Drug Database
EZ

ezetimibe + rosuvastatin (NVP1205 / NVP 1205)

✓ Approved

NVP Healthcare · HMGCR · Small Molecule

What is ezetimibe + rosuvastatin?

ezetimibe + rosuvastatin is a small molecule developed by NVP Healthcare. It is approved for therapeutic indications via oral (po).

Drug Profile

Brand NamesNVP1205, NVP 1205
CompanyNVP Healthcare
Drug ClassSmall Molecule
Molecular TargetHMGCR, NPC1L1
RouteOral (PO)
StatusApproved
Sources: ClinicalTrials.gov, NVP Healthcare

Mechanism of Action

Molecular Targets

ezetimibe + rosuvastatin acts on 2 molecular targets:

HMGCR3-hydroxy-3-methylglutaryl-CoA reductase (LDLCQ3, LGMDR28)
NPC1L1NPC1 like intracellular cholesterol transporter 1 (SLC65A2, LDLCQ7)
Want deeper analysis?Noah AI can explain complex mechanisms and compare to similar drugs.

Therapeutic Indications

ezetimibe + rosuvastatin is developed for 1 unique indication across 1 therapeutic area.

Therapeutic AreaConditionPhase
Metabolism and nutrition disordersHyperlipidaemia✓ Approved

Related Research Articles

PubMedZhonghua nan ke xue = National journal of andrology2026-11-11

[Adverse drug reaction signals of statin-induced male sexual dysfunction: Mining and analysis based on the FDA Adverse Event Reporting System].

Gao Wen W, Sun Ling L, An Xiaotong X, DU Wei W et al.

Objective To mine and analyze the adverse drug reaction (ADR) signals of statin-induced male sexual dysfunction based on the database of the FDA Adverse Event Reporting System (FAERS). Methods We searched the FAERS database for the case reports published from the first quarter of 2004 to the fourth quarter of 2023, in which statins were shown as the primary suspected drugs for sexual dysfunction ADRs in male patients, and subjected the reports to standardized processing according to the WHO Adverse Reaction Terminology. We detected the ADR signals using the reporting odds ratio (ROR), proportional reporting ratio (PRR), and Bayesian confidence propagation neural network (BCPNN). Results A total of 2 408 adverse event reports of male sexual dysfunction associated with statins as the primary suspected drug were extracted from the FAERS database, involving 2 173 patients (some patients reported multiple adverse events).The largest proportion of the patients (47.22% ［1 026/2 173］) were aged 18－65 years old, primarily from the United States (n = 897, 41.28%), the largest number of cases reported in 2010 (n = 183, 8.42%), and atorvastatin ranking the first for intervention (n= 990, 41.11%), followed by rosuvastatin (n = 639, 26.54%) and simvastatin (n = 502, 20.85%). Totally, 28 high-risk ADR signals for male sexual dysfunction were identified, among which, hypoesthesia was found related to 7 statins (atorvastatin, rosuvastatin, simvastatin, pravastatin, fluvastatin, lovastatin, and pitavastatin), and ED associated with 6 (atorvastatin, rosuvastatin, simvastatin, pravastatin, ezetimibe and lovastatin).ConclusionSufficient medication evaluation is necessitated prior to clinical application of statins, especially for patients aged 18－65 years, with caution against the development of male sexual dysfunction within 30 days of administration. Clinicians should pay attention to ADR signals beyond those listed in the drug package inserts to ensure the safety of medication.

PMID 43012181
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PubMedBritish journal of pharmacology2026-11-11

Interpretable multimodal network analysis of lipid-lowering therapies.

Dall'Olio Daniele D, Pedrelli Matteo M, Sala Claudia C, Grassi Francesca F et al.

