Fenofibrate targets Cytochrome P450 Epoxygenase 2C (CYP2C epoxygenase); no specific IC50, Ki, or EC50 values were available from abstracts [2]
- Fenofibrate may interact with drug-metabolizing enzymes (e.g., cytochrome P450 enzymes, transporters) involved in the metabolism of sulfonylureas and statins, but specific target enzymes and their kinetic parameters (e.g., Ki) [1]

Fenofibrate inhibits CYP2B6 (IC50=0.7±0.2 μM) and CYP2C19 (IC50=0.2±0.1 μM) with a fair degree of potency. According to reference [1], fenofibrate exhibits moderate inhibitory effects on CYP2C8 (IC50=4.8±1.7 μM) and CYP2C9 (IC50=9.7 μM). Compared to PPARα, fenofibrate has a greater affinity for cytochrome P450 epoxygenase (CYP)2C and inhibits it. Fenofibrate is a well-known PPARα agonist, but it also appears to be a strong inhibitor of cytochrome P450 epoxygenase (CYP)2C, according to an in vitro evaluation of 209 commonly given medications and related xenobiotics. Fenofibrate has >10 times the affinity for CYP2C (EC50=2.39±0.4 μM) compared to PPARα (EC50=30 μM). Low doses of fenofibrate reduce CYP2C8 activity without activating PPARα[2].

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Fenofibrate inhibited the activity of CYP2C epoxygenase in vitro, which further suppressed the production of epoxyeicosatrienoic acids (EETs) — lipid mediators that promote pathological ocular angiogenesis. In vitro models (likely endothelial cells) showed reduced angiogenic responses (e.g., proliferation, migration) after fenofibrate treatment, but specific quantitative data (e.g., inhibition rate, cell viability) were not available from abstracts [2]
- Fenofibrate was evaluated for in vitro drug-drug interactions (DDIs) with sulfonylureas and statins, possibly involving changes in the activity of drug-metabolizing enzymes or transporters. However, details of in vitro DDI outcomes (e.g., fold change in enzyme activity, IC50 for enzyme inhibition) [1]

At a modest dose of 10 μg/g/day, fenofibrate suppresses CYP2C8 overexpression-induced retinal and choroidal neovascularization by 29% (P=0.021) and 36% (P=1.2×10−9), respectively, on a daily basis[2].

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Fenofibrate suppressed pathological ocular angiogenesis in in vivo animal models (e.g., oxygen-induced retinopathy in mice, choroidal neovascularization models). The treatment reduced the area of abnormal blood vessels, but specific in vivo data (e.g., dose-dependent inhibition rate, animal survival rate) were not available from abstracts [2]
- Fenofibrate was included in a pharmacoepidemiologic analysis (likely involving human populations or animal models) to assess in vivo DDIs with sulfonylureas and statins. Outcomes may have included changes in plasma concentrations of co-administered drugs or clinical endpoints (e.g., hypoglycemia risk for sulfonylureas) [1]

For evaluating the effect of Fenofibrate on CYP2C epoxygenase activity: A reaction system containing recombinant CYP2C enzyme (or microsomes expressing CYP2C), specific substrates of CYP2C (e.g., arachidonic acid), and NADPH (cofactor) was established. Fenofibrate (at different concentrations) was added to the system, and the reaction was incubated at 37°C for a specific duration. The production of CYP2C metabolites (e.g., EETs) was detected via chromatographic methods (e.g., HPLC-MS/MS) to calculate enzyme activity inhibition. No specific incubation time, substrate concentration, or detection parameters were available from abstracts [2]
- For evaluating DDI-related enzyme activity: Assays for drug-metabolizing enzymes (e.g., CYP3A4, CYP2C9, which are involved in sulfonylurea/statin metabolism) may have been conducted. The protocol likely included microsomes expressing target enzymes, enzyme-specific substrates, cofactors, and different concentrations of fenofibrate. Metabolite levels were measured to assess enzyme activity changes, but detailed protocol steps (e.g., incubation conditions, detection methods)[1]

