings highlight the method's effectiveness for real-world surveillance and the critical risk of post-manufacturing NDMA generation during prolonged storage. This universal C30-based method provides a practical, reliable tool for routine screening, facilitating regulatory compliance and improved patient safety without drugspecific method development.

PMID 42283086
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PubMedJournal of cardiothoracic surgery2026-06-11

Network pharmacology and experimental evaluation of Sanwei Tanxiang Tangsan in doxorubicin-induced heart failure.

Aruna, Dulan, Damdinjav Davaadagva D, Tungalag Battulga B et al.

Heart failure (HF) is a complex syndrome characterized by inflammation, oxidative stress, and cardiomyocyte apoptosis, for which effective and well-tolerated therapies remain limited. This study sought to explore the potential mechanisms by which Mongolian medicine Sanwei Tanxiang Tangsan (STX) may be associated with AKT1/p53-related signaling in the mitigation of HF, employing network pharmacology, molecular docking, and animal experimentation. Active constituents and corresponding targets of Mongolian medicine STX were systematically screened, followed by the construction of drug-disease interaction networks to identify pivotal proteins and pathways. A doxorubicin-induced HF rat model was established, and after four weeks of intragastric administration of Mongolian medicine STX and sacubitril/valsartan (angiotensin receptor-neprilysin inhibitor, positive control), cardiac functional parameters and expression levels of AKT protein 1 (AKT1), interleukin-6 (IL-6), and p53 were assessed. Nineteen active components were identified in Mongolian medicine STX, interacting with 153 HF-associated targets, among which AKT1, IL-6, and TP53 served as the core genes. Molecular docking analysis revealed that quercetin and luteolin possessed moderate predicted binding affinities and stable interactions with the corresponding targets. Animal experiments indicated that Mongolian medicine STX significantly reduced N-terminal pro-brain natriuretic peptide levels and altered myocardial AKT1, IL-6, and p53 protein abundance. However, echocardiographic parameters showed no statistically significant improvement compared with the Model group. Mongolian medicine STX may exert cardioprotective effects in HF, as reflected by improvements in biochemical and histopathological indicators, and these effects may be associated with AKT1/p53-related signaling pathways. However, direct pathway activation and causal mechanisms were not confirmed in the present study and require further investigation.

PMID 42271471
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PubMedEuropean journal of case reports in internal medicine2026-06-10

Sacubitril/Valsartan and Elevated Prothrombin Time/International Normalized Ratio in the Absence of Anticoagulant Therapy: A Newly Recognized Potential Adverse Drug Reaction.

Diyora Tanuj T, Ranajn Ayush A

Sacubitril/valsartan is the first approved angiotensin receptor-neprilysin inhibitor (ARNI) and a cornerstone therapy for heart failure with reduced ejection fraction (HFrEF). While its clinical benefits are well established, adverse drug reactions (ADRs) beyond the recognized profile of hypotension, hyperkalaemia, and renal impairment remain incompletely characterized. We report a case of isolated elevation in prothrombin time (PT) and international normalized ratio (INR) in a 58-year-old male with HFrEF receiving sacubitril/valsartan 49/51 mg twice daily, without any concurrent anticoagulant therapy. Approximately 6 weeks after initiation, PT was 18.4 seconds and INR was 1.7. Temporary discontinuation (dechallenge) led to normalization within 2 weeks; cautious re-challenge resulted in recurrent INR elevation. Naranjo Adverse Drug Reaction Probability Scale criteria yielded a score of +9, consistent with a probable drug-induced adverse event. This case highlights a potentially underrecognized coagulopathic ADR associated with sacubitril/valsartan, manifesting as elevated PT/INR without anticoagulant use. Clinicians should consider periodic coagulation monitoring in patients on ARNI therapy. Further pharmacovigilance studies and mechanistic investigations are strongly warranted. Sacubitril/valsartan may cause isolated elevation of prothrombin time and international normalized ratio in the absence of anticoagulant therapy, liver disease, or vitamin K deficiency; a potentially underrecognized adverse drug reaction (ADR).The dechallenge-rechallenge pattern, together with a Naranjo score of +9, provides robust pharmacovigilance evidence implicating angiotensin receptor-neprilysin inhibitor therapy as the causative agent and supports baseline and periodic coagulation monitoring.Clinicians prescribing sacubitril/valsartan should be vigilant for this coagulopathic ADR, especially in patients at elevated bleeding risk, and should report cases to pharmacovigilance registries to facilitate systematic signal detection.

PMID 42266384
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PubMedInternational journal of cardiology2026-06-10

High four-pillar guideline-directed medical therapy adoption in heart failure with reduced ejection fraction: A tertiary-centre registry from eastern India, 2019-2024.