Multimodal integration of clinical and omics data could clarify the hepatic mechanisms of lipid-lowering therapies, but interpretable methods for heterogeneous data remain limited. The objective was to apply interpretable multimodal networks (IMNs), a topology-aware framework that condenses heterogeneous omics and clinical data into compact, cross-modal modules, to characterize treatment-specific hepatic responses to simvastatin and ezetimibe. In the Stockholm Study, patients scheduled for cholecystectomy were randomized for 4 weeks to simvastatin, ezetimibe, their combination or placebo. We integrated liver transcriptomics and DNA methylation with plasma/bile biochemistry, including lipoprotein functionality, on the human protein-protein interactome to build treatment-specific IMNs and evaluated selected network-derived predictions in a human hepatocyte-like model (SOAT2-only-HepG2). IMNs reduced dimensionality while preserving network topology, producing distinct molecular signatures for simvastatin, ezetimibe and combination therapy that mapped to different biological processes; the placebo network was less multimodal and more fragmented. IMNs highlighted apolipoprotein-centred modules and predicted drug effects on APOA2, PPARA and PTPRS, linked to plasma C-peptide. In SOAT2-only-HepG2 cells, selected predictions were supported experimentally, including APOA2 induction and ezetimibe-associated PTPRS upregulation. IMNs provide a practical, interactome-based route from multimodal patient data to focused, testable hypotheses about lipid-lowering therapies, yielding compact features suitable for downstream predictive modelling while retaining biological interpretability.

PMID 43010736
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PubMedInternational journal of cardiology2026-11-10

Moderate-intensity statin and ezetimibe combination therapy versus high-intensity statin on coronary atherosclerotic plaque.

Lee Joo Myung JM, Lee Sang Yoon SY, Choi Ki Hong KH, Park Taek Kyu TK et al.

Effect of moderate-intensity statin and ezetimibe is known to be non-inferior to high-intensity statin in prevention of adverse clinical events in patients with coronary atherosclerotic disease. However, data regarding regression of coronary atherosclerotic plaque remains limited. In this randomized, non-inferiority trial, patients with intermediate coronary artery stenosis were randomly assigned 1:1 to either moderate-intensity rosuvastatin (10 mg) with ezetimibe or high-intensity rosuvastatin (20 mg) group. Intravascular ultrasound (IVUS) was performed at baseline and after 12 months or longer to quantify the coronary plaque response. Primary end point was absolute changes in percent atheroma volume (PAV) between baseline and follow-up IVUS, and non-inferiority margin was as 2.5%. Secondary end point was major adverse cardiovascular events (MACE), which was a composite of cardiac death, myocardial infarction, and unplanned repeat revascularization. A total of 280 patients underwent randomization. Follow-up IVUS showed absolute changes in PAV were - 1.286 ± 3.704% and - 1.302 ± 3.586%, respectively for moderate-intensity rosuvastatin and ezetimibe group and high-intensity rosuvastatin group. Mean difference between 2 groups (0.017%; 95% confidence interval: -0.957% to 0.991%) did not exceed noninferiority margin (non-inferiority p < 0.001). Both groups showed acceptable side effect profiles without group differences. Compared with high-intensity rosuvastatin monotherapy, moderate-intensity rosuvastatin and ezetimibe was non-inferior regarding regression of coronary atherosclerotic plaque (Supported by Hanmi Pharmaceutical co., ltd; ROSUZET-IVUS ClinicalTrials.gov number, NCT03169985).

PMID 43008976
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PubMedEuropean journal of drug metabolism and pharmacokinetics2026-11-10

Feasibility of Predicting Human Enterohepatic Circulation of Ezetimibe Using In Vitro Culture Systems and PBPK Modeling.

Liang Yang Y, Tokito Fumiya F, Hu Ke K, Kono Fukino F et al.

Enterohepatic circulation (EHC) couples hepatic metabolism, biliary delivery, and intestinal recycling, making quantitative prediction difficult. We examined the feasibility and limitations of an in vitro-informed semi-mechanistic ezetimibe (EZE) model. PXB hepatocyte B-CLEAR measurements informed an apparent EZE-to-glucuronide rate input, and Caco-2 measurements provided permeability context. Gallbladder timing, intestinal and systemic rates, and an observation scale were calibrated to 24 mean total ezetimibe concentration-time observations. The observation model used a normalized parent-state proxy rather than explicitly modeled circulating parent plus glucuronide. Assay time, scale-compensation, and alternative bile-release analyses evaluated the resulting assumptions. The reconstructed apparent clearance was ( 2.610 ± 1.714 ) × 10 - 3 mL/min/well across three independent experiments. Under the stated volume and cell-content assumptions, the rate input was 1.152 h - 1 , rounding to 1.15. The saved calibration had RMSE 5.17 ng/mL and R 2 = 0.956 , but did not reproduce all local rises. Recycled return generated secondary structure; removing return eliminated it despite a comparable overall error after scale adjustment. Time-specific hepatic inputs changed exposure substantially at fixed parameters, and adjustment of the observation scale largely compensated for these changes. The workflow connects assay measurements to a calibrated EHC model but does not yet establish independent bottom-up prediction or unique physiological parameters. Better constrained assay-to-model relationships and separate parent/metabolite observations are needed.

