Drug Database
FE

fenofibrate (Triglide)

✓ Approved

SkyePharma PLC · PPARA · Small Molecule

What is fenofibrate?

fenofibrate is a small molecule developed by SkyePharma PLC. It is approved for therapeutic indications via oral (po).

Drug Profile

Brand NamesTriglide
CompanySkyePharma PLC
Drug ClassSmall Molecule
Molecular TargetPPARA
RouteOral (PO)
StatusApproved

Mechanism of Action

Molecular Targets

fenofibrate acts on 1 molecular target:

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

fenofibrate is developed for 2 unique indications across 1 therapeutic area.

Therapeutic AreaConditionPhase
Metabolism and nutrition disordersHypertriglyceridaemia✓ Approved
Metabolism and nutrition disordersDyslipidaemia✓ Approved

Related Research Articles

PubMedCureus2026-08-29

Splenic Vein Thrombosis Complicating Hypertriglyceridemia-Induced Acute Pancreatitis in Diabetic Ketoacidosis: A Rare Clinical Tetrad.

Adetiloye Adebola O AO, Asif Anim A, Salih Mohamed M, Ismail Moustafa M et al.

Diabetic ketoacidosis (DKA) is a life-threatening metabolic emergency that may be accompanied by severe hypertriglyceridemia (HTG), particularly in patients with poorly controlled type 1 or 2 diabetes mellitus. Marked HTG is a well-recognized cause of acute pancreatitis, while splenic vein thrombosis (SVT) is an uncommon vascular complication of pancreatic inflammation. The coexistence of these four conditions represents an exceptionally rare clinical presentation. SVT is clinically significant, as it may cause sinistral portal hypertension, gastric varices, and gastrointestinal bleeding. A 34-year-old man with type 2 diabetes mellitus presented with abdominal pain, nausea, vomiting, and DKA. Initial evaluation revealed severe HTG and HTG-induced acute pancreatitis (HTG-AP), with CT showing a bulky, ill-defined pancreas, peripancreatic fluid, and fat stranding. He was initially treated with intravenous insulin, aggressive fluid resuscitation, and electrolyte replacement. Persistent abdominal pain prompted repeat CT on hospital day 3, which demonstrated isolated SVT with perigastric collaterals and no portal or superior mesenteric vein involvement. Therapeutic intravenous heparin was initiated, followed by transition to oral apixaban. He was discharged in stable condition on basal-bolus insulin, atorvastatin, fenofibrate, and omega-3 acid ethyl esters with multidisciplinary follow-up. This case describes a rare clinical tetrad linking DKA, severe HTG, HTG-AP, and SVT. It highlights the importance of early recognition and prompt multidisciplinary management of both the metabolic and thrombotic complications associated with this uncommon presentation.

PubMedInternational journal of pharmaceutics2026-08-28

Polymer-free electrospun hydroxypropyl-β-cyclodextrin inserts for sustained ocular delivery of fenofibrate: a novel approach for management of posterior segment ocular disease.

Mishra Deepakkumar D, Saini Jaya J, Costa Guilherme G, Sigurðsson Hákon Hrafn HH et al.

