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fimasartan + rosuvastatin (Tubero / Tuvero)

✓ Approved

Boryung · AGTR1 · 小分子

什么是 fimasartan + rosuvastatin？

fimasartan + rosuvastatin 是一种小分子，由Boryung研发。该药已获批，用于治疗相关适应症，给药途径：Oral (PO)。

药物档案

商品名Tubero, Tuvero
公司Boryung
药物类别小分子
分子靶点AGTR1, HMGCR
给药途径Oral (PO)
状态Approved
来源： ClinicalTrials.gov, Boryung

作用机制

分子靶点

fimasartan + rosuvastatin 作用于 2 个分子靶点：

AGTR1angiotensin II receptor type 1 (HAT1R, AT1)
HMGCR3-hydroxy-3-methylglutaryl-CoA reductase (LDLCQ3, LGMDR28)
需要更深入的分析？Noah AI 可解释复杂机制并与同类药物比较。

治疗适应症

fimasartan + rosuvastatin 针对 2 个适应症，涉及 2 个治疗领域。

治疗领域疾病/病症分期
Vascular disordersHypertension✓ Approved
Metabolism and nutrition disordersHyperlipidaemiaPhase III

相关研究文献

PubMedJournal of clinical medicine2026-06-12

Rosuvastatin Attenuates Pulmonary Damage in Rats with Cecal Ligation and Puncture-Induced Sepsis.

Yıldız Safiye İnşira Sİ, Saydam Faruk F, Topçu Atilla A, Tümkaya Levent L et al.

Background/Objectives: Sepsis is a life-threatening syndrome arising from a dysregulated host response to infection, frequently leading to multiple organ dysfunction, with the lungs being among the most severely affected organs. Oxidative stress, inflammation, apoptosis, and DNA damage play key roles in the pathogenesis of sepsis-induced acute lung injury (ALI). Beyond its lipid-lowering effects, rosuvastatin possesses anti-inflammatory and antioxidant properties that may confer protective effects in sepsis. This study was designed to investigate the dose-dependent prophylactic efficacy of rosuvastatin in mitigating pulmonary damage in rats with cecal ligation and puncture (CLP)-induced sepsis. Methods: Sprague-Dawley rats were randomly divided into six groups: Sham, Sham + rosuvastatin (10 mg/kg), Sham + rosuvastatin (20 mg/kg), CLP, CLP + rosuvastatin (10 mg/kg), and CLP + rosuvastatin (20 mg/kg). Rosuvastatin was administered via oral gavage 4 h before the surgical procedures in the experimental groups. All animals were sacrificed 16 h following surgical procedures. Lung tissues were analyzed for biochemical markers, including malondialdehyde (MDA) and reduced glutathione (GSH), as well as histopathological changes and immunohistochemical expression of NF-κB/p65, caspase-3, and 8-OHdG. Results: CLP-induced sepsis significantly increased MDA levels while decreasing GSH levels, indicating enhanced oxidative stress. Rosuvastatin treatment significantly reversed these changes. Histopathological analysis revealed marked lung injury in the CLP group, including alveolar inflammation, interstitial inflammation, vascular congestion, and increased alveolar septal thickness, all of which were significantly reduced following rosuvastatin administration. Immunohistochemical findings demonstrated increased expression of NF-κB/p65, caspase-3, and 8-OHdG in the CLP group, whereas rosuvastatin significantly attenuated these expressions. No significant difference in prophylactic efficacy was observed between the 10 mg/kg and 20 mg/kg doses of rosuvastatin. Conclusions: Rosuvastatin demonstrated a protective effect against sepsis-induced pulmonary damage by reducing oxidative stress, inflammation, apoptosis, and DNA damage. These findings suggest that rosuvastatin may have prophylactic potential in sepsis; however, further support is needed from investigations of cellular pathways in different mechanistic directions.

PMID 42278973
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PubMedWound repair and regeneration : official publication of the Wound Healing Society [and] the European Tissue Repair Society2026-06-11

Topical Statin Therapy in Wound Healing: A Systemic Review of Therapeutic Outcomes.

Stratman Scott S, Campbell Caroline C, He Helen H

This systematic review evaluates the therapeutic potential of topical statin therapy in cutaneous wound healing across in vitro and in vivo animal and human studies. A PRIMSA-guided PubMed search identified 31 eligible studies evaluating simvastatin, atorvastatin, pravastatin, rosuvastatin, or mevastatin formulated a creams, ointments, hydrogels, nanoemulgels, liposomal gels, nanosponges, films, and advanced dressing for diabetic, excisional, burn, infected, pressure, vascular, and postoperative wounds. Across models, topical statins consistently accelerated wound closure and improved histological quality through convergent mechanisms, including enhanced angiogenesis and lymphoangiogenesis, promotion of re-epithelialization, modulation of collagen deposition and extracellular matrix remodelling, and attenuation of pro-inflammatory and infectious burden. Mechanistic studies demonstrated activation of intracellular signalling pathways, upregulation of vascular endothelial growth factor and CD31, macrophage polarization, restoration of epidermal growth factor receptor signalling via caveolin-1 and glucocorticoid receptor modulation, and context-dependent regulation of collagen I/III and myofibroblast activity. Clinical data, although limited, showed some initial promise in pressure ulcers and laparotomy wound healing. Safety profiles were generally favorable, with xerosis and increased transepidermal water loss reported only at higher simvastatin concentrations. Overall, topical statins represent a promising, mechanistically rational adjunct for wound management; however, heterogeneity in wound types, formulations, dosing, and comparators, together with sparse, small clinical trials, underscores the need for rigorously designed human studies to define optimal indication, concentrations, and delivery systems.