PMID 43007610
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PubMedCellular signalling2026-11-10

ESRRA facilitates hepatocellular carcinoma progression through transcriptional activation of PHF5A and serves as a potential therapeutic target of rosuvastatin.

Cai Xiang X, Wan Zhiping Z, Huang Shuying S, Chong Yutian Y et al.

The estrogen-related receptor alpha (ESRRA), a member of the estrogen receptor-related receptor family, has been implicated in tumor progression across multiple cancers. However, its function and molecular mechanisms in hepatocellular carcinoma (HCC) remain incompletely understood. Moreover, statins improve the prognosis of HCC patients in clinical trials, while the underlying mechanisms remain unclear. ESRRA expression was analyzed in public databases, clinical HCC tissues and cell lines. The effects of ESRRA and rosuvastatin on HCC cell proliferation and migration were examined in vitro (CCK-8, colony formation, EdU proliferation, wound-healing, transwell assays, and epithelial-mesenchymal transition (EMT) marker analysis) and in vivo (subcutaneous xenograft, lung metastasis, and orthotopic liver tumor models). RNA sequencing, dual-luciferase reporter assays, ChIP-qPCR, and co-IP identified ESRRA's downstream targets and pathways. ESRRA was significantly upregulated in clinical HCC specimens and cell lines. Functional assays showed that ESRRA promoted HCC cell proliferation and migration in vitro and in vivo. Mechanistically, ESRRA interacted with coactivator PGC1α and transcriptionally upregulated PHD finger protein 5 A (PHF5A), which was associated with enhanced PI3K/AKT signaling and downstream genes related to cell cycle progression and apoptosis. Furthermore, rosuvastatin exerted anti-tumor activity in HCC and potentiated lenvatinib-induced HCC cell suppression by downregulating ESRRA and inhibiting its transcriptional function via reducing intracellular cholesterol. ESRRA/PGC1α promotes HCC progression via an ESRRA-PHF5A axis that is required for PI3K/AKT pathway activity and mediates rosuvastatin's anti-tumor effect. Targeting ESRRA-PHF5A may be a therapeutic strategy for HCC.

PMID 43008960
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PubMedThe Yale journal of biology and medicine2026-11-10

Severe Atherogenic Dyslipidemia in Ataxia-Telangiectasia Despite Cachexia: Mechanistic Insights into Mitochondrial Dysfunction.

Petridis Samuele F SF, Varghese Ron T RT

Ataxia-telangiectasia is a rare autosomal recessive disorder caused by mutations in the ATM gene and characterized by progressive cerebellar degeneration, immunodeficiency, and cancer susceptibility. Metabolic complications, including dyslipidemia and insulin resistance, are increasingly recognized, but severe atherogenic lipid phenotypes remain poorly described. ATM deficiency impairs mitochondrial function, redox homeostasis, and fatty acid beta oxidation, providing a plausible basis for metabolic dysregulation. We report a 25-year-old woman with genetically confirmed ataxia-telangiectasia and extreme underweight (body mass index 12.5 kg/m²) who developed severe mixed atherogenic dyslipidemia despite modest dietary fat intake and no pathogenic variants causing monogenic familial hypercholesterolemia. Fasting triglycerides rose from 264 to 426 mg/dL, low-density lipoprotein cholesterol reached 174 mg/dL, apolipoprotein B was 156 mg/dL, lipoprotein a was 87 mg/dL, low-density lipoprotein particle number exceeded 3500 nmol/L, and small, dense low-density lipoprotein exceeded 2300 nmol/L. Concurrent diagnoses included type 2 diabetes mellitus and metabolic dysfunction-associated steatotic liver disease with fibrosis. Statin therapy was discontinued after elevated transaminases were noted in the setting of preexisting liver disease. Ezetimibe lowered low-density lipoprotein cholesterol from 174 to 149 mg/dL. After evolocumab was added to ezetimibe, low-density lipoprotein cholesterol decreased from 149 to 35 mg/dL, with triglycerides improving to 220 mg/dL and glycated hemoglobin A1c to 5.9%. This case expands the metabolic phenotype of ataxia-telangiectasia and supports careful cardiometabolic surveillance in affected adults.

PMID 43005023
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