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fenofibrate (Triglide)

✓ Approved

SkyePharma PLC · PPARA · 小分子

什么是 fenofibrate？

fenofibrate 是一种小分子，由SkyePharma PLC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Triglide
公司SkyePharma PLC
药物类别小分子
分子靶点PPARA
给药途径Oral (PO)
状态Approved
来源： ClinicalTrials.gov, SkyePharma PLC

作用机制

分子靶点

fenofibrate 作用于 1 个分子靶点：

PPARAperoxisome proliferator activated receptor alpha (NR1C1, PPAR-alpha)
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

fenofibrate 针对 2 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 disordersHypertriglyceridaemia✓ Approved
Metabolism and nutrition disordersDyslipidaemia✓ Approved

相关研究文献

PubMedThe AAPS journal2026-09-10

Dissolution Enhancement by Binding Agents: A Potential Shortcut to Improving Bioavailability?

Chronowska Maja M, Dressman Jennifer J

The poor water solubility of many drugs and drug candidates is a limiting factor to their bioavailability after oral administration. Although dissolution enhancing approaches, e.g. amorphous solid dispersions, are often used to make enabling formulations, these are usually associated with high development and manufacturing costs. This study focuses on the potential of using pharmaceutical excipients (binders) in simple tablet formulations to improve drug release and thus bioavailability. Loperamide hydrochloride, fenofibrate, compound c0 (a drug candidate) and carvedilol were chosen for this study as poorly water-soluble model compounds. Their solubility in the absence and presence of three polymeric binders, polyvinylpyrrolidone (PVP) K90, hydroxypropyl methylcellulose (HPMC) E4M and E15, and methylcellulose (MC) was tested in FaSSIF-V1 buffer and biorelevant media. Additionally, after wet granulation using PVP K90 or HPMC E15 as binders and tablet compression, the dissolution of the model compounds was tested in FaSSIF-V1 buffer and biorelevant media. Although solubilities and dissolution profiles of the model compounds were mostly improved by the binders, correlation between solubility in buffers and dissolution from the tablets in biorelevant FaSSIF-V1 was poor, indicating that dissolution experiments may be a better screening tool than solubility experiments. An important conclusion of these studies is that it is possible to increase the rate, and in some cases, the extent of dissolution of four poorly soluble drugs using wet granulation with polymeric binders, followed by tablet compression - a simple and cost-effective approach to improving drug performance.

PMID 42717179
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PubMedJournal of pharmacy & pharmaceutical sciences : a publication of the Canadian Society for Pharmaceutical Sciences, Societe canadienne des sciences pharmaceutiques2026-09-09

Fenofibrate in ophthalmology: therapeutic efficacy and mechanisms.

Ho Sean Chung-Hei SC, Lee Isabelle Xin Yu IXY, Liu Chang C, Yu Mingyi M et al.

Ophthalmic diseases are a growing global cause of visual impairment, driven by population aging and the rising prevalence of diabetes mellitus. Fenofibrate, a peroxisome proliferator-activated receptor alpha (PPARα) agonist widely used for dyslipidemia, has emerged as a candidate for therapeutic repurposing in ophthalmology. This narrative review synthesizes current preclinical and clinical evidence on fenofibrate across anterior and posterior segment diseases, including diabetic corneal neuropathy, diabetic keratopathy, dry eye disease, corneal burns, Fuchs endothelial corneal dystrophy, diabetic retinopathy, diabetic macular edema, neovascular age-related macular degeneration, and central retinal artery occlusion. Across ocular disease models, fenofibrate demonstrates neuroprotective, vascular stabilizing, and tissue-remodeling effects. These actions appear to involve modulation of shared pathogenic pathways, including PPARα-dependentregulation of inflammatory signaling, mitochondrial and lipid metabolism, and preservation of epithelial, endothelial, neuronal, and vascular integrity. Clinical evidence is strongest for diabetic retinopathy, where randomized trials support a potential adjunctive role in slowing progression and reducing interventions in patients with early-to-moderate disease. Preliminary clinical evidence for diabetic corneal neuropathy is promising but limited, whereas data for dry eye disease, corneal burns, Fuchs endothelial corneal dystrophy, neovascular age-related macular degeneration, and retinal ischemic injury remains preclinical. Emerging experimental ocular delivery strategies may improve local bioavailability while reducing systemic exposure. Overall, fenofibrate represents a biologically plausible adjunctive ophthalmic therapy, but further randomized trials, mechanistic studies, pharmacokinetic evaluation, and long-term safety assessments are required to define its therapeutic role beyond diabetic retinopathy.