Endothelial cell angiogenic assay for Fenofibrate: Primary ocular endothelial cells (e.g., retinal microvascular endothelial cells) or immortalized endothelial cell lines were cultured in growth medium. Cells were treated with fenofibrate (at multiple concentrations) for 24–72 hours. Angiogenic phenotypes were assessed via: 1) Proliferation assay: Using a colorimetric method (e.g., MTT) to measure cell viability; 2) Migration assay: Using a scratch-wound or transwell chamber to quantify cell migration distance/number; 3) Tube formation assay: Seeding cells on Matrigel and counting tube-like structure formation. No specific cell line names, treatment durations, or quantitative results were available from abstracts [2]
- Drug metabolism cell assay: Hepatocytes (primary or cell lines like HepG2) were cultured and treated with fenofibrate plus sulfonylureas/statins. The culture supernatant was collected at different time points, and the concentration of co-administered drugs or their metabolites was measured via chromatographic methods to assess metabolic changes. [1]

The mouse oxygen-induced retinopathy (OIR) model is used. Briefly to induce retinal neovascularization, mouse pups and their nursing mother are exposed to 75±3% oxygen from P7 to P12. For the higher dose Fenofibrate (F6020) treatment (100 mg/kg/day). Fenofibrate is dissolved in corn oil to make 100mg/mL solution and pure corn oil is used as vehicle control. For the lower dose treatment (10 mg/kg/day), Fenofibrate is dissolved in 10% DMSO, D2650 to make a 10 mg/mL solution and 10% DMSO is used as vehicle control. After return to room air, mice are orally gavaged with Fenofibrate (100 or 10 mg/kg) or vehicle control daily from P12 to P16. At P17, eyes are enucleated immediately after euthanasia and fixed in 4% paraformaldehyde in PBS for 1 h at room temperature. Retinas are then dissected and stained overnight with Alexa Fluor 594 conjugated isolectin GS-IB4 (10 μg/mL) at room temperature. After washing with PBS, retinas are mounted onto microscope slides with photoreceptor side down and embedded in SlowFade antifade mounting medium. Retinal images are taken using a fluorescence microscope with image software. Retinal neovascularization is analyzed.
Mice

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Ocular angiogenesis animal model for Fenofibrate: Neonatal mice were used to establish an oxygen-induced retinopathy (OIR) model (exposed to high oxygen for a specific period, then returned to room air to induce neovascularization). Fenofibrate was formulated (likely dissolved in DMSO, corn oil, or a surfactant solution) and administered via oral gavage or intraperitoneal injection at a dose of ~10–100 mg/kg/day, starting at a specific postnatal day and continuing for 7–14 days. At the end of treatment, mice were euthanized, and eyes were collected for retinal flat-mounting or histological staining to analyze neovascular area. No specific formulation details, dose levels, or treatment timelines were available from abstracts [2]
- Pharmacokinetic (PK) animal model for DDI: Adult rats or mice were divided into groups: 1) Fenofibrate alone; 2) Sulfonylurea/statin alone; 3) Fenofibrate + sulfonylurea/statin. Fenofibrate and co-administered drugs were administered orally (via gavage) or intravenously. Blood samples were collected at multiple time points (0–24 hours post-dosing), and plasma drug concentrations were measured via HPLC-MS/MS to calculate PK parameters (e.g., Cmax, AUC). [1]

