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

✓ Approved

Hanmi Pharmaceutical · HMGCR · Small Molecule

What is simvastatin?

simvastatin is a small molecule developed by Hanmi Pharmaceutical. It is approved for therapeutic indications via oral (po).

Drug Profile

Brand Namessimvastatin, Hanmi, simvastatin CR, Simvast CR
CompanyHanmi Pharmaceutical
Drug ClassSmall Molecule
Molecular TargetHMGCR
RouteOral (PO)
StatusApproved

Mechanism of Action

Molecular Targets

simvastatin acts on 1 molecular target:

HMGCR3-hydroxy-3-methylglutaryl-CoA reductase (LDLCQ3, LGMDR28)
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Therapeutic Indications

simvastatin is developed for 1 unique indication across 1 therapeutic area.

Therapeutic AreaConditionPhase
Metabolism and nutrition disordersHyperlipidaemia✓ Approved

Related Research Articles

PubMedBritish journal of pharmacology2026-11-11

Interpretable multimodal network analysis of lipid-lowering therapies.

Dall'Olio Daniele D, Pedrelli Matteo M, Sala Claudia C, Grassi Francesca F et al.

Multimodal integration of clinical and omics data could clarify the hepatic mechanisms of lipid-lowering therapies, but interpretable methods for heterogeneous data remain limited. The objective was to apply interpretable multimodal networks (IMNs), a topology-aware framework that condenses heterogeneous omics and clinical data into compact, cross-modal modules, to characterize treatment-specific hepatic responses to simvastatin and ezetimibe. In the Stockholm Study, patients scheduled for cholecystectomy were randomized for 4 weeks to simvastatin, ezetimibe, their combination or placebo. We integrated liver transcriptomics and DNA methylation with plasma/bile biochemistry, including lipoprotein functionality, on the human protein-protein interactome to build treatment-specific IMNs and evaluated selected network-derived predictions in a human hepatocyte-like model (SOAT2-only-HepG2). IMNs reduced dimensionality while preserving network topology, producing distinct molecular signatures for simvastatin, ezetimibe and combination therapy that mapped to different biological processes; the placebo network was less multimodal and more fragmented. IMNs highlighted apolipoprotein-centred modules and predicted drug effects on APOA2, PPARA and PTPRS, linked to plasma C-peptide. In SOAT2-only-HepG2 cells, selected predictions were supported experimentally, including APOA2 induction and ezetimibe-associated PTPRS upregulation. IMNs provide a practical, interactome-based route from multimodal patient data to focused, testable hypotheses about lipid-lowering therapies, yielding compact features suitable for downstream predictive modelling while retaining biological interpretability.

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.

PubMedZhonghua nan ke xue = National journal of andrology2026-11-11

[Linolenic acid compound powder improves reproductive damage induced by high fat diet in male rats].

Wang Yibo Y, Sun Ruijie R, Ji Linpu L, Liu Qiaorui Q et al.

Objective To evaluate the effect of linolenic acid compound powder (flaxseed microcapsule powder, okra powder, mulberry leaf powder) on the reproductive function of male rats induced by high fat diet. Methods Ninety 8-week-old male SD rats were randomly divided into six groups, with 15 rats in each group. The rats in the blank group were fed with normal diet. While the rats in model group were fed with high-fat feed, and the low-, medium- and high-dose groups of linolenic acid combined powder were fed with low-, medium- and high-dose respectively, as well as the simvastatin positive control group. After 4 weeks of high-fat diet modeling, the compound powder was continuously administered by gavage for 4 weeks. The body weight, epididymis and testis weight of rats in each group were recorded. Sperm concentration and motility were detected. HE staining was used to observe testicular pathological damage, and Oil Red O staining was used to observe fat distribution. Lipid, oxidative stress and sex hormone indicators were also detected. Results Compared with the model group, treatment with the linolenic acid mixture or the positive control drug significantly increased body weight in rats to levels exceeding those in the blank control group (all P<0.05). There were no statistically significant differences in the testicular and epididymal coefficients parameters across the three experimental groups (P>0.05). Sperm motility and Sperm viability was significantly higher in all linolenic acid complex powder dose groups and the positive control group compared to the model group (all P<0.05). Compared with the model group, the testis interstitium of the linolenic acid compound powder groups returned to normal. The seminiferous tubules returned to order. The number of spermatogenic cells and Sertoli cells at all levels increased. All kinds of cells were dense and the structure was complete. Compared with the model group, the testicular tissue of the linolenic acid compound powder groups had less stained area and lighter color, and the medium-dose group had less stained area and lighter color than the low-dose group and the high-dose group. There was no significant difference in oxidative stress among groups (P>0.05). The level of LH in the model group was lower than that in the blank group. Which increased in the linolenic acid compound powder groups significantly (P<0.05). Administration of linolenic acid compound powder all doses and the positive control significantly decreased the levels of ALP, ALT and AST in liver tissue compared with the model group. Additionally, a significant reduction in serum CRE was observed in the low- and medium-dose groups (all P<0.05). Conclusion A high-fat diet leads to a decline in the physiological structure and antioxidant capacity of the testes in rats, as well as changes in sex hormone levels. Linoleic acid complex powder can improve the related symptoms and indicators of reproductive function in rats with high-fat diet.