Tripathi Suyash S

Whether dedicated tertiary heart-failure programmes in low- and middle-income countries can approach guideline-directed medical therapy (GDMT) targets, and whether temporal trends reflect prescribing optimisation or case-mix shift, remains unresolved. We characterise four-pillar GDMT adoption in an eastern Indian tertiary centre with systematic robustness testing. Repeated cross-sectional analysis in a prospective HFrEF registry (2022-2024 primary cohort, n = 319 patients). Half-yearly adoption assessed by Cochran-Armitage trend tests (Benjamini-Hochberg FDR), MI-adjusted logistic regression (m = 20), and Bayesian regression. Robustness: delta-adjusted MI, tipping-point, FMI, sacubitril-valsartan target-dose, E-value, time-by-diabetes interaction, quarterly ITS at ≥ 8 bins. Four-pillar composite rose from 48.6% (H12022) to 76.3% (H2 2024); MI-adjusted OR per half-year 1.24 (95% CI 1.05-1.47; p = 0.013). SGLT2 inhibitor drove the composite (OR 1.51; 1.22-1.86; p < 0.001); RAAS-i 1.24, MRA 1.11 and beta-blocker 0.98 not significant. Bayesian regression concurred (SGLT2i posterior probability 0.972; four-pillar 0.896). SGLT2i trend was robust to delta-adjusted MI, tipping-point beyond +/- 50 mL/min/1.73 m^2, and unmeasured confounding (E-value point 1.76; CI lower 1.44). Time-by-diabetes interaction was null; sacubitril-valsartan target-dose attainment 20.0%. Quarterly ITS at ≥ 8 bins returned non-significant level and slope changes at every feasible policy event. Tertiary specialist care approached but did not reach the four-pillar prescription ceiling (76.3%; residual 23.7-percentage-point gap). The SGLT2i trend was robust to MNAR, unmeasured confounding, and diabetes case-mix shift; quarterly ITS at ≥ 8 bins detected no policy-event association. Sacubitril-valsartan target-dose attainment (20.0%), single-centre design, and fragile non-SGLT2i E-values constrain generalisability.

PMID 42263948
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PubMedDrug design, development and therapy2026-06-10

Sacubitril/Valsartan Fails to Ameliorate Cisplatin-Induced Cognitive Impairment.

Alshammari Abdullah Obaid AO, Aldubayan Maha A MA, Alwashmi Ahmad H AH, Alhowail Ahmad H AH

Chemotherapy-induced cognitive impairment ("chemobrain") is mechanistically linked to oxidative stress, neuroinflammation, and apoptotic pathway dysregulation. Angiotensin receptor-neprilysin inhibitors and angiotensin II type-1 receptor blockers, such as sacubitril/valsartan (VS), have demonstrated neuroprotective potential; however, their effects in cisplatin (CIS)-induced neurotoxicity models remain poorly characterized. Forty male Wistar rats were randomized into four groups: Control, CIS (5 mg/kg, i.p). VS alone (≈40 mg/kg/day in drinking water), and CIS+VS, receiving three doses over 7 days. Cognitive performance was assessed 24 hours after the final dose via the Y-maze and novel object recognition test (NORT). Survival and body weight were monitored throughout. Hippocampal levels of reactive oxygen species (ROS), malondialdehyde (MDA), TNF-α, IL-1β, IL-6, total NF-κB, BAX, and total caspase-3 were quantified by ELISA, complemented by histopathological analysis. CIS produced dose-limiting toxicity, with 40% mortality and approximately 13% body weight loss over 8 days. The CIS+VS group exhibited greater toxicity, with 50% mortality and approximately 16% weight loss, while the control and VS animals gained weight. Both CIS and CIS+VS groups demonstrated significant impairment in spatial and recognition memory, as reflected by reduced novel-arm entries and time spent in the Y-maze, and diminished novel object exploration in NORT relative to controls. Hippocampal oxidative stress, neuroinflammatory, and apoptosis-related signaling markers were markedly elevated following CIS and remained comparably elevated in the CIS+VS group, consistent with persistent neuroinflammation. Histopathological examination confirmed severe hippocampal tissue damage in both CIS-treated groups, with no attenuation observed in the CIS+VS group. CIS induces significant cognitive deficits accompanied by elevated neurotoxicity markers. Under the tested dosing schedule, adjunctive VS failed to rescue cognitive function or attenuate hippocampal neuro-injury. These findings reinforce oxidative stress, neuroinflammation, and apoptotic signaling as key mechanistic drivers of chemobrain and indicate that VS confers no neuroprotective benefit in this model.

PMID 42266512
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