The management of ocular angiogenesis remains challenging due to limitations in drug solubility, bioavailability, and conventional delivery approaches. Polymer-free electrospun hydroxypropyl-β-cyclodextrin (HPβCD) inserts loaded with fenofibrate were developed for sustained episcleral drug delivery. Fenofibrate-HPβCD inclusion complexes were characterized using 1H NMR, FTIR, and DSC. Phase solubility studies were conducted at temperatures ranging from 4 to 50°C to determine complexation parameters. Electrospun inserts were prepared from solutions containing 25-150% w/v HPβCD with fenofibrate loadings of 2.5-10% w/w and processed under optimized conditions. Fiber morphology was evaluated using scanning electron microscopy. Drug content, complexation efficiency, in vitro release, and ex vivo transscleral permeation were assessed using validated HPLC methods. Biocompatibility was evaluated using ARPE-19 retinal pigment epithelial cells and HET-CAM irritation assays. Anti-angiogenic efficacy was determined through wound-healing, and fibrin bead sprouting assays. Spectroscopic analysis confirmed inclusion complex formation through characteristic peak shifts and intensity changes. Electrospinning produced uniform fibers with diameters ranging from 2.04-2.75 μm and drug loadings up to 8.56% (w/w). Higher drug loadings resulted in decreased complexed drug fractions (74% at 2.5% loading vs. 23% at 10% loading). In vitro release profiles showed sustained drug release over 168 h with minimal burst effect (<2%), achieving 19-35% cumulative release. Ex vivo transscleral permeation studies demonstrated 0.35-0.5% drug penetration within 24 h, compared to undetectable levels for free fenofibrate. All formulations-maintained cell viability above 85%, with minimal irritation observed in HET-CAM assays. Anti-angiogenic studies revealed significant dose-dependent activity: wound closure decreased from 45.13% (control) to 8.12% (10% w/w), Fibrin bead sprouting was reduced by approximately 44% in length (276 ± 140 µm vs 493 ± 142 µm for media only) and 49% in number (3.4 ± 1.6 vs 6.6 ± 2.6 for media only) for the 10% w/w formulation. The polymer-free HPβCD electrospinning approach successfully addresses fenofibrate's solubility limitations while providing sustained drug release and preserved biological activity. The excellent biocompatibility profile and significant anti-angiogenic efficacy demonstrate the potential for clinical translation in treating ocular neovascular diseases.

PubMedMedicine2026-08-22

Fenofibrate-associated rhabdomyolysis complicated by dialysis-requiring acute kidney injury presenting with atypical clinical manifestations: A case report and literature review.

Fang Yumei Y, Jiang Yan Y

Rhabdomyolysis (RM) may cause acute kidney injury (AKI), but the classic triad of myalgia, muscle weakness, and dark-colored urine is often absent. Fenofibrate-associated RM is rare and may be overlooked in older patients with chronic kidney disease (CKD), reduced renal reserve, or polypharmacy. A 70-year-old man with CKD was admitted with nausea, poor appetite, and a marked increase in serum creatinine for 1 week. Two months earlier, atorvastatin had been discontinued, and micronized fenofibrate had been started for hypertriglyceridemia. He had no obvious myalgia, muscle weakness, or dark-colored urine. Serum creatinine rapidly increased from approximately 130 μmol/L to 1132-1202 μmol/L. Peak creatine kinase (CK) was 28,831 U/L, and serum myoglobin was 915 ng/mL, accompanied by metabolic acidosis, hypocalcemia, and hyperphosphatemia. Based on the temporal association with fenofibrate exposure, marked muscle enzyme elevation, improvement after drug withdrawal, and absence of common alternative triggers, the patient was diagnosed with probable fenofibrate-associated rhabdomyolysis complicated by KDIGO stage 3 AKI superimposed on underlying CKD. Fenofibrate was discontinued immediately. The patient received fluid therapy, correction of metabolic acidosis, electrolyte monitoring and management, and supportive kidney care. Because he initially refused dialysis, intermittent hemodialysis (IHD) was initiated on hospital day 10 for persistent uremic symptoms, severe AKI, and metabolic derangements. Net ultrafiltration was set at 0 mL to avoid further volume depletion. After IHD and supportive treatment, gastrointestinal symptoms improved, urine output increased, and CK and renal function gradually improved. Dialysis frequency was reduced after discharge, and IHD was discontinued 5 weeks later. At 8 months after discharge, serum creatinine had decreased to 157 μmol/L, and CK and myoglobin remained normal. In older patients with CKD, eGFR should be calculated before fenofibrate is prescribed, and dosing should follow the product label. Unexplained renal deterioration or nonspecific symptoms after fenofibrate exposure should prompt measurement of CK and myoglobin. Immediate drug withdrawal and supportive treatment are essential, whereas IHD should be reserved for standard AKI indications.

PubMedThe British journal of ophthalmology2026-08-21

Association of fenofibrate use with progression of ocular disease in individuals with diabetes.

