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simvastatin (simvastatin, Hanmi / simvastatin CR / Simvast CR)

✓ Approved

Hanmi Pharmaceutical · HMGCR · 小分子

什么是 simvastatin？

simvastatin 是一种小分子，由Hanmi 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simvastatin, Hanmi, simvastatin CR, Simvast CR
公司Hanmi Pharmaceutical
药物类别小分子
分子靶点HMGCR
给药途径Oral (PO)
状态Approved
来源： ClinicalTrials.gov, Hanmi Pharmaceutical

作用机制

分子靶点

simvastatin 作用于 1 个分子靶点：

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

simvastatin 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 disordersHyperlipidaemia✓ Approved

相关研究文献

PubMedZhongguo Zhong yao za zhi = Zhongguo zhongyao zazhi = China journal of Chinese materia medica2026-08-03

[Study on Huanglian Jiedu Decoction improving ox-LDL-induced LC3-related phagocytosis dysfunction in RAW264.7 macrophages by activating ERK5].

Wang Song-Fan SF, Jiang Ying-Yi YY, Li Xing-Yuan XY, Li Xiao-Hui XH et al.

To investigate whether the anti-atherosclerotic(AS) effect of Huanglian Jiedu Decoction(HLJDD) is associated with activation of extracellular signal-regulated kinase 5(ERK5) and the consequent improvement of microtubule-associated protein 1 light chain 3(LC3)-associated phagocytosis(LAP) dysfunction in macrophages. RAW264.7 cells were randomly divided into the normal control group, oxidized low-density lipoprotein(ox-LDL) group, HLJDD group, simvastatin(simva) group, and RAW264.7-ERK5 gene knockout(ERK5-KO) group. According to the experimental protocol, cells in each group were treated for 24 h with normal control rat serum, ox-LDL, HLJDD-containing serum, or simva-containing serum. Apoptotic Jurkat cells were added to each group and co-cultured for 90 min. After removal of the supernatant, LC3-Ⅱ labeling was performed to observe LAPosomes in macrophages, and the clearance of apoptotic Jurkat cells was assessed. The expression levels of phosphorylated(p)-ERK5, ERK5, LAP-related signaling molecules [T-cell immunoglobulin and mucin-domain-containing molecule-4(TIM-4), vacuolar protein sorting 34(VPS34), Beclin-1, RUN domain Beclin-1-interacting and cysteine-rich domain-containing protein(Rubicon), autophagy-related protein 5(ATG5), and autophagy-related protein 7(ATG7)], pro-inflammatory cytokines [interleukin-1β(IL-1β), interleukin-6(IL-6)], and anti-inflammatory cytokines [interleukin-10(IL-10), transforming growth factor-β(TGF-β)] were measured. RESULTS:: showed that, compared with the control group, the ox-LDL group exhibited decreased LAPosome percentage and reduced clearance of apoptotic cells, downregulated expression of p-ERK5, TIM-4, VPS34, Beclin-1, Rubicon, ATG5, and ATG7, increased IL-1β and IL-6 levels, and no significant changes in IL-10 or TGF-β expression. Compared with the ox-LDL group, the HLJDD and simva groups showed increased LAPosome percentage and enhanced apoptotic cell clearance, upregulated expression of p-ERK5, TIM-4, VPS34, Beclin-1, Rubicon, ATG5, and ATG7, decreased IL-1β and IL-6 levels, and increased IL-10 and TGF-β expression. Compared with the HLJDD group, the ERK5-KO group exhibited significantly reduced expression of ERK5 and p-ERK5, and all other indicators were reversed. In conclusion, HLJDD may ameliorate macrophage LAP dysfunction and exert anti-AS effects by activating ERK5.

PMID 42543371
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PubMedSkin health and disease2026-08-02

Efficacy and safety of topical statins for porokeratosis: a systematic review and practice-guided synthesis.

Shanshal Mohammed M, Uthayakumar Aarthy A, Moon Emily E, Bala Laksha L

Porokeratosis comprises keratinization disorders with few consistently effective, nondestructive treatments. Topical inhibition of the mevalonate pathway with statins is biologically plausible, but the clinical evidence is scattered across small reports. To consolidate fragmented data into a pragmatic framework for clinicians and to highlight priorities for future controlled trails. We performed a PRISMA-based systematic review of PubMed, Embase, Scopus and ClinicalTrials.gov to 8 December 2025, including all study designs that reported patient-level outcomes with topical statins. Thirty-three studies involving 162 patients met the inclusion criteria: three small, randomized trials and predominantly case series and case reports. In nonrandomized studies with analysable data (n = 98), most patients achieved partial improvement (n = 67/98 68.4%), whereas complete or near-complete clearance was less frequent (n = 16/98; 16.3%); disseminated superficial actinic porokeratosis (DSAP) appeared most responsive. Randomized evidence showed clinical improvement with topical statins but did not support routine addition of cholesterol to statin formulations. Topical statins were generally well tolerated, with several patch test-confirmed cases of simvastatin allergic contact dermatitis but no serious systemic adverse events. Certainty of evidence (GRADE) was low for DSAP improvement and serious harms, and very low for other subtypes, reflecting small sample sizes, risk of bias and heterogeneity. Overall, topical statin monotherapy emerges as a mechanism-based, field-directed option for porokeratosis, particularly DSAP, most often yielding partial rather than complete clearance with a favourable safety signal.

