Drug Database
PI

pitavastatin + valsartan (Livalsartan / Livasartan)

✓ Approved

JW Pharmaceutical · AGTR1 · Small Molecule

What is pitavastatin + valsartan?

pitavastatin + valsartan is a small molecule developed by JW Pharmaceutical. It is approved for therapeutic indications via oral (po).

Drug Profile

Brand NamesLivalsartan, Livasartan
CompanyJW Pharmaceutical
Drug ClassSmall Molecule
Molecular TargetAGTR1, HMGCR
RouteOral (PO)
StatusApproved
Sources: ClinicalTrials.gov, JW Pharmaceutical

Mechanism of Action

Molecular Targets

pitavastatin + valsartan acts on 2 molecular targets:

AGTR1angiotensin II receptor type 1 (HAT1R, AT1)
HMGCR3-hydroxy-3-methylglutaryl-CoA reductase (LDLCQ3, LGMDR28)
Want deeper analysis?Noah AI can explain complex mechanisms and compare to similar drugs.

Therapeutic Indications

pitavastatin + valsartan is developed for 2 unique indications across 2 therapeutic areas.

Therapeutic AreaConditionPhase
Metabolism and nutrition disordersHypercholesterolaemia✓ Approved
Vascular disordersHypertension✓ Approved

Related Research Articles

PubMedFrontiers in endocrinology2026-07-25

A multi-center, open-label, observational study to evaluate the efficacy and safety of LivaloZet® tablets in patients with dyslipidemia and metabolic syndrome: PIVOT study protocol.

Joung Kyong Hye KH, Ku Bon Jeong BJ

Dyslipidemia accompanied by metabolic syndrome substantially elevates cardiovascular risk by clustering multiple risk factors, including abdominal obesity, hypertension, hyperglycemia, and atherogenic dyslipidemia. The prevalence of both conditions is rising in Korea, underscoring the need for effective and metabolically safe lipid-lowering therapy. LivaloZet® Tablet (pitavastatin/ezetimibe fixed-dose combination) addresses this need by combining complementary cholesterol-lowering mechanisms with the glucose-neutral profile of pitavastatin. The PIVOT study is a multi-center, non-interventional, prospective observational study enrolling up to 10,000 Korean adult patients with dyslipidemia accompanied by metabolic syndrome who have been prescribed LivaloZet® Tablets (pitavastatin/ezetimibe 2/10 mg or 4/10 mg) by their treating physician as part of routine clinical care. Metabolic syndrome is defined according to the modified NCEP-ATP III criteria for the Asian population. Assessments are conducted at baseline, Week 24, and Week 48. The primary endpoint is the percent change in low-density lipoprotein cholesterol (LDL-C) from baseline at Week 24. Secondary endpoints include LDL-C changes at Week 48, changes in the full lipid panel, and LDL-C target achievement rates by cardiovascular risk group. Exploratory endpoints encompass glucose metabolism parameters (HbA1c, HOMA-IR, HOMA-β), medication adherence and persistence, and high-sensitivity C-reactive protein. Safety is assessed through adverse events, laboratory tests, and vital signs, including systematic monitoring of AST, ALT, and creatine kinase for statin-related hepatotoxicity and myopathy. The study was approved by the Institutional Review Board of Chungnam National University Hospital (2025-07-065) and is registered at ClinicalTrials.gov (NCT07523971). The PIVOT study will generate prospective large-scale real-world evidence on the LDL-C-lowering effectiveness and safety patterns associated with use of a pitavastatin/ezetimibe fixed-dose combination in Korean patients with dyslipidemia accompanied by metabolic syndrome. The inclusion of glucose metabolism and inflammatory markers will provide descriptive information on the metabolic safety profile of this regimen. As a non-randomized, single-arm observational study, this design cannot establish causal effects or comparative efficacy versus other lipid-lowering regimens. Findings should be interpreted descriptively, acknowledging potential confounding by indication, selection bias, and inter-laboratory variability.

PMID 42500128
Read full article →
PubMedPharmacology & therapeutics2026-07-24

Biomarker-guided pharmacotherapy in cardiovascular-kidney-metabolic syndrome: A three-dimensional framework for precision drug selection and monitoring.

Li Yafeng Y, Song Wenzhu W, Huan Chengyu C, Xu Keman K et al.