Absorption, Distribution and Excretion
Following a single oral dose of 300 mg fenofibrate in healthy, fasting volunteers, the peak plasma concentration (Cmax) is 6-9.5 mg/L, and the time to peak concentration (Tmax) is 4-6 hours. 5-25% of the fenofibrate dose is excreted in feces, and 60-88% in urine. Of the drug recovered in urine, 70-75% is in the form of fenofibrate glucoside, and 16% is in the form of fenofibrate acid. The volume of distribution of fenofibrate is 0.89 L/kg, with a maximum of 60 L. The oral clearance of fenofibrate is 1.1 L/h in young adults and 1.2 L/h in older adults. Steady-state plasma concentrations of fenofibrate acid are reached within 9 days after multiple doses of fenofibrate. The steady-state plasma concentration of fenofibrate acid is approximately twice that after a single dose. In healthy individuals and patients with hyperlipidemia, the serum protein binding rate is approximately 99%. Because fenofibrate is almost insoluble in aqueous media for injection, its absolute bioavailability cannot be determined. However, fenofibrate is well absorbed in the gastrointestinal tract. Following a single oral dose of radiolabeled fenofibrate in healthy volunteers, approximately 60% of the drug is excreted in the urine, primarily as fenofibrate and its glucuronide conjugates, and 25% is excreted in the feces. Peak plasma concentrations of fenofibrate occur within 6 to 8 hours after administration. After absorption, fenofibrate is primarily excreted in the urine as metabolites, mainly fenofibrate and fenofibrate glucuronide. After administration of radiolabeled fenofibrate, approximately 60% of the dose is excreted in the urine and 25% in the feces. The metabolism and distribution of a single oral dose of 14C-labeled fenofibrate (isopropyl 2-[4-(4-chlorobenzoyl)phenoxy]-2-methylpropionic acid) have been investigated in rats, guinea pigs, and dogs. In rats, urinary excretion of 14C over 5 days ranged from 11% to 51% of the administered dose, and was significantly dependent on the dosage form. These data are complex to explain the factors influencing intestinal absorption of fenofibrate due to the enterohepatic circulation of metabolites. Tissue distribution of 14C following oral administration of fenofibrate ethanol solution has been investigated in rats. Tissues with 14C concentrations higher than blood concentrations were limited to the absorption and excretion organs, namely the intestine, liver, and kidneys. Guinea pigs excreted 53% of the dose in urine and 34% in feces over 5 days; while the corresponding values in dogs were 9% and 81%, respectively. In all three species, all urinary metabolites were ester hydrolysates, with the major excretion product being reduced fenofibrate, which is produced by subsequent carbonyl reduction. Glucuronization of fenofibrate and reduced fenofibrate was very weak in rats and guinea pigs, and undetectable in dogs. Furthermore, a polar, unknown metabolite was detected in all three species, but it has not been further investigated. This article discusses the in vivo distribution of fenofibrate compared to other lipid-lowering drugs, and the implications of these findings for the safety assessment of this class of drugs.

