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

PubMedTherapeutic advances in neurological disorders2026-08-28

The impact of concomitant use of rosuvastatin or atorvastatin plus clopidogrel on the platelet inhibition and clinical outcomes in acute large-vessel minor stroke or TIA: A randomized controlled multi-center trial, the ROCATIS-1 trial.

Zeinhom Mohamed G MG, Sayed Ismaiel Mohamed Gamal MG, Khalil Mohamed Fouad Elsayed MFE, Elmesallami Ahmad Galal AG et al.

Although clopidogrel is commonly used for ischemic stroke secondary prevention, 20-50% of patients experienced clopidogrel failure and recurrence of ischemic events. We aimed to evaluate the benefits or hazards of adding atorvastatin or rosuvastatin to clopidogrel on the clopidogrel-induced inhibition of platelet activation and vascular events prevention. Our multi-center, randomized, single-blinded, parallel-group trial was conducted between 10th April 2024 and 10th May 2026. 600 first-ever, large-vessel minor ischemic stroke or TIA patients received 40 mg of atorvastatin or 20 mg of rosuvastatin during the first 24 hours of stroke onset once daily till the 90th day after stroke onset. Both groups received open-label 300 mg loading doses of aspirin and clopidogrel during the first 24 hours after stroke onset, followed by 75 mg clopidogrel and 100 mg aspirin once daily for 3 weeks, then 75 mg clopidogrel only until the end of the follow-up period. We followed up with our patients for 3 months. The change in the percentage of platelet maximum aggregation at 3 months of treatment compared with baseline while using adenosine diphosphate (ADP), 5 µM/L as an agonist was 54.4 (51.0-57.1) in the rosuvastatin group compared with 49.2 (45.5-52.3) in the atorvastatin group with P-value 0.003. 22 (7.3%) patients in the rosuvastatin group and 40 (13.3%) patients in the atorvastatin group experienced a composite of a new stroke, MI, or death due to vascular insults (HR 0.52; 95% CI, 0.33-0.81; P-value= 0.004), moreover, 12 (4.0%) patients in the rosuvastatin group and 19 (6.3%) in the atorvastatin group experienced recurrent stroke either ischemic or hemorrhagic, with (HR 0.60; 95% CI, 0.32-1.10; P-value 0.10). Compared with combining atorvastatin with clopidogrel in African large-vessel minor stroke or TIA, combining rosuvastatin with clopidogrel yielded higher rates of clopidogrel-induced platelet aggregation inhibition, significantly lower rates of a composite of recurrent stroke, MI, and death due to vascular events at three months. There were no significant differences between rosuvastatin and atorvastatin regarding drug-related side effects. Our findings are hypothesis-generating and require confirmation in a double-blinded, multinational randomized trial before they can inform practice.

PMID 42662137
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PubMedLipids in health and disease2026-08-28

Increased LDL-C reduction with ezetimibe in ketogenic diet-induced hypercholesterolemia.

Gonzalez Jorge J, Wageman Joshua J, Buchanan Laura L, Kalayjian Tro T et al.

Several case reports and a meta-analysis have documented significant increases in cholesterol levels among individuals following a ketogenic diet. However, the mechanistic drivers of this phenotype remain incompletely understood. Here, we describe a retrospective case series of 14 patients with ketogenic diet-induced hypercholesterolemia who experienced larger-than-expected LDL-C reductions after ezetimibe therapy. In a subset of participants with available genetic data, no biallelic sitosterolemia-associated variants were identified in the loci assessed. We hypothesize that chronically low insulin levels may alter hepatic cholesterol homeostasis through changes in ACAT2-mediated cholesterol esterification and in NPC1L1/ABCG5/G8-mediated cholesterol handling. The magnitude of LDL-C reduction achieved with ezetimibe in this cohort suggests that altered cholesterol absorption may contribute importantly to this phenotype. This hypothesis-generating framework offers a plausible mechanistic explanation and supports further prospective study of precision lipid management in ketogenic diet-induced hypercholesterolemia.

PMID 42661192
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PubMedInternational journal of pharmaceutics: X2026-08-28

Impact of adsorption-based solidification on the pharmaceutical performance and antidyslipidemic efficacy of simvastatin-ezetimibe SNEDDS.