Cardiovascular-kidney-metabolic (CKM) syndrome, formally defined by the American Heart Association in 2023, affects approximately 90% of US adults, who meet criteria for stage 1 or higher. The rapid convergence of multiple drug classes on CKM pathways-SGLT2 inhibitors, finerenone, GLP-1 receptor agonists, ARNI, and interleukin-directed therapies-has created an urgent need for pharmacologically grounded frameworks that guide drug selection, interpret biomarker responses, and monitor target engagement across interconnected organ systems. This review proposes a three-dimensional biomarker-guided approach to precision pharmacotherapy in CKM syndrome. In the organ-specific dimension, we map key biomarkers to their corresponding drug targets and elucidate the molecular mechanisms underlying drug-biomarker interactions: SGLT2 inhibitors attenuate myocardial injury through metabolic substrate shifting toward ketone body utilization and, based on preclinical evidence, NHE1 inhibition; neprilysin selectivity of sacubitril/valsartan explains the differential natriuretic peptide response; and tubuloglomerular feedback mediates the renoprotective hemodynamic effects of SGLT2 inhibitors. In the pathway-specific dimension, we identify cross-system biomarkers-hs-CRP, IL-6, galectin-3, GDF-15, and FGF21-that reveal shared druggable targets spanning the IL-1β/NLRP3 inflammasome axis (canakinumab, colchicine), IL-6 trans-signaling (ziltivekimab), and FGF21/β-klotho metabolic signaling. In the temporal dimension, we demonstrate how serial biomarker trajectories serve as pharmacodynamic readouts that distinguish therapeutic drug effects from disease progression, including the initial eGFR dip with SGLT2 inhibitors and natriuretic peptide changes during combination therapy. Central to this framework is the concept of "pharmacological phenotyping"-using multi-biomarker panels to define drug-responsive pathophysiological states that directly inform therapeutic selection, analogous to companion diagnostics in oncology. We further present a comprehensive drug-biomarker interaction matrix with pharmacological rationale and analyze the emerging drug development pipeline, including RNA-based Lp(a) therapeutics, FGF21 analogues, galectin-3 inhibitors, and in vivo CAR-T anti-fibrotic approaches. This framework provides a practical roadmap for biomarker-guided precision pharmacotherapy in CKM syndrome.

PMID 42492739
Read full article →
PubMedPakistan journal of pharmaceutical sciences2026-07-23

Formulation and evaluation of sustained-release pitavastatin-loaded chitosan nanoparticles for enhanced anti-hyperlipidemic activity.

Arshad Amina A, Zaman Muhammad M, Riaz Humayun H, Haider Muhammad Sajjad MS et al.

Pitavastatin (PVN), a BCS class-II drug, exhibits poor aqueous solubility leading to limited oral bioavailability and therapeutic efficacy. This study aimed to enhance the solubility and anti-hyperlipidemic efficacy of Pitavastatin (PVN) by encapsulating it in chitosan-based polymeric nanoparticles. Pitavastatin-loaded chitosan nanoparticles (NPs) were prepared using the ionic gelation method. Formulations were characterized by particle size, zeta potential, drug loading, In-vitro drug release and surface morphology. Fourier transform infrared spectroscopy (FTIR), X-ray diffraction (XRD), thermal analysis (TGA and DSC), ex-vivo intestinal permeability and in-vivo pharmacodynamic analysis were also performed. The size of PVN-loaded NP ranged from 219.9±1.11 to 292.7±2.29 nm with PDI 0.2-0.4, surface charge of +28.4 ± 0.43 to 32.5 ± 1.02 mV and entrapment efficiency 65±1.12-93±1.23%. Solubility in different media (PBS (pH 6.8), 0.1N HCl (pH 1.2) and distilled water showed a 56-102-fold increase compared to PVN. SEM analysis revealed a smooth surface and spherical geometry of the NP. FTIR analysis confirmed that there was no physicochemical interaction between PVN and chitosan in NP formulations (NP1-NP5). XRD and thermal analysis indicated the amorphous nature of PVN-loaded NP. In-vitro drug release from NP formulations (NPI-NP5) ranged from 80.97±4.80 to 81±3.90% indicating sustained release, while ex-vivo intestinal permeability was 1.5-fold higher than PVN. The optimized formulation (NP1) followed Higuchi release model, indicating Fickian diffusion. Pharmacodynamic analysis of lipid profiles in hyperlipidemic albino rats suggested that NP1 reduced low-density lipoprotein (LDL) by 33±1.24 %, total cholesterol by 29±2.13% and triglycerides by 23±1.21%, showing better results than PVN. Chitosan-based Pitavastatin nanoparticles successfully enhanced drug solubility and provided sustained release, leading to improved ex-vivo permeability and greater in-vivo anti-hyperlipidemic activity in albino rats. This approach represents a promising strategy for enhancing therapeutic potential of Pitavastatin.

