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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

PubMedEuropean journal of pharmaceutical sciences : official journal of the European Federation for Pharmaceutical Sciences2026-05-23

Modulation of Remimazolam Placental Transfer via OATP2B1 by Rosuvastatin in an In Vitro 3D Placental Barrier Model.

Sato Satoshi S, Chaki Tomohiro T, Narumi Katsuya K, Hirahata Tomoki T et al.

Fetal exposure to anesthetics via the placenta during the perinatal period may adversely affect central nervous system development. Organic anion-transporting polypeptide 2B1 (OATP2B1) functions as an active transport carrier across the blood-placental barrier and can be modulated by interactions with rosuvastatin (RSV). This study hypothesized that drug interactions could alter OATP2B1-mediated transport of remimazolam (RMZ), thereby modulating its placental permeability. First, an in vitro 3D blood-placental barrier model was used to assess the permeability of RMZ with a single administration (100 nM RMZ) and co-administration with RSV (0.1, 1, and 10 nM). RMZ permeability was significantly decreased from 2 to 4 hours in the RMZ alone group (p < 0.001), whereas at 3-4 hours post-dose it was significantly decreased by 15-71% in the groups treated with 1 nM or 10 nM RSV in combination, compared to the RMZ alone group. Next, intracellular uptake assays using OATP2B1-overexpressing human embryonic kidney 293 cells (HEK293) confirmed carrier-mediated transport of RMZ. Uptake was time-dependent, markedly higher than in non-expressing cells, and decreased by 57.6-61.1% in the presence of RSV. These findings demonstrate that RMZ is transported via OATP2B1 through a non-high-affinity binding site and that placental transfer of RMZ can be modulated by drug interactions that alter OATP2B1 function. Considering the differences in OATP2B1 localization between in vivo and in vitro conditions, modification of OATP2B1 transport function by RSV may potentially contribute to increased fetal exposure to RMZ at the blood-placental barrier.

PMID 42173384
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PubMedJournal of ethnopharmacology2026-05-23

Shenling Jiangzhi Formula Alleviates Atherosclerosis in ApoE-/- Mice by Inhibiting Vascular Inflammation via the NF-κB/NLRP3 Pathway.

Kong Qinghe Q, Niu Yingshuo Y, Yao Jianming J, Hou Xuemei X et al.

Atherosclerosis (AS) falls into the categories of "blood stasis" and "vascular impediment" in traditional Chinese medicine (TCM) theory. Its core pathogenesis is spleen deficiency with excessive dampness, and intermingling of phlegm and stasis. Shenling Jiangzhi Formula (SJF), a clinically common prescription for treating AS, possesses the effects of replenishing qi and invigorating the spleen, tonifying the kidney and resolving turbidity, promoting blood circulation and dredging collaterals, clearing the liver and detoxifying. However, its specific pharmacological mechanism remains unclear. To characterize the chemical components of SJF and explore its pharmacodynamic substances, observe the regulatory effects of SJF on plaque formation and inflammatory response in the AS model of ApoE-/- mice, and clarify the pharmacodynamic effects and anti-AS mechanism of SJF. UPLC-Q-Exactive Orbitrap MS/MS technology was used to analyze the chemical components of SJF and attribute each component to its source medicinal materials. Network pharmacology and molecular docking techniques were utilized to screen the core targets and active components of SJF against AS, followed by molecular docking verification. ApoE-/- mouse AS model was established using a combination of a high-fat diet and an intermittent water environment (sleep deprivation) model and rosuvastatin gavage was used as the positive control. ELISA was used to detect the serum concentrations of blood lipids (TC, TG, LDL-C, HDL-C), inflammatory cytokines (hs-CRP, IL-1β, IL-6, IL-18, NF-κB, MCP-1), and other relevant markers (Hb, TMAO, Orexin A); HE staining and Oil Red O staining were performed to observe cell morphology and aortic plaque area; Western blotting was used to detect the expression levels of IL-1β, IL-18, NF-κB p65, p-NF-κB p65, NLRP3, Caspase-1, cleaved Caspase-1 (p20), and ASC proteins in the aorta. A total of 313 chemical components were identified from SJF, including terpenoids, flavonoids, anthraquinones, etc. On this basis, network pharmacology combined with molecular docking technology was used for screening, and the active components of SJF for treating AS were found to be luteolin, quercetin, kaempferol, isorhamnetin, β-sitosterol, and arachidonic acid, with key therapeutic targets including IL-1β, MMP9, IL-6, CXCL8, etc. HE staining and Oil Red O staining showed that compared with the model group, the aortic intimal thickness of the administration group was thinner and atherosclerotic plaques were reduced. In addition, SJF could reduce blood lipid levels, down-regulate the expression of inflammatory factors, and increase hemoglobin concentration to improve the hypoxic microenvironment of AS lesions, thereby alleviating vascular endothelial injury, inhibiting macrophage foam cell formation, and plaque lipid deposition. Mechanistic studies suggested that SJF may suppress atherosclerotic plaque progression, possibly through inhibition of the NF-κB/NLRP3 signaling pathway, which could contribute to its anti-AS effects. SJF improves AS-related inflammatory responses by inhibiting the activation of the NF-κB/NLRP3 signaling pathway, reduces abnormal blood lipid levels, accelerates lipid metabolism, decreases lipid deposition, inhibits the development of atherosclerotic plaques, and exerts anti-AS effects.