Oliver Courtney C, Berkenstock Meghan K MK, Sachdeva Mira M MM

Fenofibrates may slow progression of diabetic retinopathy (DR). This study used the large international TriNetX database to evaluate progression of retinopathy and development of cataracts, primary open angle glaucoma (POAG) and diabetic macular oedema (DME) in patients with diabetes with and without fenofibrate use. In this retrospective cohort study, ICD10 codes and RxNorm were used to identify patients in the TriNetX database aged ≥18 years with a diagnosis of diabetes mellitus (DM), with mild or moderate non-proliferative diabetic retinopathy (NPDR) and with and without fenofibrate use from December 2014 through December 2024. ORs were calculated to analyse the proportion of individuals with mild or moderate NPDR using fenofibrate who developed vision-threatening DR (VTDR, defined as severe NPDR or proliferative DR), cataracts, POAG or DME compared with those not taking fenofibrate. Those with cataracts, POAG or DME at baseline were excluded from their respective outcomes analyses. After propensity score matching, 4316, 4200, 4073 and 4571 individuals prescribed fenofibrate were compared with the same number who were not prescribed fenofibrate for progression to VTDR, cataract, POAG or DME, respectively. The ORs for DR progression (OR 0.528, 95% CI 0.333 to 0.838; p=0.0059), cataract (OR 0.585, 95% CI 0.441 to 0.774; p=0.0002) and DME (OR 0.316, 95% CI 0.243 to 0.411; p<0.0001) development were lower for individuals taking fenofibrate compared with those not taking fenofibrate. Fenofibrate use is associated with significantly lower risk of developing VTDR, cataracts and DME in patients with mild or moderate NPDR.

PubMedReproductive biology2026-08-21

Corrigendum to: "Effect of ginger extract and/or fenofibrate on the associated infertility of experimentally induced obese Wistar Albino male rats" [Reprod Biol 26 (2): 101208].

Elsayed Mohamed H MH, Abd El-Rheem Samia M SM, Almadaly Essam A EA, Elkattawy Azza M AM et al.

PubMedGut2026-08-21

Activation of the KPNA2-mediated nuclear import of PPARα by KIF13B mitigates alcohol-associated liver steatosis.

Lu Kaikai K, Mei Si S, Zhang Lianxin L, Lian Li-You LY et al.

Alcohol-associated liver disease (ALD) is a major global health burden with no approved targeted therapies. Emerging evidence implicates kinesin family member 13B (KIF13B) in lipid metabolism, primarily in cardiovascular disease but its role in ALD remains unexplored. To investigate the role and underlying mechanism of KIF13B in ALD pathogenesis and evaluate its therapeutic potential. ALD was modelled in global and hepatocyte-specific Kif13b knockout mice using the modified chronic-plus-binge ethanol-feeding model (the NIAAA model). Human liver tissues from patients with ALD were analysed for clinical relevance. In vitro studies employed primary mouse hepatocytes and HepG2 cells treated with ethanol and palmitic acid. Hepatic KIF13B expression was markedly reduced in both ethanol-fed mice and patients with ALD. KIF13B deficiency exacerbated ethanol-induced steatosis by impairing peroxisome proliferator-activated receptor alpha (PPARα) nuclear translocation without affecting its total expression. Mechanistically, KIF13B directly bound and stabilised karyopherin subunit alpha 2 (KPNA2), a critical nuclear import factor, thereby facilitating PPARα nuclear localisation and transcriptional activation of fatty acid oxidation genes. While the PPARα agonist fenofibrate effectively alleviated steatosis in wild-type mice, its efficacy was blunted in Kif13b-deficient mice. Conversely, the KPNA2-targeting compound foslinanib restored PPARα nuclear transport and ameliorated steatosis in Kif13b-deficient settings. Notably, combined treatment with fenofibrate and the KPNA2-targeting compound foslinanib exerted a more pronounced therapeutic effect in ameliorating hepatic steatosis. This study identifies KIF13B as a novel regulator of hepatic lipid homeostasis in ALD via the KIF13B-KPNA2-PPARα axis, enhancing KPNA2 mediated nuclear import, particularly in combination with PPARα activation, represents a promising therapeutic strategy for ALD.

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