PMID 42489300
Read full article →
PubMedAmerican journal of cardiovascular disease2026-07-23

Retrospective real-world study on effectiveness and safety of sacubitril/valsartan in Indian patients with heart failure.

Mehta Ashwani A, Mehta Kapil Dev KD, Mangaonkar Komal K

This study aimed to evaluate the clinical, biochemical, and functional outcomes of sacubitril/valsartan therapy in Indian patients with heart Failure (HF) with reduced ejection fraction (HFrEF) in routine practice. We conducted a retrospective, single-centre, observational study at The Heart Clinic, New Delhi, India. Adult patients (≥18 years) with the New York Heart Association (NYHA) class II-IV HF who were newly initiated on sacubitril/valsartan and had ≥12 months of follow-up were included in the study. Clinical, echocardiographic, and biochemical data were extracted from the electronic medical records. The primary outcomes at 12 months were changes in left ventricular ejection fraction (LVEF), NYHA classification, N-terminal pro-B-type natriuretic peptide (NT-proBNP) levels, estimated glomerular filtration rate (eGFR), and the number of patients receiving the maximum dose of sacubitril/valsartan. The secondary outcomes were cardiovascular and all-cause mortality. A total of 300 patients were analyzed (mean age, 61.3 years; 69.7% male). Hypertension (266 patients, 88.7%), diabetes (163 patients, 54.3%), and chronic kidney disease (153 patients, 51%) were the most frequent comorbidities. At 12 months, the mean LVEF increased significantly from 29.57% to 34.66% (absolute gain of 5.09%, P<0.0001). A significant improvement in functional ability was observed, with 282 patients (94%) classified as NYHA class II at 12 months compared with 22 patients (7.3%) at baseline (P<0.0001), and the NT-proBNP levels decreased from 2344.5 ± 1951.8 pg/mL to 564 ± 410.3 pg/mL (P<0.0001). Renal function remained stable (mean change in eGFR +2.01 mL/min/1.73 m2, P=0.088). Over half of the cohort (52.3%) achieved a target dose of 200 mg twice daily. No cardiovascular or all-cause deaths were observed. In this real-world Indian cohort, sacubitril/valsartan was associated with significant improvements in systolic function, functional class, and NT-proBNP levels, with preserved renal function and good tolerability. These findings support the use of sacubitril/valsartan as a cornerstone therapy for HFrEF management in routine clinical practice.

PMID 42488489
Read full article →
PubMedCardiology research and practice2026-07-23

Dapagliflozin Augmentation of Sacubitril/Valsartan Therapy in Patients With Heart Failure Following PCI-Treated Acute Myocardial Infarction: A Meta-Analysis of Clinical Efficacy and Safety.

Tang Tang T, Yu Huimin H, Zhang Yun Y, Li Shuang S et al.

