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HCID 3339Erstellt: 31. Oktober 2026

Fenofibrat

Fenobrate · FINOFIBRATE · sedufen · Fenoglide · propan-2-yl 2-[4-(4-chlorobenzoyl)phenoxy]-2-methyl-propanoate · lf-178 · lipsin · Lipirex

https://huagongshe.com/de/chemical/3339

Molekülstruktur von Fenofibrat

Identifikatoren & physikalische Daten

CAS No.49562-28-9
SummenformelC20H21ClO4
Durchschnittliche Molmasse360,8 g/mol
Monoisotopische Masse360,1128368 g/mol
SMILESCC(C)OC(=O)C(C)(C)Oc1ccc(C(=O)c2ccc(Cl)cc2)cc1
InChIKeyYMTINGFKWWXKFG-UHFFFAOYSA-N
PubChem CID3339
ChEMBLCHEMBL672
ChEBICHEBI:5001
EC No.256-376-3
DTXSIDDTXSID2029874
Lokaler NameFenofibrat

Chemische & physikalische Eigenschaften

XLogP5,2
Polarare Oberfläche (TPSA)52,6
H-Brücken-Donoren0
H-Brücken-Akzeptoren4
Frei drehbare Bindungen7
Schwere Atome25
Formalladung0
Komplexität458
StoffklassenPharmaceutical
ArzneimittelPharmaceuticals -> Used in Switzerland
LogP (Verteilungskoeffizient)5.35.1
Color/FormCrystals from isopropanolWhite solid
LöslichkeitPractically insoluble in waterslightly soluble in methanol, ethanolsoluble in acetone, ether, benzene, chloroform7.07e-04 g/LPractically insoluble in water, very soluble in methylene chloride, slightly soluble in ethanol (96 per cent)0.8mg/L(25 ºC)
Human DrugsBreast FeedingLactationMilk, HumanAnticholesteremic AgentsHypolipidemic AgentsFibric AcidsFDA approved drugs -> Active ingredient
Schmelzpunkt79-8280-81 °C80.5 °C80-810C
Physical DescriptionSolid
Collision Cross Section192.8 Ų [M+H]+ [CCS Type: DTBuffer gas: N2Ionization: ESI+Dataset: TOXCASTSource Identifier: DTXSID2029874]172.51 Ų [M+Na]+ [CCS Type: TWMethod: calibrated with polyalanine and drug standards]190.5 Ų [M+H]+ [CCS Type: TW
Other Experimental PropertiesStable under ordinary conditions
Siedepunkt469.8±35.0 °C(Predicted)
Dichte1.177±0.06 g/cm3(Predicted)
Lagerbedingungenroom temp
Aggregatzustandpowder
Farbeoff-white
Merck14,3978
Henry-Konstante2.2×103 mol/(m3Pa) at 25℃, HSDB (2015)
BCS Class2
Hauptanwendungenforensics and toxicologypharmaceutical (small molecule)
InChIInChI=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
InChIKeyYMTINGFKWWXKFG-UHFFFAOYSA-N
SMILESC(OC(C)C)(=O)C(OC1=CC=C(C(=O)C2=CC=C(Cl)C=C2)C=C1)(C)C
EPA chemische InformationenPropanoic acid, 2-[4-(4-chlorobenzoyl)phenoxy]-2-methyl-, 1-methylethyl ester (49562-28-9)

