北京若生智能科技有限公司
Drug Database
RO

rosuvastatin + ezetimibe (ID 1805 / ID1805 / Droptop)

✓ Approved

Ildong Pharmaceutical · HMGCR · 小分子

什么是 rosuvastatin + ezetimibe？

rosuvastatin + ezetimibe 是一种小分子，由Ildong Pharmaceutical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ID 1805, ID1805, Droptop
公司Ildong Pharmaceutical
药物类别小分子
分子靶点HMGCR, NPC1L1
给药途径Oral (PO)
状态Approved
来源： ClinicalTrials.gov, Ildong Pharmaceutical

作用机制

分子靶点

rosuvastatin + ezetimibe 作用于 2 个分子靶点：

HMGCR3-hydroxy-3-methylglutaryl-CoA reductase (LDLCQ3, LGMDR28)
NPC1L1NPC1 like intracellular cholesterol transporter 1 (SLC65A2, LDLCQ7)
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

rosuvastatin + ezetimibe 针对 1 个适应症，涉及 1 个治疗领域。

治疗领域疾病/病症分期
Metabolism and nutrition disordersHypercholesterolaemia✓ Approved

相关研究文献

PubMedRomanian journal of internal medicine = Revue roumaine de medecine interne2026-10-26

Achieving Risk-Specific Absolute LDL-C Threshold with PCSK9 Inhibitors: A Real-World, Single-Center Analysis.

Ciobanu Dana Mihaela DM, Berchișan Antonia A, Mălan Cosmina C, Rusu Adriana A et al.

Proprotein convertase subtilisin/kexin type 9 (PCSK9) inhibitors emerged as an effective treatment for hypercholesterolemia in clinical trials, however real-world evidence shows considerable heterogeneity. We aimed to assess the effectiveness and safety of injectable PCSK9 inhibitors in real-world patients. Our retrospective analysis included 45 consecutive adults, 18 (40%) men, mean age 57.4 years, inadequately controlled on, or intolerant to, statins and/or ezetimibe, and newly initiated on alirocumab 75 mg or 150 mg, evolocumab 140 mg, or inclisiran 284 mg. Biochemical parameters and adverse events were recorded at baseline and when LDL-C reached the risk-specific absolute threshold or the lowest LDL-C closest to it after starting PCSK9 inhibitors (<55 mg/dL very high, <70 mg/dL high cardiovascular risk, per European Society of Cardiology). LDL-C was also assessed at standardized time points (3, 6, 12, 18, 24 months). At 3 and 6 months, LDL-C decreased by a median of 54.4% and 59.2% (both p < 0.001), with 52.4% and 50.0% of patients below threshold. The best LDL-C reduction was 66.9% (from 145 mg/dL to 50 mg/dL; p < 0.001) at a median time to first documented threshold attainment of 5 months. In an exploratory analysis, no significant association was detected between LDL-C reduction and sex, diabetes, statin intensity or ezetimibe use. No clinically relevant hepatic or muscular toxicity was attributed to PCSK9 inhibitors. In real-world patients aiming to achieve the absolute LDL-C threshold on PCSK9 inhibitors, treatment was associated with marked LDL-C reduction after a median of 5 months.

PMID 42928644
阅读全文 →
PubMedDaru : journal of Faculty of Pharmacy, Tehran University of Medical Sciences2026-10-25

Association between perioperative statin-ezetimibe therapy and reoperation following arthroscopic rotator cuff repair: A TriNetX database study.

Mahatme Ronak R, Gangavaram Anish A, Muthusamy Nishanth N, Moore Shawn S et al.