PMID 42273908
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PubMedDiabetology & metabolic syndrome2026-06-10

Real-world comparative outcomes of atorvastatin, rosuvastatin, and lovastatin-niacin fixed-dose combination in metabolic dysfunction-associated steatotic liver disease: hepatic, metabolic, and economic perspectives.

Tsai Yi Tseng YT, Mudiyanselage Sriyani Padmalatha Konara SPK, Tsai Yi-Jing YJ, Maithreepala Sujeewa Dilhani SD et al.

Metabolic dysfunction-associated steatotic liver disease (MASLD) is a rising global health burden linked to dyslipidemia, metabolic syndrome, and hepatic inflammation. Statins are widely prescribed in MASLD, but comparative evidence on their efficacy, safety, and cost-effectiveness remains limited. To evaluate and compare the clinical effectiveness and cost-efficiency of atorvastatin, rosuvastatin, and lovastatin-niacin fixed-dose combination [LN-FDC; commercially distributed as Linicor in Taiwan] (lovastatin plus niacin) in improving liver enzymes and lipid profiles in MASLD patients. This retrospective cohort study analyzed electronic medical records from a teaching hospital in southern Taiwan. Of 984 screened patients, 729 were included after 1:1 propensity score matching by age, sex, and baseline ALT. Patients received daily atorvastatin (20 mg), rosuvastatin (10 mg), or LN-FDC (20/500 mg) for six months. Primary outcomes were ALT and AST changes and treatment response (≥ 30% decline); secondary outcomes included lipid profiles, adverse events, and cost-effectiveness. All three regimens were associated with statistically significant reductions in liver biochemistry and lipid markers over six months. LN-FDC was associated with the most substantial reductions in ALT and AST, with 53.5% achieving ≥ 30% AST decline versus < 30% with atorvastatin or rosuvastatin (p < 0.001). For ALT, LN-FDC was associated with a higher ALT response rate by six months (39.9% responders vs. ~31% in comparators, p = 0.048). While atorvastatin and rosuvastatin were associated with greater HDL-C improvements, LN-FDC was associated with decreased triglycerides and a low incremental cost-effectiveness ratio. Adverse events were infrequent but showed variation across groups. Specifically, Higher flush reactions were observed in LN-FDC patients, while higher gastrointestinal intolerance and liver enzyme elevations were shown in the atorvastatin group, and higher hyperglycemia was associated with rosuvastatin. LN-FDC appeared to be associated with greater reductions and favorable cost patterns for improving hepatic inflammation and triglycerides in MASLD, though atorvastatin and rosuvastatin could increase HDL-C. Statin therapy thus provides dual hepatic and cardiovascular benefits in MASLD, with treatment choice guided by patient-specific metabolic and economic considerations.

PMID 42265807
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PubMedJournal of biomedical materials research. Part B, Applied biomaterials2026-06-10

Preparation and Characterization of Biopolymeric-Based Orally Dissolving Mucoadhesive Hydrogels Loaded With Rosuvastatin for the Effective Treatment of Aphthous Ulcer.

Dey Ishika I, Ghosh Koushik K, Hazra Ahana A, Maitra Debashis D et al.