PMID 42713229
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PubMedFASEB journal : official publication of the Federation of American Societies for Experimental Biology2026-09-08

Fenofibrate Protects Against Antipsychotic-Induced Hyperglycemia Through Weight Loss and FGF21 Dependent Mechanisms.

Akcan Michael M, Jeromson Stewart S, Baranowski Bradley J BJ, Bellucci Annalaura A et al.

Antipsychotic (AP) medications, such as olanzapine, cause acute weight gain independent of hyperglycemia through a glucagon-dependent mechanism. Previous work has shown that exercise, a ketogenic diet, and fasting can protect against acute AP-induced hyperglycemia and attenuate increases in glucagon. As these interventions all increase circulating concentrations of fibroblast growth factor 21 (FGF21), we hypothesized that increasing endogenous FGF21 through treatment with fenofibrate would protect against AP-induced hyperglycemia. Male C57BL/6J mice were fed a low-fat diet with or without fenofibrate (0.2% w/w) for 1 week prior to an acute olanzapine (OLZ) challenge. Fenofibrate reduced food intake and caused weight loss while protecting against OLZ-induced increases in serum glucagon and blood glucose. Pair feeding mice with the same amount of food as fenofibrate-treated animals conferred a similar degree of protection against OLZ-induced hyperglycemia. Furthermore, an acute oral gavage with fenofibrate, despite increasing circulating FGF21 concentrations to a similar level as fenofibrate feeding, failed to protect against OLZ-induced glucose excursions. The effects of fenofibrate on weight loss and protection against OLZ-induced hyperglycemia were attenuated in FGF21-/- mice. Fenofibrate attenuated both OLZ-induced hyperlipidemia and increases in whole-body fatty acid oxidation, with the latter effects being dependent upon FGF21. Together, our findings demonstrate that fenofibrate protects against acute olanzapine-induced hyperglycemia and hyperlipidemia in a weight loss and FGF21-dependent manner.

PMID 42709008
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PubMedThe Journal of clinical endocrinology and metabolism2026-09-07

Associations between fenofibrate use and sight-threatening diabetic retinopathy in type 2 diabetes: UK real-world evidence.

Tan Luyuan L, Cooper Jennifer M JM, Gokhale Krishna K, Sainsbury Christopher C et al.

Half of individuals with type 2 diabetes (T2D) also experience dyslipidaemia. In a phase IV clinical trial, fenofibrate was shown to reduce the risk of referable diabetic retinopathy (DR) comparing to placebo in people with background diabetic retinopathy (BDR). We aimed to generate comprehensive real-world evidence on the effects of fenofibrate on the risk of sight-threatening diabetic retinopathy (STDR) in individuals with T2D, compared with statins. This propensity score-matched, prevalent new-user comparative effectiveness trial emulation study included adults (≥18 years) with T2D, receiving either statins or fenofibrate, as recorded in Clinical Practice Research Datalink (a UK primary care database) from 1 January 2000 to 30 June 2022. The primary outcome was incident STDR. After propensity score matching, competing risk Cox proportional hazard regression models were used to estimate the crude and adjusted hazard ratios (aHR) in both intention-to-treat (ITT) and per-protocol (PP) analyses. Data from 16,337 fenofibrate new users and their matched 25,764 statin users were included in this study. Participants were followed up for up to 12 years. Fenofibrate use was associated with a reduced risk of developing STDR (aHR: ITT 0.87, 95% CI 0.82-0.93; PP 0.80, 0.74-0.87) in comparison with the statin group. The results were consistent across sensitivity analysis and subgroups based on age, sex, ethnicity, and lipid levels. However, the protective effect was not observed in South Asians. Fenofibrate use was associated with a reduced risk of STDR in individuals with T2D in the real-world clinical practice. These fundings suggest that fenofibrate could be considered as a DR preventive therapy for individuals with T2D.