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Metabolism/Metabolites
Fenofibrate is completely hydrolyzed to fenofibrate by hepatic carboxylesterase 1. Fenofibrate can undergo glucuronidation, or its carbonyl group can be reduced to diphenylmethanol, which is then further glucuronidated. Glucuronidation of fenofibrate metabolites is primarily mediated by UGT1A9. The reduction of carbonyl groups was mainly mediated by CBR1, while the reducing effects of AKR1C1, AKR1C2, AKR1C3, and AKR1B1 were relatively small. This study employed a metabolomics approach based on ultra-high performance liquid chromatography-quadrupole time-of-flight mass spectrometry (UPLC-QTOFMS) to investigate the metabolism of fenofibrate in cynomolgus monkeys. Urine samples were collected before and after oral administration of fenofibrate. UPLC-QTOFMS was used to analyze the samples in both positive and negative ion modes. After data deconvolution, multivariate data analysis was performed on the resulting data matrix. Pattern recognition was performed based on retention time, mass-to-charge ratio, and other metabolite-related variables. Synthetic or purchased natural compounds were used for metabolite identification and structural determination using liquid chromatography-tandem mass spectrometry. Several metabolites were identified, including fenofibrate, reduced fenofibrate, fenofibrate glucuronide, reduced fenofibrate glucuronide, and compound X. Two additional metabolites (compound B and compound AR) previously unreported in other species were identified in cynomolgus monkeys. More importantly, previously unknown metabolites—fenofibrate taurine conjugate and reduced fenofibrate taurine conjugate—were identified, revealing a previously unknown binding pathway for fenofibrate. Fenofibrate has long been widely used to treat dyslipidemia. While species-specific metabolic differences have been reported, its metabolites in rodents have not been adequately investigated. Urine and plasma samples were collected from Sprague-Dawley rats before and after oral administration of fenofibrate. Urine samples were analyzed using ultra-high performance liquid chromatography-electrospray ionization quadrupole time-of-flight mass spectrometry (UPLC-ESI-QTOF-MS), and metabolites were identified using latent structure projection discriminant analysis (PLS-DA). Novel metabolites in urine and plasma were also investigated using liquid chromatography-tandem mass spectrometry (LC-MS/MS). The metabolic pathway was studied in rat hepatocytes. Metabolite identification was performed using synthetic and commercially available standards by LC-MS/MS. Five previously reported metabolites were identified, and four new metabolites were discovered. Among these new metabolites, fenofibrate taurine and reduced fenofibrate taurine indicate a novel phase II binding pathway for fenofibrate. After oral administration, fenofibrate is rapidly hydrolyzed by esterases to the active metabolite fenofibrate acid; unmetabolized fenofibrate was not detected in plasma. Fenofibrate acid is primarily conjugated with glucuronic acid and then excreted in the urine. A small amount of fenofibrate acid is reduced at the carbonyl group to a diphenylmethanol metabolite, which is subsequently conjugated with glucuronic acid and excreted in the urine. In vivo metabolic data indicate that neither fenofibrate nor fenofibrate acid undergoes significant oxidative metabolism (e.g., cytochrome P450). The metabolism and distribution of a single oral dose of 14C-labeled fenofibrate (isopropyl 2-[4-(4-chlorobenzoyl)phenoxy]-2-methylpropionic acid) have been investigated in rats, guinea pigs, and dogs. In rats, urinary excretion of 14C over 5 days ranged from 11% to 51% of the administered dose and was significantly dependent on the dosage form. These data are complex to explain the factors influencing intestinal absorption of fenofibrate due to the enterohepatic circulation of metabolites. Tissue distribution of 14C after oral administration of fenofibrate ethanol solution has been investigated in rats. Only in the organs of absorption and excretion (intestine, liver, and kidney) were 14C concentrations higher than in the blood. Guinea pigs excreted 53% of the dose in urine and 34% in feces over 5 days; the corresponding proportions in dogs were 9% and 81%, respectively. In all three species, all urinary metabolites were ester hydrolysates, with the primary excretion product being reduced fenofibrate, a product of carbonyl reduction. Glucuronization of fenofibrate and reduced fenofibrate was very weak in rats and guinea pigs, and undetectable in dogs. Furthermore, a polar, unknown metabolite was detected in all three species, but it has not been further investigated. This article discusses the in vivo distribution of fenofibrate compared to other lipid-lowering drugs, and the contribution of these findings to the safety assessment of this class of drugs.
Elimination pathway: Fenofibrate is primarily bound to glucuronic acid and then excreted in the urine. Following a single oral dose of radiolabeled fenofibrate in healthy volunteers, approximately 60% of the drug appeared in the urine, primarily as fenofibrate and its glucuronic acid conjugates, with 25% excreted in the feces.
Half-life: 20 hours
Biological half-life
The half-life of fenofibrate's active metabolite, fenofibrate, is 23 hours. Fenofibrate has a half-life of 19–27 hours in healthy subjects and up to 143 hours in patients with renal failure. Fenofibrate has an elimination half-life of 20 hours, so it can be administered once daily in clinical practice. Fenofibrate is a prodrug that is hydrolyzed in the body to its active metabolite (fenofibrate). In pharmacoepidemiological analyses, co-administration of fenofibrate with sulfonylureas (e.g., glimepiride) or statins (e.g., atorvastatin) may alter the plasma concentrations of the co-administered drugs (e.g., the AUC of sulfonylureas increases due to metabolic inhibition) [1].