Hyperlipidemia (HLD) impairs tendon healing and is associated with increased revision risk following arthroscopic rotator cuff repair (ARCR). While statins may partially mitigate this effect, residual dyslipidemia may impair healing. Ezetimibe, through inhibition of intestinal cholesterol absorption, has demonstrated favorable effects on tendon healing in preclinical studies. This study evaluated whether perioperative statin-ezetimibe therapy is associated with improved postoperative outcomes following ARCR compared with statin monotherapy and patients without HLD. A retrospective cohort study was conducted using the TriNetX Research Network. Adult patients undergoing ARCR were stratified into three cohorts based on HLD status and perioperative (± 6 months) lipid-lowering therapy: (1) documented HLD treated with statin-ezetimibe prescriptions, (2) patients without documented HLD or lipid-lowering therapy prescriptions, and (3) documented HLD treated with statin monotherapy prescriptions. Primary comparisons were predefined between cohort 1 and cohorts 2 and 3. Propensity score matching (1:1) adjusted for demographics and comorbidities. Tear size and presence of fatty atrophy and fatty infiltration were not adjusted for. Outcomes occurring within 5 years included revision rotator cuff repair (RCR), conversion to shoulder arthroplasty, and secondary shoulder arthroscopy. After matching, 1,066 patients were included in cohorts 1 and 2 and 1,114 patients in cohorts 1 and 3. Compared with patients without HLD, statin-ezetimibe therapy demonstrated similar rates of revision RCR (5.4% vs. 6.4%; RR 0.853; p = 0.358), conversion to shoulder arthroplasty (RR 1.227; p = 0.470), and secondary arthroscopy (RR 0.846; p = 0.260). Compared with statin monotherapy, statin-ezetimibe therapy was associated with lower rates of revision RCR (5.6% vs. 8.0%; RR 0.697; p = 0.023) and secondary shoulder arthroscopy (7.3% vs. 9.6%; RR 0.757; p = 0.048), while arthroplasty rates remained similar (RR 1.261; p = 0.400). Among patients with HLD undergoing ARCR, perioperative statin-ezetimibe therapy was associated with lower reoperation rates compared with statin monotherapy and postoperative outcomes comparable to patients without HLD. These findings support further investigation of intensified lipid-lowering therapy, while accounting for tear size and fatty infiltration.

PMID 42927533
阅读全文 →
PubMedPeerJ2026-10-25

Effectiveness and safety of atorvastatin/ ezetimibe fixed-dose combination in hypercholesterolemia: a systematic review and network meta-analysis.

Qian Juying J, Zhang Xingxin X, Li Qing Q, Chen Sisi S

Many patients fail to achieve low-density lipoprotein cholesterol (LDL-C) targets with statin monotherapy, calling for a combination of statins and ezetimibe. This systematic review and network meta-analysis evaluated the comparative effectiveness and safety of atorvastatin monotherapy, atorvastatin/ezetimibe free-equivalent combination (AS/EZ FEC), and fixed-dose combination (AS/EZ FDC) in patients with hypercholesterolemia. Randomized controlled trials were retrieved from electronic databases. Primary outcomes were the percentage change in LDL-C from baseline and LDL-C goal attainment, analyzed using mean difference (MD) and risk ratio (RR) with 95% confidence intervals (CI). Treatments were ranked via surface under the cumulative ranking curve (SUCRA). The two combination therapies were compared to AS alone for their safety profiles and tolerability. Forty-six trials (n = 10,567) were included. AS/EZ FDC reduced LDL-C more than AS alone (MD -13.94%, 95% CI [-18.90% to -9.10%]), with similar results for AS/EZ FEC (MD -12.41%, 95% CI [-14.61% to -10.22%]). SUCRA rankings for LDL-C reduction were FDC (86.2%), FEC (63.8%), and AS (0.0%). For LDL-C goal attainment, the RR was 1.87 (95% CI [1.47-2.39]) for FEC vs. monotherapy, 1.80 (95% CI [0.85-3.81]) for FDC vs. monotherapy. No significant differences in safety profiles were observed between treatments. AS/EZ combination therapies provide greater improvements in LDL-C reduction and goal attainment compared with AS monotherapy, with FDC ranking highest in LDL-C reduction. Treatment with AS/EZ FEC or FDC did not increase the risk of adverse events compared to AS monotherapy and was well tolerated. These findings support FDC use when intensive LDL-C lowering is required.

PMID 42927391
阅读全文 →
PubMedJCEM case reports2026-10-25

Persistent atherogenic lipoprotein changes during lorlatinib therapy.

Shibue Kimitaka K, Kunimasa Kei K, Hamasaki Akihiro A

Lorlatinib, a third-generation anaplastic lymphoma kinase (ALK)/ROS1 tyrosine kinase inhibitor, frequently induces hypercholesterolemia and hypertriglyceridemia, but longitudinal qualitative lipoprotein changes remain incompletely characterized. We describe a 52-year-old woman with ALK-rearranged non-small cell lung cancer who developed persistent dyslipidemia despite lipid-lowering therapy. Before lorlatinib, total cholesterol was 164 mg/dL (SI [International System of Units]: 4.24 mmol/L) (reference range, 148-248 mg/dL [SI: 3.83-6.41 mmol/L]), low-density lipoprotein (LDL) cholesterol was 52 mg/dL (SI: 1.34 mmol/L) (reference range, 65-139 mg/dL [SI: 1.68-3.59 mmol/L]), and triglycerides were 54 mg/dL (SI: 0.61 mmol/L) (reference range, 30-117 mg/dL [SI: 0.34-1.32 mmol/L]). Within 3 weeks after lorlatinib initiation, these increased to 340, 245, and 166 mg/dL, respectively. Longitudinal profiling showed persistent apolipoprotein B (ApoB) elevation, increased oxidized LDL, and a prominent pre-β-lipoprotein fraction. Subclinical hypothyroidism was later detected, and pitavastatin was switched to rosuvastatin. This case highlights the potential value of ApoB and qualitative lipid assessment during prolonged lorlatinib therapy.