To systematically review the efficacy and safety of dapagliflozin and sacubitril/valsartan (SV) in patients with heart failure (HF) following percutaneous coronary intervention (PCI)-treated acute myocardial infarction (AMI) and to provide evidence for clinical practice. Seven electronic databases were systematically searched from their inception to July 25, 2024. Following literature screening, data extraction, and risk of bias assessment, 14 randomized controlled trials involving 1310 patients were included. A meta-analysis was subsequently conducted using RevMan 5.4 and Stata 18. Meta-analysis results showed that dapagliflozin combined with SV was superior to the control in improving left ventricular ejection fraction (LVEF) (WMD = 3.79, 95% CI: 2.70∼4.87; p < 0.001) and reducing N-terminal pro-brain natriuretic peptide (NT-proBNP) levels (WMD = -83.49, 95% CI: -129.33∼-37.65; p = 0.0004). This combination also significantly reduced left ventricular end-diastolic diameter (LVEDD) (WMD = -2.27, 95% CI: -3.64∼-0.90; p = 0.001), left ventricular end-systolic diameter (LVESD) (WMD = -3.29, 95% CI: -3.98∼-2.59; p < 0.001), left ventricular remodeling index (LVRI) (WMD = -0.08, 95% CI: -0.10∼-0.06; p < 0.001), and left ventricular mass index (LVMI) (WMD = -8.84, 95% CI: -12.25∼-5.43; p < 0.001), while increasing the 6-min walking distance (6MWD) (WMD = 51.74, 95% CI: 32.33∼71.14; p < 0.001). Compared with SV monotherapy, adding dapagliflozin reduced major adverse cardiovascular event (MACE) incidence (OR = 0.24, 95% CI: 0.15∼0.39; p < 0.001). However, no significant difference in adverse drug events (ADEs) was observed. Subgroup analyses revealed no significant differences in NT-proBNP (WMD = -194.85, 95% CI: -396.53∼6.82; p = 0.06), LVEDD (WMD = -1.50, 95% CI: -3.90∼0.89; p = 0.22), or the incidence of ADE (OR = 1.26, 95% CI: 0.74∼2.14; p = 0.39) when the follow-up duration was short (≤ 12 w). Additionally, significant heterogeneity was observed across studies for most outcomes. However, this heterogeneity was markedly reduced in the long-term follow-up subgroup (≥ 24 w), and the results were consistent with those of previous meta-analyses. Current evidence suggests that early initiation of dapagliflozin combined with SV offers superior efficacy and cardiovascular benefits for patients with HF following PCI-treated AMI. These benefits become increasingly evident with sustained treatment. Nevertheless, these conclusions warrant validation through more high-quality evidence.

PMID 42491272
Read full article →
PubMedFrontiers in pharmacology2026-07-23

Pharmacovigilance assessment of gout: a real-world study using the FAERS database.

Ren Honghao H, Yao Nannan N, Ren Xiaodong X, Su Yani Y et al.

Drug intervention is a key method for preventing gout, various drugs have been implicated as potential risk factors in individual studies. This study aims to comprehensively identify drugs linked to the development of gout. Data were obtained from the FDA Adverse Event Reporting System (FAERS), and disproportionality analysis was employed to quantitatively assess the associations between drugs and gout. Four complementary signal detection methods-Reporting Odds Ratio (ROR), Proportional Reporting Ratio (PRR), Bayesian Confidence Propagation Neural Network (BCPNN), and Multi-item Gamma Poisson Shrinker (MGPS)-were utilized. To further delineate exposure-outcome relationships and identify influential predictors, least absolute shrinkage and selection operator (LASSO) logistic regression was implemented. Time-to-onset (TTO) analysis was conducted to examine the temporal dynamics between drug initiation and the occurrence of gout. Finally, a comprehensive assessment of the therapeutic indications of the drugs was performed. A total of 35 drugs were ultimately identified as potentially associated with the onset and progression of gout. Among these, several agents have been previously reported in the literature as having possible links to gout development. In addition, a number of novel candidates were detected for which evidence of an association with gout remains limited or has not been clearly established. These include Lenalidomide, Sacubitril valsartan, Ruxolitinib, Treprostinil, Octreotide, Selexipag, Rosuvastatin, Sitagliptin, Riociguat, Epoprostenol, Patiromer, Dasabuvir ombitasvir paritaprevir ritonavir, Tafamidis, Sparsentan, and Iloprost. Furthermore, TTO analysis suggested that approximately 75% of gout events occurred within 0.6 years following initiation of therapy. These pharmacotherapeutic agents are employed across diverse clinical settings, encompassing haematological malignancies, cardiovascular diseases, and pulmonary hypertension. These findings suggest the potential for targeted monitoring of drug-associated gout in clinical practice. When administering these medications, it may be crucial to regularly assess patients' uric acid levels and maintain heightened awareness for the possible onset of gout.

PMID 42488563
Read full article →

+7342 more articles available with a free account

Sign up free to view all articles →

Ask about pitavastatin + valsartan