PMID 42702803
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PubMedDiabetes research and clinical practice2026-09-04

Effect of fenofibrate on diabetic retinopathy progression: an RCT-Only systematic review and meta-analysis incorporating the LENS trial.

Bhandari Manish M, Devkota Sandesh S, Dhital Rubina R, Subedi Sunil S et al.

Diabetic retinopathy (DR) causes preventable vision loss, yet treatments remain reactive. Fenofibrate showed ophthalmic benefits in cardiovascular trials, and LENS (2024) expanded the evidence. Under a pre-registered PRISMA 2020 protocol we searched four databases to June 25, 2026 for randomized trials of fenofibrate reporting an ophthalmic outcome in adults with diabetes, applied RoB 2 and GRADE, and pooled dichotomous outcomes as random-effects risk ratios (RR). Ten studies met inclusion criteria: six completed with extractable results and four ongoing; three completed trials contributed to the primary pooled outcome. All enrolled predominantly type 2 diabetes (one trial 26% type 1, no type-specific estimate). For DR progression, three trials (N = 3,756) gave RR 0.77 (95% CI 0.68-0.88;HKSJ 0.60-0.99; I2 0%; moderate certainty), 45 fewer events per 1,000; stratification gave 0.80 (0.68-0.93) for the LENS composite and 0.70 (0.55-0.90) for ETDRS step-based definitions (difference P = 0.37). Need for retinal treatment fell under the conventional model (RR 0.68, 0.57-0.82) but at low certainty: 90.2% of the weight came from one pre-anti-VEGF-era trial and the HKSJ interval crossed the null (0.42-1.11), so this outcome is not firm evidence about contemporary treatment need. No trial found benefit for visual acuity or function (low certainty); macular edema evidence was not combinable (very low certainty). Venous thromboembolism was increased (RR 1.52, 1.12-2.06), an estimate derived entirely from FIELD (103/4,755 vs 68/4,767). In adults with diabetes, predominantly type 2, fenofibrate slows structural DR progression but is not established as vision-preserving.

PMID 42697514
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PubMedNature communications2026-09-04

PPARα activation overcomes fibroinflammatory liver microenvironment-associated anti-PD-1 resistance in hepatocellular carcinoma by mediating GSDME-dependent pyroptosis.

Chen Peng P, Xiong Kai K, Huang Kuiyuan K, Dong Zheyu Z et al.

The fibroinflammatory liver microenvironment (FILM), characterized by collagen-rich stroma and immunosuppressive inflammation, is prevalent in hepatocellular carcinoma (HCC) and correlates with poor response to programmed cell death protein 1 (PD-1) blockade. Here, we show that FILM suppresses gasdermin E (GSDME)-dependent pyroptosis and promotes immune suppression and anti-PD-1 resistance. Mechanistically, FILM-associated cancer-associated fibroblasts recruit and polarize macrophages toward a nitric oxide synthase 2 (NOS2)⁺ inflammatory phenotype. NOS2+ macrophage-derived nitric oxide induces SP1 S-nitrosylation, impairs SP1 binding to the peroxisome proliferator-activated receptor alpha (PPARA) promoter and transcriptionally represses PPARA in HCC cells. PPARα downregulation reduces pyruvate dehydrogenase kinase 4 (PDK4) expression, mitochondrial reactive oxygen species production, caspase-3 activation and GSDME cleavage. Conversely, ligand activation of tumor intrinsic PPARα restores the PDK4-ROS-caspase-3-GSDME axis, enhances dendritic cell and CD8⁺ T cell activation, and sensitizes HCC to anti-PD-1 therapy. The clinically approved PPARα agonist fenofibrate enhances anti-PD-1 efficacy in HCC models in male mice and is associated with improved clinical benefit in a retrospective cohort of patients with HCC. We propose a FILM-NOS2-SP1-PPARα-PDK4 axis that controls pyroptotic immunogenicity and immunotherapy response, supporting PPARα activation as a strategy to overcome FILM-associated immune resistance in HCC.

PMID 42693091
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