PMID 42923625
阅读全文 →
PubMedEuropean journal of pharmacology2026-10-25

Interleukin-17D Deficiency Attenuates Atherosclerosis by Diminishing Macrophage Inflammation and Promoting M2 Phenotype.

Hou Jingyuan J, Gu Xiaodong X, Li Xia X, Zhao Junli J et al.

Macrophages are central to atherosclerosis by driving vascular inflammation, plaque growth, and instability. Although interleukin-17D (IL-17D) has been linked to endothelial inflammation, its role in macrophage-mediated atherosclerosis remains unclear. This study investigated the function and mechanism of macrophage IL-17D in atherosclerosis. Using IL-17D knockout, macrophage-specific IL-17D knockdown, and macrophage-specific Spi-B knockdown mouse models on an ApoE-/- background, we assessed aortic lesion burden, necrotic core formation, macrophage accumulation, inflammatory responses, and macrophage polarization. Mechanistic studies were performed using transcriptomic analysis, ChIP-PCR, and luciferase reporter assays. IL-17D deficiency markedly reduced atherosclerotic plaque formation in the whole aorta and aortic root, decreased necrotic core size, and limited macrophage accumulation and vascular inflammation. Both in vitro and in vivo, IL-17D deficiency promoted M2 macrophage polarization while suppressing pro-inflammatory cytokines and chemokines. Macrophage-specific IL-17D knockdown similarly attenuated atherosclerotic lesion development and inflammation. Mechanistically, IL-17D deficiency activated the Spi-B-STAT6 transcriptional axis. Macrophage-specific Spi-B knockdown reversed the anti-atherosclerotic effects of IL-17D deficiency, confirming its functional importance. Rosuvastatin suppressed IL-17D expression, and IL-17D repression contributed to its anti-inflammatory and anti-atherogenic effects. These findings identify macrophage-derived IL-17D as a key regulator of atherosclerosis. Targeting IL-17D may promote protective M2 polarization and alleviate vascular inflammation, offering a potential therapeutic strategy for atherosclerotic disease.

PMID 42926082
阅读全文 →
PubMedNutrition, metabolism, and cardiovascular diseases : NMCD2026-10-25

Extreme cardiovascular risk as a major barrier to LDL-C target achievement: insights from ITACARE-P registry.

Giallauria Francesco F, Cuomo Gianluigi G, Faggiano Andrea A, Vallefuoco Giuseppe G et al.

Achieving low-density lipoprotein cholesterol (LDL-C) targets remains challenging in secondary cardiovascular prevention despite the availability of effective lipid-lowering therapies. The 2025 ESC/EAS dyslipidaemia guidelines introduced an "extreme cardiovascular risk" category requiring LDL-C levels <40 mg/dL, potentially increasing the difficulty of target attainment. We aimed to identify clinical and therapeutic predictors of LDL-C target achievement according to the 2025 ESC/EAS recommendations and estimate the probability of goal attainment across different risk categories and treatment strategies. This sub-analysis of the multicentre ITACARE-P registry included 1904 outpatients with established atherosclerotic cardiovascular disease. Missing data were handled using multiple imputation, and stable predictors were selected through Elastic Net regularization across 20 imputed datasets. A multivariable generalized linear mixed-effects model was internally validated using 1000 bootstrap resamples. Overall, 38% of patients achieved guideline-recommended LDL-C targets. Independent predictors of target attainment included PCSK9 inhibitor therapy (OR = 7.65), high-intensity statins (OR = 4.73), ezetimibe (OR = 2.64), male sex (OR = 1.99), diabetes mellitus (OR = 1.99), coronary artery disease (OR = 2.73), participation in cardiac rehabilitation (OR = 1.81), and high physical activity (O = 1.54). Current smoking, prior dyslipidaemia, and longer disease duration were associated with lower odds of achievement. Very-high-risk patients were more likely to achieve LDL-C targets than extreme-risk patients (OR = 5.66). Predicted target attainment ranged from 9.8% to 88.6% according to treatment intensity and risk category. Model discrimination was good (optimism-corrected AUC = 0.782). LDL-C target attainment under the 2025 ESC/EAS guidelines remains suboptimal, particularly among extreme-risk patients. Earlier therapeutic intensification and individualized lipid-lowering strategies may be necessary to improve real-world goal achievement.

PMID 42928029
阅读全文 →

注册免费账户还可查看另外 9575 篇文献

免费注册查看全部文献 →

了解更多rosuvastatin + ezetimibe