The primary objective of this study was to develop and evaluate a sustained-release mucoadhesive hydrogel loaded with Rosuvastatin (RSV) to enhance the treatment of aphthous ulcers. By leveraging the pleiotropic anti-inflammatory and tissue-repair properties of RSV, the study aimed to overcome the rapid clearance and low efficacy associated with conventional oral gels and mouthwashes. Mucoadhesive hydrogels were formulated using Carbopol 934 and sodium alginate via a freeze-thaw crosslinking technique. Four formulations (F1-F4) were prepared and evaluated for morphology, swelling behavior, viscosity, mucoadhesive strength, drug entrapment efficiency, pH, in vitro drug release, antimicrobial activity, cytocompatibility, and in vivo therapeutic efficacy. Antimicrobial activity was assessed against Streptococcus mutans (ATCC 10231) and Staphylococcus aureus (MTCC 2940), while cytocompatibility was determined using an MTT assay on fibroblast cells. The formulated mucoadhesive hydrogel showed good swelling behavior, thermal stability, and controllable biodegradability. The four formulations (F1, F2, F3, and F4) exhibited significant entrapment efficiency (72.14% ± 1.5% to 95.12% ± 0.28%), and the pH was 6.7. The optimized formulation (F3) demonstrated sustained RSV release of 96.8% ± 1.4% over 8 h. We found that F3 may inhibit the growth of both Streptococcus mutans (ATCC 10231) and Staphylococcus aureus (MTCC 2940) (MRSA), which are common aphthous ulcer infectious bacteria. Cytocompatibility studies confirmed that F3 supported fibroblast viability and enhanced cell proliferation. In vivo evaluation further demonstrated improved healing of oral ulcers, supported by histopathological findings indicating enhanced tissue regeneration and reduced inflammation. The RSV-loaded mucoadhesive hydrogel (F3) exhibited high drug entrapment, sustained release, effective antimicrobial activity, and excellent biocompatibility, leading to significant therapeutic efficacy in an animal model. These findings suggest that the developed hydrogel is a promising and safe alternative for the treatment of aphthous ulcers, warranting further clinical investigation.

PMID 42267512
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PubMedCureus2026-06-10

Reassessment of Long-Term Guideline-Directed Therapy for Peripheral Arterial Occlusive Disease in Primary Care.

Park Joomong J

Peripheral arterial occlusive disease is a manifestation of systemic atherosclerosis associated with increased risks of cardiovascular events, limb complications, and mortality. Guideline-directed medical therapy, including antiplatelet agents and statins, is recommended for secondary prevention, whereas cilostazol and exercise therapy are primarily intended for symptomatic relief of claudication. We report the case of a 68-year-old man with previously diagnosed peripheral arterial occlusive disease who presented to a primary care clinic with worsening intermittent claudication while receiving cilostazol without documented antiplatelet or statin therapy. His comorbidities included hypertension, type 2 diabetes mellitus with complications, chronic kidney disease, prior ischemic stroke, and former tobacco use. Physical examination revealed diminished pulses in the affected limb and a relatively cool foot without ulceration or acute infection. Laboratory evaluation showed serum creatinine 1.44 mg/dL (reference range: 0.70-1.30 mg/dL), estimated glomerular filtration rate 49 mL/min/1.73 m² (reference range: ≥60 mL/min/1.73 m²), and glycated hemoglobin 5.7% (reference range: 4.0%-5.6%). Aspirin 100 mg daily and rosuvastatin 10 mg daily were initiated for cardiovascular risk reduction. Cilostazol was later resumed for symptomatic management, and aspirin was changed to clopidogrel because of gastrointestinal intolerance. At the fourth week follow-up, the patient reported a modest increase in walking distance, although causality could not be established. This case highlights the importance of periodic medication reconciliation, reassessment of long-term vascular risk management, and recognition that symptomatic therapy should not substitute for guideline-directed secondary prevention in patients with established peripheral arterial occlusive disease.

PMID 42266296
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PubMedComparative biochemistry and physiology. Toxicology & pharmacology : CBP2026-06-06

Rosuvastatin calcium and pravastatin sodium regulate the antioxidant system in zebrafish liver through the PI3K/Nrf2/ARE signaling pathway.

Xie Y I N G YING, Wang X I A N R U I XIANRUI, Mu Q U A N L I N G QUANLING, Ding C U N B A O CUNBAO

Rosuvastatin calcium (ROV) and pravastatin sodium (PRA) are common drugs used for the treatment and prevention of cardiovascular diseases. They have been frequently detected in the global aquatic environment, but their toxic effects and molecular mechanisms on the antioxidant system of fish remain unclear. In this study, zebrafish were exposed to ROV or PRA for 48 h to investigate their effects on the hepatic antioxidant response system of zebrafish and the possible underlying molecular mechanisms. The results showed that after exposure to the two drugs, the levels of reactive oxygen species (ROS), glutathione (GSH), and malondialdehyde (MDA) increased, while the activities of catalase (CAT) and superoxide dismutase (SOD) were inhibited. Exposure to ROV (5 mg/L) upregulated the activities of glutathione peroxidase (GPx) and glutathione S-transferase (GST), as well as the mRNA levels of phosphatidylinositol 3-kinase (PI3K) and CAT. However, the protein levels of nuclear factor erythroid 2-like protein (Nrf2) and SOD were suppressed. Exposure to PRA (10 mg/L) also increased the mRNA levels of PI3K, CAT, and GPx, while inhibiting Nrf2 and SOD proteins. The inhibitory effects on Nrf2 and SOD proteins were reversed after the addition of the PI3K activator 740YP. Molecular docking showed that both ROV and PRA could bind stably to PI3K. In conclusion, both ROV and PRA can induce hepatic oxidative damage in zebrafish, and the mechanism may be related to the disruption of the PI3K-mediated Nrf2/ARE pathway.

PMID 42248540
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