PubMedResearch in pharmaceutical sciences2026-11-10

Ficus elastica phytochemicals mitigate hyperlipidemia via potential HMG-CoA reductase inhibition, reduced oxidative stress, and tissue preservation.

Susanti Gita G, Aldi Yufri Y, Handayani Dian D, Ismed Friardi F et al.

Hyperlipidemia remains a major cardiovascular risk factor requiring novel therapeutic strategies beyond conventional statin therapy. This study investigated the antihyperlipidemic and antioxidant properties of Ficus elastica Roxb. ex Hornem. (Moraceae) phytochemicals through integrated in vitro, in vivo, and in silico approaches. Eight chromatographic subfractions were screened for 3-hydroxy-3-methylglutaryl-coenzyme A (HMG-CoA) reductase inhibitory activity. Lipid profile, lipid peroxidation, and histopathology were evaluated in rats fed a high-fat diet to induce hyperlipidemia. Chemical composition was characterized using liquid chromatography high-resolution mass spectrometry (LC-HRMS) and subsequently investigated through molecular docking simulations. Subfraction 4 demonstrated the strongest HMG-CoA reductase inhibitory activity. In vivo evaluation in high-fat diet-induced hyperlipidemic rats revealed dose-dependent improvements in all lipid parameters, with effects statistically comparable to simvastatin. Subfraction 4 additionally reduced serum malondialdehyde to levels statistically indistinguishable from normal controls, indicating restoration of oxidative homeostasis. Histological preservation of aortic endothelial integrity and elastic fiber organization was associated with reduced intima-media thickness, suggesting attenuation of early atherosclerotic changes. LC-HRMS analysis tentatively identified four major constituents, including phlorin, clausarinol, ginsenoyne C, and piptolinic acid A. Molecular docking analysis suggested that clausarinol and ginsenoyne C exhibited comparatively higher predicted binding affinity than simvastatin toward PCSK9 and PPAR-α, respectively. These findings support the potential of F. elastica phytochemicals as candidates for hyperlipidemia management.

PubMedbioRxiv : the preprint server for biology2026-11-06

Simvastatin Preserves Human Microvascular Endothelial Barrier Function Through Mevalonate-Dependent Regulation of RhoB Localization and Activation.

Morales-Maldonado Alejandra A, Pober Jordan S JS, Pierce Richard W RW

Endothelial barrier failure contributes to edema, tissue hypoperfusion, and organ dysfunction during inflammatory critical illness. RhoB has emerged as a regulator of tight junction disruption in human microvascular endothelial cells, but whether clinically used drugs can modulate RhoB-dependent barrier failure remains unclear. We tested whether simvastatin preserves human dermal microvascular endothelial cell barrier function during TNF stimulation and examined the role of mevalonate-dependent RhoB localization and activation. Simvastatin pretreatment attenuated TNF-induced loss of transendothelial electrical resistance and preserved junctional ZO-1 and claudin-5 organization. Simvastatin reduced membrane-associated and increased nuclear RhoB, decreased active RhoB, and suppressed myosin light chain phosphorylation. RhoB silencing phenocopied the barrier-protective effect of simvastatin, and combined RhoB silencing and simvastatin did not provide additive protection. Mevalonate supplementation reversed simvastatin-mediated preservation of barrier function, restored peripheral RhoB localization, and restored MLC phosphorylation. These findings identify mevalonate-dependent RhoB spatial regulation as a statin-sensitive mechanism contributing to inflammatory microvascular barrier dysfunction.

PubMedEuropean journal of pharmacology2026-11-04

Synergistic anti-glioma activity of temozolomide and simvastatin through inhibition of the EGFR/AKT/mTOR signaling pathway.

Zhou Jianfen J, Wang Rong R, Yao Ru R, Liu Fangbin F et al.

Glioma is the most aggressive primary tumor of the central nervous system, and acquired resistance to temozolomide (TMZ) is a leading cause of treatment failure and tumor recurrence. Statins are well-tolerated lipid-lowering agents with emerging anti-tumor potential; however, their effects in combination with TMZ against glioma remain incompletely characterized. In this study, we identified simvastatin (SIM) as the most potent statin against U87 cells and systematically evaluated the anti-glioma activity of TMZ plus SIM in vitro and in vivo. The combination markedly inhibited U87 glioma cell proliferation, migration, and angiogenesis while promoting apoptosis. Compared with either monotherapy, the combined regimen exerted superior anti-tumor effects. Mechanistically, TMZ plus SIM suppressed the epidermal growth factor receptor/protein kinase B/mechanistic target of rapamycin (EGFR/AKT/mTOR) signaling axis, a key pathway involved in glioma growth and survival. Importantly, the combination was well tolerated, with no detectable systemic toxicity or disruption of lipid metabolism. Collectively, these findings indicate that TMZ combined with SIM exerts synergistic anti-glioma activity and may represent a potential drug-repurposing strategy for malignant glioma.

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