PMID 42539922
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PubMedComputational biology and chemistry2026-07-31

A reproducible computational transcriptomic framework for cell-type-resolved fibroinflammatory-AKT remodeling in human heart failure.

Li YiMeng Y

Human heart failure involves multicellular transcriptional remodeling, but public transcriptomic studies often remain disconnected from cell-type localization and perturbational interpretation. We developed a reproducible computational workflow integrating human left-ventricular bulk transcriptomes, donor-level cell-type pseudobulk results from a human heart-failure single-cell/single-nucleus atlas, external snRNA-seq support, curated module scoring, focused ligand-receptor prioritization and LINCS/L1000 perturbational matching. Cross-cohort analysis identified 14,358 same-direction HF-associated genes, including 1633 replicated HF-up and 785 replicated HF-down genes. Donor-level pseudobulk analysis localized disease remodeling to cardiomyocyte, fibroblast and myeloid compartments. Activated fibroblast and inflammatory myeloid programs defined a fibroinflammatory remodeling axis connected to context-dependent AKT-associated transcriptional shifts. External snRNA-seq support was strongest for fibroblast activation and AKT-associated remodeling, with etiology-dependent heterogeneity across validation resources. L1000FWD screening prioritized safety-aware perturbational hypotheses, including glimepiride and simvastatin as interpretable candidates requiring experimental validation. This study provides a computational transcriptomic framework linking reproducible human HF signatures, cell-type-resolved fibroinflammatory remodeling and perturbational genomic prioritization without claiming drug efficacy or AKT causality.

PMID 42537336
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PubMedAdvanced healthcare materials2026-07-30

A Cathepsin-Triggered Size-Shrinkable Nanoparticle Enhances Fibrous Cap Penetration to Relieve Atherosclerosis.

Liang Xiaoya X, Xu Maochang M, Wu Daobin D, He Xinghui X et al.

In the microenvironment of atherosclerosis (AS), excessive migration of vascular smooth muscle cells led to the formation of a thick fibrous cap. This structure acted as a physical barrier and hindered efficient drug delivery to lesional macrophages. An optimal strategy for balancing long circulation with effective penetration involved the use of size-tunable nanoformulations. Leveraging highly expressed cathepsin K (CTSK) in atherosclerotic plaques, this work reported CTSK-responsive, size-shrinkable nanoparticles (PDE@Mn3O4/SIM) by encapsulating trimanganese tetraoxide (Mn3O4) and simvastatin (SIM) within CTSK-cleavable block copolymers (PDE) to achieve controlled drug release and deep penetration within plaque sites. The resulting nanoparticles underwent rapid degradation and released smaller Mn3O4 nanozymes, facilitating penetration into plaque macrophages. In vitro, the nanoparticles reduced reactive oxygen species levels and enhanced cholesterol efflux in macrophages. More importantly, they prolonged blood circulation and selectively accumulated in atherosclerotic plaques with high enzyme expression. They also markedly decreased macrophage infiltration and lipid deposition in plaques of AS mouse models. Collectively, these findings indicated that nanoparticles with CTSK-responsive and size-regulating properties achieved deep plaque penetration and precise macrophage targeting, serving as an effective anti-atherosclerotic therapeutic strategy. HIGHLIGHTS: 1 Utilizing endogenously overexpressed cathepsin K in plaques as a biological stimulus could achieve precise and on-demand drug release. 2 By taking advantage of the size restriction imposed by fibrous caps, we designed microenvironment-adaptive and size-transformable nanoparticles for deep penetration. 3 Co-delivery of Mn3O4 nanozyme and SIM elicited synergistic antioxidative, antiinflammatory and lipid-modulating activities to combat atherosclerosis.

PMID 42527963
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PubMedOphthalmology. Retina2026-07-30

Sustained High-Intensity Lipophilic Statin Use and Risk of Age-Related Macular Degeneration: A Target Trial Emulation.

Bantounou Maria Anna MA, Emfietzoglou Maria M, Keenan Tiarnán D L TDL, Baroutis Konstantinos G KG et al.