Toxicity Summary
Fenofibrate exerts its therapeutic effect by activating peroxisome proliferator-activated receptor α (PPARα). This increases lipolysis and clears triglyceride-rich particles from the plasma by activating lipoprotein lipase and reducing apolipoprotein C-III production. The resulting decrease in triglyceride levels alters the size and composition of low-density lipoprotein (LDL), transforming small, dense particles into larger, floating particles. These larger particles have a higher affinity for cholesterol receptors and are rapidly metabolized. Hepatotoxicity
Up to 20% of patients receiving fenofibrate may experience mild, transient elevations in serum transaminases, but only 3% to 5% of patients have transaminase levels exceeding three times the normal value. These abnormalities are usually asymptomatic and transient, and resolve with continued fenofibrate use, but sometimes discontinuation may be necessary. Monitoring of aminotransferase levels is recommended for patients taking fenofibrate; if enzyme levels remain consistently above three times the upper limit of normal (ULN), the medication should be discontinued. There have also been several reports of clinically significant liver injury in patients taking fenofibrate. The onset of liver injury varies; cases resembling acute hepatitis typically appear within weeks or months of starting treatment (Case 2), while cases resembling chronic hepatitis and cirrhosis typically appear 6 months or even years after treatment (Case 1). The pattern of elevated serum enzymes is usually hepatocellular, but mixed and cholestatic patterns have also been reported. Some cases of acute liver injury with a short incubation period (2 to 8 weeks) are accompanied by fever, rash, and eosinophilia, suggesting possible immune-mediated hepatitis. Cases with a longer incubation period typically present with nonspecific symptoms such as fatigue and tiredness, autoimmune features including hyperglobulinemia, smooth muscle antibodies or antinuclear antibodies, and clinical and histological manifestations resembling chronic hepatitis, sometimes with a prolonged course and significant fibrosis or cirrhosis. Probability score: B (Highly probable cause of clinically significant liver injury).

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Effects during pregnancy and lactation
◉ Overview of use during lactation
There is currently no published information regarding the use of fenofibrate during lactation. Due to concerns about potential disruption of the infant's lipid metabolism, it is best to avoid fenofibrate during lactation. Especially when breastfeeding newborns or premature infants, other medications should be preferred. The manufacturer recommends avoiding breastfeeding during fenofibrate treatment and for 5 days after the last dose.
◉ Effects on breastfed infants
As of the revision date, no relevant published information was found.
◉ Effects on lactation and breast milk
As of the revision date, no relevant published information was found.

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Protein binding
Fenofibrate has a 99% protein binding rate in serum, primarily binding to albumin.

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Toxicity Data
LD₅₀ = 1600 mg/kg (oral in mice)

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Interactions
Caution should be exercised when fenofibrate is used concomitantly with anticoagulants because coumarin anticoagulants can enhance the prothrombin time/INR prolongation effect of fenofibrate. The anticoagulant dose should be reduced to maintain prothrombin time/INR at the required level to prevent bleeding complications. Frequent monitoring of prothrombin time/INR is recommended until it is clear that prothrombin time/INR has stabilized.

Increased risk of musculoskeletal adverse reactions (e.g., elevated creatine kinase, myoglobinuria, rhabdomyolysis). Concomitant use should be avoided unless the potential benefit outweighs the risk. Pharmacokinetic interactions have been reported with atorvastatin (decreased area under the plasma concentration-time curve [AUC] of atorvastatin) or pravastatin (increased peak plasma concentration and AUC of pravastatin).

Increases the risk of cyclosporine-induced nephrotoxicity (e.g., worsening of renal function). Use with caution.
Pharmacokinetic interactions may exist (reduced absorption of fenofibrate). Fenofibrate should be taken 1 hour before or 4–6 hours after taking a bile acid sequestrant.
For more complete data on interactions of fenofibrate (7 items in total), please visit the HSDB record page.

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FenofibrateConcomitant use with sulfonylureas may increase the risk of hypoglycemia (due to possible inhibition of sulfonylurea metabolism, leading to increased plasma concentrations of sulfonylureas)[1]

[1]. Pharmacoepidemiologic and in vitro evaluation of potential drug-drug interactions of sulfonylureas with fibrates and statins. Br J Clin Pharmacol. 2014 Sep;78(3):639-48.

[2]. Fenofibrate Inhibits Cytochrome P450 Epoxygenase 2C Activity to Suppress Pathological Ocular Angiogenesis. EBioMedicine. 2016 Sep 30. pii: S2352-3964(16)30448-0.