PMID 42173415
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PubMedJournal of primary care & community health2026-05-22

Candesartan, Metoprolol and Rosuvastatin Associated to Lower 30-Days Mortality in Adult COVID-19 Patients - A Register Study in Finland before COVID-19 Vaccines.

Hyvärinen Anna A, Helminen Mika M, Broas Markku M, Syrjälä Hannu H

Elderly people with chronic diseases are at risk for having severe COVID-19 disease. We were interested whether the drugs prescribed for the chronic diseases are associated with lower mortality in COVID-19 patients.We used Finnish national registry data for analysis of potential associations of 73 prescription drugs to mortality among 6082 adult COVID-19 patients between 1.1.2020 and 30.6.2020, before COVID-19 vaccinations were available. Adjusted odds ratios (aORs) with 95 percent confidence intervals (95% CIs) for different medications are presented.The use of three cardiovascular drugs was associated with lower 30 days all-cause mortality rate: candesartan (aOR 0.34, 95% CI 0.16-0.72, p=0.005), metoprolol (aOR 0.37, 95% CI 0.16-0.88, p=0.024) and rosuvastatin (aOR 0.44, 95% CI 0.21-0.94, p=0.034).In conclusion, COVID-19 patients who used cardiovascular drugs candesartan, metoprolol or rosuvastatin have lower 30 days all-cause mortality than other COVID-19 patients.

PMID 42169481
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PubMedDrug design, development and therapy2026-05-21

Efficacy and Safety of Fimasartan/Indapamide Combination Therapy versus Fimasartan Monotherapy in Patients with Essential Hypertension Inadequately Responding to Fimasartan 30 mg (FINEDUO): A Randomized, Double-Blind, Multicenter, Phase III Study.

Youn Jong-Chan JC, Lee So-Young SY, Yu Cheol Woong CW, Sung Ki-Chul KC et al.

Effective blood pressure (BP) control in hypertension frequently requires combination therapy, particularly in patients whose BP is inadequately controlled by monotherapy. This study evaluated the efficacy and safety of fimasartan (FMS) and indapamide (IND) sustained release (SR) combination therapy. In this randomized, double-blind, phase III trial, patients with hypertension who remained uncontrolled after a 4-week run-in with FMS 30 mg, were randomized to FMS 30 mg/IND SR 1.5 mg or FMS 30 mg, followed by forced titration to FMS 60 mg/IND SR 1.5 mg or FMS 60 mg after 4 weeks. The primary endpoint was the change in sitting systolic BP (SiSBP) at week 8. Secondary endpoints included changes in sitting diastolic BP (SiDBP), BP control rates, response rates, and safety outcomes. Two hundred forty-eight patients were randomized (FMS/IND SR, n=126; FMS, n=122). At week 8, the least square mean reduction in SiSBP was greater with FMS/IND SR than with FMS (-17.9 vs -7.4 mmHg, P<0.0001). Significant improvements were also observed for SiSBP at week 4, SiDBP at week 4 and 8, and BP control rates and response rates. The safety profile was comparable between groups, with no significant differences in adverse events, including patients aged 65 years and older. FMS/IND SR combination therapy demonstrated superior antihypertensive efficacy, rapid BP control, and comparable safety to FMS monotherapy. This regimen may serve as an effective therapeutic option, particularly in elderly or high-risk hypertensive patients. https://www.clinicaltrials.gov, NCT05878561.

PMID 42163997
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PubMedDrug metabolism and disposition: the biological fate of chemicals2026-05-17

Impact of SLCO1B1 and ABCB1 variants on statin efficacy and toxicity in a Tunisian population.

Abbes Houwaida H, Yassine Khalij, Meksi Maha M, Meddeb Ayoub A et al.