Priani Sani Ega SE, Sopyan Iyan I, Chaerunisaa Anis Yohana AY, Wilar Gofarana G

Simvastatin and ezetimibe are widely used in combination therapy for dyslipidemia; however, their poor aqueous solubility limits oral bioavailability. This study aimed to develop and characterize liquid and solid self-nanoemulsifying drug delivery systems (L-SNEDDS and S-SNEDDS) containing simvastatin and ezetimibe and to evaluate the impact of adsorption-based solidification on their physicochemical characteristics, dissolution behavior, and antidyslipidemic efficacy. An optimized L-SNEDDS composed of Capryol® 90, Cremophor® RH40, and Transcutol® HP was successfully converted into S-SNEDDS by adsorption onto Neusilin® US2. The optimized L-SNEDDS exhibited rapid self-emulsification, high transmittance, and a globule size of 24.47 ± 0.55 nm, whereas S-SNEDDS readily reconstituted into a nanoemulsion with a globule size of 35.51 ± 0.32 nm. Adsorption-based solidification did not alter the chemical integrity of either drug and maintained both drugs predominantly in an amorphous or molecularly dispersed state. S-SNEDDS markedly increased the apparent solubility of both drugs, and both formulations substantially enhanced drug dissolution compared with the drug suspension, although dissolution from S-SNEDDS was slightly lower than that from L-SNEDDS. In a Poloxamer 407-induced dyslipidemia model, both formulations significantly reduced total cholesterol, LDL-C, and triglyceride levels compared with the dyslipidemic control and produced greater lipid-lowering effects than the drug suspension, while no significant differences were observed between L-SNEDDS and S-SNEDDS. These findings suggest that adsorption-based solidification preserved the pharmaceutical and therapeutic performance of the optimized L-SNEDDS while providing the practical advantages of a solid dosage form, supporting S-SNEDDS as a promising oral lipid-based delivery system for simvastatin-ezetimibe combination therapy.

PMID 42662858
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PubMedEuropean journal of clinical microbiology & infectious diseases : official publication of the European Society of Clinical Microbiology2026-08-28

Selective statin therapy and nasal staphylococcal colonisation: a retrospective case-control study.

Abbas Zahraa Z, Hughes Jeffery J, Sunderland Bruce B, Parsons Richard R et al.

Nasal Staphylococcus aureus (S. aureus) colonisation is a key risk factor for serious infections. Statins, used for hypercholesterolaemia and cardiovascular disease prevention, have been linked to gut microbiome dysbiosis, but their impact on nasal bacterial colonisation remains unclear. To examine whether statin use, individual statins, and statin dose intensity are associated with nasal S. aureus colonisation, and whether associations differ between methicillin-sensitive S. aureus (MSSA) and methicillin-resistant S. aureus (MRSA) colonisation. A retrospective case-controlled study included 4,005 nasal swabs obtained from 3,983 patients at a tertiary hospital in Western Australia. Swabs were classified as S. aureus-positive (MRSA or MSSA); controls were negative. Statin exposure and dose intensity were assessed, and multivariable logistic regression adjusted for confounders. Statin use was associated with increased odds of nasal S. aureus colonisation (OR 1.34; p < 0.001), driven by MSSA. Atorvastatin (OR 1.31; p = 0.005) and rosuvastatin (OR 1.56; p < 0.001) were independently associated with colonisation. A dose-response effect was observed: moderate-intensity (OR 1.26; p = 0.024) and high-intensity therapy (OR 1.47; p < 0.001) increased the odds of colonisation. MRSA showed no association. Diabetes was independently associated with S. aureus colonisation (OR 1.27; p = 0.004). Statin therapy, particularly atorvastatin and rosuvastatin at moderate to high dose intensities, was associated with increased nasal S. aureus colonisation. These findings may have implications for infection prevention in high-risk patients, though they do not diminish the established cardiovascular benefits of statins. Prospective studies are required to confirm causality, elucidate mechanisms, and determine whether these findings should inform screening or decolonisation strategies.

