Drug Database
FI

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

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
Read full article →
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
Read full article →
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
Read full article →
PubMedBiochemical pharmacology2026-11-08

GPR146 as a therapeutic target: Linking lipid metabolism with macrophage inflammation in atherosclerosis.

Liu Qing Q, Wang Yifei Y, Geng Yu Y, Xue Yajun Y et al.

Atherosclerosis is driven by dyslipidemia and chronic inflammation. GPR146 has emerged as a regulator of cholesterol metabolism; however, whether GPR146 links lipid metabolism with macrophage inflammation during atherosclerosis remains unclear. Apolipoprotein E-deficient (ApoE-/-) mice were fed a high-fat diet for 12 weeks, followed by 4 weeks of intervention with adeno-associated virus (AAV)-mediated hepatic GPR146 knockdown or rosuvastatin treatment. Atherosclerotic lesions and plaque composition were assessed using Oil Red O staining and immunofluorescence. Lipid profiles, oxidized low-density lipoprotein (ox-LDL), and inflammatory markers were evaluated using enzymatic assays, ELISA, and qPCR, respectively. In ox-LDL-stimulated THP-1-derived macrophages, GPR146 was silenced to examine lipid accumulation, inflammatory responses, transcriptomic alterations, and the potential involvement of the JAK-STAT signaling pathway. GPR146 expression increased in atherosclerotic lesions, particularly in macrophage-rich regions. Hepatic GPR146 knockdown reduced atherosclerotic lesion burden, circulating total cholesterol and low-density lipoprotein cholesterol (LDL-C) levels, ox-LDL accumulation, and inflammatory activation within plaques. In macrophages, GPR146 silencing suppressed ox-LDL-induced lipid accumulation, accompanied by reduced CD36 expression and decreased foam cell formation. GPR146 silencing also attenuated pro-inflammatory macrophage activation, as evidenced by reduced expression of inflammatory mediators. Transcriptomic analysis implicated JAK-STAT signaling, with reduced JAK2 and STAT3 expression following GPR146 silencing. Pharmacological inhibition of the JAK-STAT signaling partially recapitulated the anti-inflammatory effects associated with GPR146 knockdown. Together, these findings suggest that GPR146 contributes to lipid metabolic regulation and macrophage inflammatory responses during atherosclerosis and may represent a therapeutic target warranting further investigation.

PMID 42998850
Read full article →
PubMedJournal of cardiovascular pharmacology and therapeutics2026-11-06

Genome-Wide and Exome-Wide Significant Genetic Variants Influencing Rosuvastatin Therapy: A Scoping Review.

Dermota Tjaša T, Rojnik Tamara T, Božič Mijovski Mojca M

BackgroundCardiovascular diseases remain the leading cause of mortality worldwide, with elevated low-density lipoprotein cholesterol representing a major risk factor. Rosuvastatin is widely used for cardiovascular prevention due to its potent lipid-lowering effects. Significant interindividual variability exists in its pharmacokinetics (PK), pharmacodynamic (PD) response, and susceptibility to adverse effects, which is not fully understood.ObjectiveGenome-wide association studies (GWAS) and exome-wide association studies (ExWAS) have emerged as powerful approaches to identify genetic determinants that influence drug response. This review aimed to summarize evidence from such studies investigating the influence of genetic variation on rosuvastatin PK, PD, and intolerance.DesignA systematic literature search was performed in PubMed and Web of Science to identify GWAS and ExWAS studies examining associations between single-nucleotide polymorphisms (SNPs) and rosuvastatin PK, PD, or intolerance. Eligible English-language studies published up to July, 2025 were independently screened by two reviewers, and data were extracted from the included studies.ResultsSix eligible studies were included, and relevant data were extracted. Genome-wide significant associations were observed for SLCO1B1, affecting rosuvastatin plasma concentrations, while variants in ABCG2, LPA, APOE, and PCSK9 were linked to PD effects. Common variants in TMEM9 and KLF12 were associated with rosuvastatin intolerance. Additional SNPs were identified at sub-genome-wide or exome-wide significance levels.ConclusionLimitations across studies included treatment with different statins and small sample sizes, which may obscure conclusions. Overall, these findings highlight the potential of pharmacogenomic research to guide personalized rosuvastatin therapy by identifying individuals at higher risk of altered drug response or adverse events.

PMID 42992644
Read full article →
PubMedThe American journal of case reports2026-11-06

Severe Rosuvastatin-Associated Rhabdomyolysis and Dialysis-Requiring Acute Kidney Injury in an Octogenarian Patient: A Case Report.

De Melo Luiza Mendonça Pessoa LMP, Passos Mauro De Deus MD, Ferreira Dilson Palhares DP

BACKGROUND Statins are fundamental to dyslipidemia management, but high-potency rosuvastatin can cause myotoxicity in vulnerable older patients. We present a probable case of rosuvastatin-associated rhabdomyolysis causing stage 3 acute kidney injury requiring hemodialysis in an 87-year-old woman with polypharmacy, highlighting clinical management and outcomes. CASE REPORT An octogenarian presented with progressive muscle weakness and inability to ambulate 20 days after starting rosuvastatin (20 mg/day), ezetimibe (10 mg/day), and evogliptin (5 mg/day). Laboratory tests revealed creatine kinase above 4267 U/L, serum creatinine 6.13 mg/dL, blood urea 220 mg/dL, severe hyponatremia (122 mEq/L), bicarbonate 15 mEq/L, and elevated transaminases (AST 419 U/L; ALT 342 U/L). Direct bilirubin (0.2 mg/dL) and gamma-glutamyl transferase (28 U/L) levels were normal, excluding primary hepatocellular or cholestatic liver injury. Urinalysis findings supported myoglobinuria. Refractory oliguria despite aggressive intravenous fluid resuscitation required emergency hemodialysis with sodium correction to prevent osmotic demyelination; rhabdomyolysis prompted rosuvastatin cessation. Concomitant nephrotoxic and renally cleared medications were temporarily withheld. During a 30-day hospital stay with 8 hemodialysis sessions, dialytic support was discontinued on Day 23 (serum creatinine 1.61 mg/dL). After physical rehabilitation, the patient was discharged on Day 30 with full motor strength (MRC grade 5/5). At 3 months, serum creatinine had stabilized (1.40 mg/dL; eGFR 38 mL/min/1.73 m²; creatine kinase 62 U/L) and independent ambulation continued. CONCLUSIONS Statin-associated rhabdomyolysis in older adults can be followed by renal recovery with dialysis independence and functional recovery through early drug cessation, fluid resuscitation, and timely dialytic support. Formal Naranjo assessment (score 5) classified the reaction as "probable," highlighting the multifactorial risks of geriatric polypharmacy.

PMID 42993685
Read full article →

+5275 more articles available with a free account

Sign up free to view all articles →

Ask about fimasartan + rosuvastatin