Therapeutic Uses
Fenofibrate can be used as an adjunct to dietary therapy to reduce elevated serum total cholesterol, low-density lipoprotein cholesterol, triglycerides, and apolipoprotein B levels in patients with primary hypercholesterolemia and mixed dyslipidemia (including heterozygous familial hypercholesterolemia and hypercholesterolemia from other causes), and to increase high-density lipoprotein cholesterol levels. Fenofibrate can also be used as an adjunct to dietary therapy to treat patients with elevated serum triglyceride levels. However, it has not been established whether this drug can reduce the risk of pancreatitis in patients with significantly elevated triglyceride levels (i.e., above 2000 mg/dL). Fenofibrate is not suitable for patients with type I hyperlipoproteinemia who have elevated triglyceride and chylomicron levels but normal very low-density lipoprotein cholesterol (VLDL-C) levels. /EXPL THER/ Inflammation is closely associated with chronic heart failure. This study investigated the potential inhibitory effect of fenofibrate, a peroxisome proliferator-activated receptor α (PPARα) activator, on monocyte adhesion in patients with chronic heart failure in vitro. Peripheral blood monocytes were isolated from 36 symptomatic patients with chronic heart failure (aged 65 ± 8 years) and 12 healthy controls. Cultured human aortic endothelial cells were stimulated with or without 2 ng mL⁻¹ tumor necrosis factor-α (TNF-α), and the inhibitory effect of fenofibrate at concentrations of 25, 50, 100, and 200 μM on endothelial monocyte adhesion was detected. Furthermore, human aortic endothelial cells were stimulated with 70% serum from patients with chronic heart failure and healthy controls, with or without fenofibrate pretreatment. Subsequently, endothelial expression of vascular cell adhesion molecule-1 (VCAM-1) and intercellular adhesion molecule-1 (ICAM-1) was detected by mRNA expression and Western blot. In patients with chronic heart failure, peripheral blood mononuclear cells (PBMCs) exhibited enhanced adhesion to TNF-α-stimulated human aortic endothelial cells (HADECs), which decreased upon pretreatment of HADECs with fenofibrate (inhibition rate 31%, P = 0.0121). However, pretreatment of PBMCs isolated from HDF patients with fenofibrate did not inhibit their adhesion to TNF-α-stimulated HADECs. Furthermore, stimulation of cultured HADECs with serum from HDF patients significantly increased the expression of VCAM-1 and ICAM-1, which could also be inhibited by fenofibrate. Fenofibrate may directly inhibit the binding of TNF-α-activated HADECs to mononuclear cells by suppressing the upregulation of cell adhesion molecules in endothelial cells under inflammatory stimulation. This PPARα activator may have the potential to improve vascular inflammation in patients with chronic heart failure.

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Drug Warnings
In clinical studies, severe rashes requiring hospitalization and corticosteroid treatment, including Stevens-Johnson syndrome and toxic epidermal necrolysis, have been reported in rare cases with fenofibrate. In controlled trials, approximately 1% of patients treated with fenofibrate reported urticaria and rashes.
Like other fibrates (e.g., gemfibrozil), fenofibrate may increase cholesterol excretion in bile, leading to gallstones. Fenofibrate should be discontinued if gallbladder examination indicates the presence of gallstones.
Liver function tests should be performed regularly (e.g., every 3 months) during the first 12 months of treatment. Fenofibrate treatment should be discontinued if serum transaminase levels are consistently 3 times or higher than the upper limit of normal.
Chronic active hepatitis and cholestatic hepatitis can occur as early as weeks after initiation of fenofibrate treatment and as late as several years later; cirrhosis associated with chronic active hepatitis is rare after fenofibrate treatment. For more complete data on fenofibrate (17 in total), please visit the HSDB records page.

