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fimasartan + rosuvastatin (Tubero / Tuvero)

✓ Approved

Boryung · AGTR1 · Small Molecule

What is fimasartan + rosuvastatin?

fimasartan + rosuvastatin is a small molecule developed by Boryung. It is approved for therapeutic indications via oral (po).

Drug Profile

Brand NamesTubero, Tuvero
CompanyBoryung
Drug ClassSmall Molecule
Molecular TargetAGTR1, HMGCR
RouteOral (PO)
StatusApproved
Sources: ClinicalTrials.gov, Boryung

Mechanism of Action

Molecular Targets

fimasartan + rosuvastatin 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

fimasartan + rosuvastatin is developed for 2 unique indications across 2 therapeutic areas.

Therapeutic AreaConditionPhase
Vascular disordersHypertension✓ Approved
Metabolism and nutrition disordersHyperlipidaemiaPhase III

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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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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PubMedCurrent hypertension reviews2026-08-24

Emerging Pharmacological Therapies for Hypertension.

Mahajan Pritesh P, Pagar Ashish A, Baviskar Kajal K, Kachave Ramanlal R

This review provides a general overview of the physiological effects and pharmacokinetic properties that affect the absorption, distribution, metabolism, and elimination of recently developed antihypertensive drugs, such as fimasartan, azilsartan, zilebesiran, aprocitentan, and esaxerenone. It provides an opportunity to understand the pharmacologic properties of drugs like esaxerenone, a non-steroidal selective mineralocorticoid receptor antagonist; aprocitentan, a dual endothelin receptor antagonist; and zilebesiran, a small interfering RNA (siRNA) therapeutic that inhibits hepatic angiotensinogen synthesis. Mechanistic differences among these agents are also highlighted; for instance, fimasartan and azilsartan inhibit the angiotensin II receptor, whereas other medications alter mineralocorticoid activity or endothelial pathways. The review further discusses the clinical implications of these mechanisms in hypertension management and supports informed therapeutic decisionmaking by providing a detailed understanding of the pharmacological and mechanistic profiles of these emerging antihypertensive therapies.

PMID 42634574
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PubMedMedicina clinica2026-08-24

Comparative efficacy and safety of rosuvastatin versus atorvastatin after acute ischemic stroke or transient ischemic attack: A systematic review and exploratory meta-analysis.

Cueva-Cañola Luis E LE, Beltran-De la Fuente Andrea C AC, Ramírez Navarro Diana I DI, Carrión-Cuéllar Astrid G AG et al.

Acute ischemic stroke (AIS) and transient ischemic attack (TIA) are leading causes of mortality and disability. High-intensity statins are central to secondary prevention, with guidelines recommending atorvastatin or rosuvastatin; however, comparative evidence post-stroke is limited. This study systematically reviewed literature comparing both agents after AIS/TIA. The protocol was registered in PROSPERO (CRD420261287374). PubMed, Embase, and Ovid MEDLINE were searched from inception to January 17, 2026, using predefined terms for statins and AIS/TIA. Five studies were included (one randomized trial and four cohort studies). Compared with atorvastatin, rosuvastatin was associated with greater improvements in lipid and inflammatory markers. Despite these differences, rates of recurrent stroke and all-cause mortality were similar between treatments. However, rosuvastatin was associated with lower rates of hemorrhagic stroke and more favorable composite cardiovascular outcomes. Evidence suggests biological differences but is insufficient to establish clinical superiority of either statin.

PMID 42636678
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