Statins are the cornerstone treatment for coronary artery disease treatment. However, they exhibit considerable interindividual variability in both pharmacokinetics and pharmacodynamics. This variability was assessed by investigating 9 genetic variants impact across 5 pharmacogenes (ABCB1, CYP3A4, CETP, APOC1, and SLCO1B1) in 279 Tunisian coronary patients newly started on statins. Regarding myopathy, carrying the variant allele G of SLCO1B1 rs2306283 reduced myopathy risk (odds ratio [OR] = 0.322, P = .008) compared with a allele. Conversely, the variant allele C of SLCO1B1 rs4149056 appeared to increase myopathy occurrence (OR = 4.799, P = .001) compared with T allele. Stratifying by statin type, the associations were only significant for atorvastatin, not for rosuvastatin, with a protective effect for rs2306283 (OR = 0.502, P = .046) and at risk of rs4149056 (OR = 4.290, P = .003). Sex analysis revealed no significant differences between sexes and safety for rs4149056. However, for rs2306283, the protective effect was more pronounced in men (OR = 0.348, P = .015) compared with women. Concerning efficacy, the variant alleles C of ABCB1 rs1045642 and rs1128503 were found to be significantly associated with nonresponse to statins for both low density lipoprotein cholesterol (LDL-c; OR = 0.350, P = .023 and OR = 0.292, P = .011, respectively) and non-high-density lipoprotein cholesterol (non-HDL-c; OR = 0.302, P = .007 and OR = 0.200, P = .002, respectively) compared with T allele. Stratifying by statin type, the association was only significant with atorvastatin, not with rosuvastatin, for both LDL-c (rs1045642, OR = 0.331, P = .013 and rs1128503, OR = 0.249, P = .004), and non-HDL-c (rs1045642, OR = 0.363, P = .011 and rs1128503, OR = 0.207, P = .001). Sex analysis revealed significant association between efficacy and ABCB1 only in men, for both LDL-c (rs1045642, OR = 0.355, P = .013 and rs1128503, OR = 0.325, P = .012), and non-HDL-c (rs1045642, OR = 0.272, P = .001 and rs1128503, OR = 0.400, P = .023). Our findings substantiate the clinical utility of genetic biomarkers in predicting statins response. SIGNIFICANCE STATEMENT: Although statins remain a cornerstone therapy for acute coronary syndromes, significant interindividual variability in efficacy and toxicity exists. These findings suggest that SLCO1B1 variants may influence the occurrence of statin-induced myopathy, whereas ABCB1 polymorphisms may affect statin efficacy. This highlights the potential of pharmacogenetic screening to optimize the benefit-risk balance of statin therapy.

PMID 42142508
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PubMedClinical therapeutics2026-05-16

Assessing the Potential Clinical Drug-Drug Interactions Between D-1553 (Garsorasib) and CYP450 Enzymes/Transporters via a Cocktail Approach.

Chen Qian Q, Ding Qichen Q, Sun Chan C, He Zijian Z et al.

This Phase I drug-drug interaction study in healthy Chinese male subjects evaluated: (1) the perpetrator effects of D-1553 (garsorasib) on cytochrome P450 enzymes (CYP3A4, CYP1A2), hepatic (OATP1B1/1B3), renal uptake transporters (OAT1/3), and efflux transporter P-glycoprotein (P-gp); and (2) the victim potential with itraconazole (200 mg daily) or omeprazole (20 mg daily). The study comprised three cohorts. Cohort 1 received D-1553 tablets (400 mg twice daily) co-administered with a cocktail of probe substrates: midazolam, caffeine, rosuvastatin, furosemide, and digoxin. Cohort 2 received D-1553 co-administered with the strong CYP3A4 and P-gp inhibitor itraconazole. Cohort 3 received D-1553 co-administered with the proton-pump inhibitor omeprazole. A total of 45 healthy male subjects were enrolled in the study, and 44 subjects were included in the safety and pharmacokinetic (PK) analyses. Plasma concentrations of D-1553 and concomitant drugs were quantified using validated liquid chromatography-tandem mass spectrometry (LC-MS/MS) methods. Tolerability was also evaluated. In the substrate cocktail assessment, D-1553 significantly inhibited CYP3A4 (midazolam AUC ratio: 2.04) but not CYP1A2 (caffeine AUC ratio: 1.18), and reduced exposures of rosuvastatin and furosemide (AUC ratio: 0.59 and 0.41, respectively), likely via intestinal OATP2B1 inhibition. Meanwhile, no clinically relevant effect on P-gp was shown (digoxin AUC ratio: 1.19). Co-administration with itraconazole increased D-1553 exposure (AUC ratio: 1.46), whereas omeprazole decreased its exposure (AUC ratio: 0.85). All AEs were mild and no serious AEs were reported. D-1553 acts as a moderate inhibitor of CYP3A4 and a weak inhibitor of P-gp, while reducing the absorption of specific transporter substrates, likely via intestinal OATP2B1. Co-administration with strong CYP3A4 inhibitors moderately increases D-1553 exposure, whereas acid-reducing agents like omeprazole have no clinically relevant effect. These findings provide a targeted scientific basis for guiding the clinical co-administration of D-1553 with concomitant medications.

PMID 42140797
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