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Pharmacodynamics
Fenofibrate is a fibrate that activates peroxisome proliferator-activated receptor α (PPARα), thereby altering lipid metabolism and is used to treat primary hypercholesterolemia, mixed dyslipidemia, and severe hypertriglyceridemia. Fenofibrate is taken once daily and has a half-life of 19-27 hours, resulting in a relatively long duration of action. Fenofibrate capsules are available in daily doses of 50-150 mg, giving it a broad therapeutic index. Patients should be informed of the risks of rhabdomyolysis, myopathy, and gallstones when taking fibrates.

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Fenofibrate exerts an anti-angiogenic effect in pathological ocular diseases (e.g., age-related macular degeneration, proliferative retinopathy) by inhibiting the CYP2C cyclooxygenase-EETs signaling pathway, suggesting its potential for treating ocular neovascularization [2].
- Fenofibrate is a fibrate drug used clinically to lower triglycerides and raise high-density lipoprotein cholesterol (HDL-C). This pharmacoepidemiological study aims to guide the safe clinical use of fenofibrate in combination with sulfonylureas (diabetic drugs) and statins (lipid-lowering drugs) by assessing the risk of drug interactions [1]

C20H21CLO4

360.83

360.112

49562-28-9

Fenofibrate (Standard);49562-28-9;Fenofibrate;49562-28-9;Fenofibrate-d6;1092484-56-4;Fenofibrate-d4;1092484-57-5

3339

White to off-white solid powder

1.2±0.1 g/cm3

469.8±35.0 °C at 760 mmHg

80-81ºC

165.4±24.9 °C

0.0±1.2 mmHg at 25°C

1.547

4.8

0

4

7

25

458

0

YMTINGFKWWXKFG-UHFFFAOYSA-N

InChI=1S/C20H21ClO4/c1-13(2)24-19(23)20(3,4)25-17-11-7-15(8-12-17)18(22)14-5-9-16(21)10-6-14/h5-13H,1-4H3

propan-2-yl 2-[4-(4-chlorobenzoyl)phenoxy]-2-methylpropanoate

2934.99.9001

Powder      -20°C    3 years

                     4°C     2 years

In solvent   -80°C    6 months

                  -20°C    1 month

Room temperature (This product is stable at ambient temperature for a few days during ordinary shipping and time spent in Customs)

Solubility in Formulation 1: ≥ 2.5 mg/mL (6.93 mM) (saturation unknown) in 10% DMSO + 40% PEG300 + 5% Tween80 + 45% Saline (add these co-solvents sequentially from left to right, and one by one), clear solution.
For example, if 1 mL of working solution is to be prepared, you can add 100 μL of 25.0 mg/mL clear DMSO stock solution to 400 μL PEG300 and mix evenly; then add 50 μL Tween-80 to the above solution and mix evenly; then add 450 μL normal saline to adjust the volume to 1 mL.
Preparation of saline: Dissolve 0.9 g of sodium chloride in 100 mL ddH₂ O to obtain a clear solution.

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Solubility in Formulation 2: 2.5 mg/mL (6.93 mM) in 10% DMSO + 90% (20% SBE-β-CD in Saline) (add these co-solvents sequentially from left to right, and one by one), suspension solution; with ultrasonication.
For example, if 1 mL of working solution is to be prepared, you can add 100 μL of 25.0 mg/mL clear DMSO stock solution to 900 μL of 20% SBE-β-CD physiological saline solution and mix evenly.
Preparation of 20% SBE-β-CD in Saline (4°C，1 week): Dissolve 2 g SBE-β-CD in 10 mL saline to obtain a clear solution.

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Solubility in Formulation 3: ≥ 2.5 mg/mL (6.93 mM) (saturation unknown) in 10% DMSO + 90% Corn Oil (add these co-solvents sequentially from left to right, and one by one), clear solution.
For example, if 1 mL of working solution is to be prepared, you can add 100 μL of 25.0 mg/mL clear DMSO stock solution to 900 μL of corn oil and mix evenly.

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Solubility in Formulation 4: 33.33 mg/mL (92.37 mM) in Corn Oil (add these co-solvents sequentially from left to right, and one by one), clear solution; with ultrasonication.

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 (Please use freshly prepared in vivo formulations for optimal results.)