PMID 42663902
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PubMedDrug metabolism and disposition: the biological fate of chemicals2026-08-28

Identification of Gln422 in transmembrane domain 9 as a key amino acid residue for the selective transport of ginsenoside Re by organic anion transporting polypeptide 1B3.

Liu Han H, Chen Shuang S, Zhang Chen C, Dong Yao Y et al.

Organic anion transporting polypeptide (OATP) 1B1 and 1B3 are the 2 highly homologous liver-specific uptake transporters. Although they share many common substrates, OATP1B3 exhibits selective transport for some protopanaxatriol-type ginsenosides such as ginsenoside Re. In this study, we successfully identified Gln422 (Q422) in transmembrane domain 9 as a key residue for OATP1B3's selectivity toward ginsenoside Re. Substitution of Q422 with bulky residues tyrosine and phenylalanine will almost totally destroy OATP1B3's transport for ginsenoside Re, which is not due to the reduction of transporter's surface expression but due to the reduction of its transport activity per se. Kinetic studies showed that the decreased transport activity of Q422Y was mainly due to its reduced turnover number. Molecular docking indicated that the Q422Y mutation might cause steric hindrance for ginsenoside Re binding/translocation. Q422 plays a significant role in the transport of protopanaxatriol-type ginsenoside Rg1 and notoginsenoside R1. However, it only has a trivial effect on the transport of estradiol-17β-glucuronide, estrone-3-sulfate, and rosuvastatin. Taken together, Q422 is crucial for ginsenoside transport by OATP1B3, but its role is substrate dependent. SIGNIFICANCE STATEMENT: Protopanaxatriol-type ginsenosides are primarily eliminated via hepatobiliary excretion. They are transported by organic anion transporting polypeptide (OATP) 1B3 but not by OATP1B1. This study successfully identified that Q422 in transmembrane domain 9 plays a pivotal role in OATP1B3's uptake for ginsenosides Re, Rg1, and notoginsenoside R1. The naturally occurring Q422H variant may largely compromise OATP1B3's function and thus impair the hepatobiliary excretion of these ginsenosides. These findings would advance our knowledge of the molecular mechanism for OATP1B3's selectivity toward protopanaxatriol-type ginsenosides.

PMID 42664884
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PubMedSleep medicine2026-08-28

Lipid-lowering agent use and changes to sleep.

Belghiti Mariam M, Virk Manraj M, Costa Yakdehikandage S YS, Berger Sarah S et al.

There is mixed evidence as to whether lipid-lowering agents impact sleep, with some patients reporting significant sleep disruption after starting these medications. Our objective was to determine the relationship between use of lipid-lowering agents and objective measures of sleep quality recorded via in-laboratory polysomnography. In this cross-sectional retrospective study, we examined data from patients who underwent diagnostic in-laboratory polysomnography at Sunnybrook Sleep Laboratory, an academic tertiary care sleep center. Self-reported questionnaires were used to ascertain use of any lipid-lowering agent and medical comorbidities. Multivariable linear regression models were utilized to analyze the association between use of lipid-lowering agents, including specific classes, with objective polysomnography-derived measures of sleep (i.e. sleep efficiency, total sleep time, REM latency, sleep onset latency, and wake time after sleep onset). We included 3754 patients (mean age±SD = 54.7 ± 16.4 years; 47.5% male; mean BMI±SD = 29.0 ± 6.64 kg/m2). Overall, 1055 patients were found to be using lipid-lowering agents with atorvastatin being the most common, followed by rosuvastatin, cholesterol absorption inhibitors, simvastatin, pravastatin, fibrates, and bile acid sequestrants. After adjusting for age, sex, body mass index, relevant comorbidities, obstructive sleep apnea and its severity, habits that worsen sleep, and other medication classes that impact sleep, the use of atorvastatin was found to significantly decrease sleep efficiency (β = -1.95; 95% CI = -3.71 to -0.19; p = 0.030). The use of other lipid-lowering agents, regardless of medication class, did not significantly impact sleep. The use of atorvastatin may be associated with negative impacts to patients' sleep, though the magnitude of change is small. Clinicians should be aware of these effects and counsel patients accordingly.

PMID 42664635
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