To evaluate whether sustained high-intensity lipophilic statin exposure is associated with reduced risk of incident nonexudative age-related macular degeneration (AMD) and progression from nonexudative to exudative AMD. Target trial emulation retrospective cohort study. Data were obtained from the Mass General Brigham database (2005-2025). For incident nonexudative AMD, hypertensive adults ≥55 years old were included if they were treated or untreated with high-intensity lipophilic statins (atorvastatin 40-80 mg or simvastatin 40-80 mg) within 2 years following the hypertension date. For progression to exudative AMD, adults ≥55 years old with hypertension and nonexudative AMD were included if they were treated or untreated within 1 year before the nonexudative AMD date. Sustained exposure was defined as ≥80% cumulative exposure during the exposure window. Exposed and unexposed individuals were propensity-score matched 1:1 on demographics, diabetes, obesity, healthcare utilization, calendar time. Subdistribution hazard ratios (sHR) accounting for the competing risk of death and inverse probability of censoring weighting (IPCW) hazard ratios (HR) were estimated for exposed vs. unexposed, adjusting for cardiovascular and chronic kidney disease. Sensitivity analyses included: positive-control (cataract), negative-control [posterior vitreous detachment (PVD)], any statin vs no exposure. Incident clinically documented nonexudative AMD and progression to exudative AMD. Over 2.8±1.8 years, 68/8,633 participants (0.79%) in the high-intensity lipophilic statin-exposed cohort and 88/8,633 (1.02%) in the unexposed cohort developed nonexudative AMD (sHR=0.53, 95%-CI, 0.38-0.74; P=0.0002; IPCW HR=0.53, 95%-CI, 0.37-0.76; P=0.0005). In the progression cohort, over 2.1±1.6 years, 66/1,082 high-intensity lipophilic statin-exposed participants (6.10%) and 85/1,082 unexposed participants (7.86%) progressed to exudative AMD (sHR=0.62, 95%-CI, 0.45-0.87; P=0.006; IPCW HR=0.61, 95%-CI, 0.43-0.87; P=0.006). Any statin use was not associated with AMD. For cataract, the sHR was 1.18 (95%-CI, 1.03-1.34; P=0.015), and the IPCW HR was 1.20 (95%-CI, 1.05-1.38; P=0.007). For PVD, the sHR was 1.00 (95%-CI, 0.81-1.22; P=0.96), and the IPCW HR was 1.00 (95%-CI, 0.81-1.24; P=0.99). High-intensity lipophilic statin exposure was associated with lower clinically documented nonexudative AMD and progression to exudative AMD risk, whereas any statin exposure was not. These findings support regimen-specific statin effects on AMD risk. Confirmation in prospective studies and randomized trials with retinal outcomes is needed.

PMID 42526538
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PubMedInternational journal of geriatric psychiatry2026-07-29

Dementia Risk With Combined Statin and Antihypertensive Drugs That Increase Versus Decrease Angiotensin-II Formation: Findings From the 45 and Up Study.

Belachew Eyayaw Ashete EA, Peterson Gregory M GM, Salahudeen Mohammed S MS, Bezabhe Woldesellassie M WM

Hypertension and dyslipidaemia are key modifiable risk factors of dementia, and the combined use of statins and antihypertensive medications (AHMs) may offer protective benefits. However, evidence on specific combinations remains limited. This study examined associations between dementia risk and the use of statins with angiotensin-II (Ang-II) promoting AHMs (drugs that increase Ang-II formation) compared with statins combined with Ang-II suppressing AHMs (drugs that decrease Ang-II formation). This was a prospective study using data from the 45 and Up Study cohort, a large population-based cohort in New South Wales, Australia. Participants aged ≥ 45 years with hypertension and dyslipidaemia were included if they had concurrent statin and AHM use. Exposure groups were defined as either users of statins and Ang-II promoting AHMs (angiotensin II receptor blockers [ARBs], thiazides, and dihydropyridine calcium channel blockers [DHP CCBs]) or statins and Ang-II suppressing AHMs (angiotensin-converting enzyme inhibitors [ACEIs], beta-blockers [BBs], and non-DHP CCBs). Medication exposure was determined based on a proportion of days covered (PDC ≥ 80%). Baseline characteristics of the two groups were balanced using 1:1 pair propensity score matching. The Cox proportional hazards model was used to estimate hazard ratios (HRs) adjusted for diet, physical activity, comorbidities, and concomitant medications. Among 34,610 matched participants (17,305 per group; a mean age [standard deviation (SD)] of 65.8 (8.8) years; a mean follow-up (SD) of 12.4 (5.1) years), use of a statin plus Ang-II promoting AHM was associated with a 12% lower dementia risk (HR, 0.88; 95% CI, 0.79-0.98) and 13% lower all-cause mortality (HR, 0.87; 95% CI, 0.82-0.93) compared to statin plus Ang-II suppressing AHM combinations. Combinations of rosuvastatin or atorvastatin with Ang-II promoting AHMs (HR, 0.43; 95% CI, 0.36-0.50 and HR, 0.74; 95% CI, 0.64-0.84, respectively) conferred greater benefit compared with simvastatin combined with Ang-II promoting AHMs. The effects were consistent across both sexes, with the protective association observed only in the 65-74-year age group, and combinations involving ARBs demonstrated superior benefit compared to those with ACEIs. Findings were robust across sensitivity analyses, including applying a competing-risks model for death. Combined therapy with a statin plus Ang-II promoting AHMs, particularly rosuvastatin or atorvastatin with an ARB, was associated with lower dementia risk, suggesting cognitive benefits may inform therapy selection. Future randomised trials should confirm these findings and explore underlying mechanisms.

PMID 42522377
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