Sicherheit & Vorschriften

GHS-EinstufungThis chemical does not meet GHS hazard criteria for 1.3% (2 of 159) of reports.WarningH373 (85.5%): May causes damage to organs through prolonged or repeated exposure [Warning Specific target organ toxicity, repeated exposure]P260, P273, P319, and P501 (click each P-code to see the statement)Aggregated GHS information provided per 159 reports by companies from 17 notifications to the ECHA C&L Inventory. Each notification may be associated with multiple companies.
Regulatorische InformationenREACH registered substance: Fenofibrate (EC: 256-376-3)
Weitere SicherheitsinformationenIMAP assessments - Propanoic acid, 2-[4-(4-chlorobenzoyl)phenoxy]-2-methyl-, 1-methylethyl ester: Environment tier I assessment
FDA-AnforderungenThe Approved Drug Products with Therapeutic Equivalence Evaluations List identifies currently marketed prescription drug products, incl fenofibrate, approved on the basis of safety and effectiveness by FDA under sections 505 of the Federal Food, Drug, and Cosmetic Act.
Hazard Classes and CategoriesSTOT RE 2 (85.5%)
LagerbedingungenStore at 25 °C (77 °F)excursions permitted to 15-30 °C (59-86 °F). ... Protect from moisture.
EntsorgungsverfahrenSRP: At the time of review, criteria for land treatment or burial (sanitary landfill) disposal practices are subject to significant revision. Prior to implementing land disposal of waste residue (including waste sludge), consult with environmental regulatory agencies for guidance on acceptable disposal practices.
WechselwirkungenCaution should be exercised when anticoagulants are given in conjunction with Tricor because of the potentiation of coumarin-type anticoagulants in prolonging the prothrombin time/INR. The dosage of the anticoagulant should be reduced to maintain the prothrombin time/INR at the desired level to prevent bleeding complications. Frequent prothrombin time/INR determinations are advisable until it has been definitely determined that the prothrombin time/INR has stabilized.Increased risk of adverse musculoskeletal effects (i.e., increased CK, myoglobinuria, rhabdomyolysis). Avoid concomitant use unless potential benefit outweighs risk. Pharmacokinetic interaction reported following concomitant use with atorvastatin (decreased area under the plasma concentration-time curve [AUC] of atorvastatin) or pravastatin (increased peak plasma concentration and AUC of pravastatin).

Anwendungen & Verwendung

Verwenden

Fenofibrate has been used:to study its effect on plasma lipids, liver phenotype and gene expressionto study its impact on endothelium-dependent vasodilatation of thoracic aortato administer to NASH knock-in mice along with a high fat diet (HFD) to study its effect

Increased risk of cyclosporine-induced nephrotoxicity (i.e., deterioration in renal function). Use with caution.
Potential pharmacokinetic interaction (decreased absorption of fenofibrate). Fenofibrate should be administered 1 hour before or 4-6 hours after a bile acid sequestrant.
For more Interactions (Complete) data for Fenofibrate (7 total), please visit the HSDB record page.
Gesundheitliche AuswirkungenInvestigated as a teratogen and reproductive hazard.
HepatotoxicityMild, transient serum aminotransferase elevations develop in up to 20% of patients receiving fenofibrate, but values above 3 times normal in only 3% to 5%. These abnormalities are usually asymptomatic and transient, resolving even with continuation of fenofibrate, but they occasionally may require drug discontinuation. Monitoring of aminotransferase levels is recommended at baseline and periodically during therapy and discontinuation if enzymes persist above 3 times the upper limit of normal (ULN) or if symptoms of liver injury arise.
UmweltverhaltenTERRESTRIAL FATE: Based on a classification scheme(1), an estimated Koc value of 3,800(SRC), determined from a structure estimation method(2), indicates that fenofibrate is expected to have slight mobility in soil(SRC). Volatilization of fenofibrate from moist soil surfaces is not expected to be an important fate process(SRC) given an estimated Henry's Law constant of 4.5X10-9 atm-cu m/mole(SRC), using a fragment constant estimation method(3). Fenofibrate is not expected to volatilize from dry soil surfaces(SRC) based upon an estimated vapor pressure of 6.2x10-7 mm Hg at 25 °C(SRC), determined from a fragment constant method(4). Fenofibrate was 64% removed during passage through a municipal sewage treatment planthowever, removal could be attributed to adsorption to sludge(5).AQUATIC FATE: Based on a classification scheme(1), an estimated Koc value of 3,800(SRC), determined from a structure estimation method(2), indicates that fenofibrate is expected to adsorb to suspended solids and sediment(SRC). Volatilization from water surfaces is not expected(3) based upon an estimated Henry's Law constant of 4.5X10-9 atm-cu m/mole(SRC), developed using a fragment constant estimation method(4). According to a classification scheme(5), an estimated BCF of 320(SRC), from an estimated log Kow of 5.2(6) and a regression-derived equation(7), suggests the potential for bioconcentration in aquatic organisms is high, provided the compound is not metabolized by the organism(SRC). Fenofibrate was 64% removed during passage through a municipal sewage treatment planthowever, removal could be attributed to adsorption to sludge(8).ATMOSPHERIC FATE: According to a model of gas/particle partitioning of semivolatile organic compounds in the atmosphere(1), fenofibrate, which has an estimated vapor pressure of 6.2X10-7 mm Hg at 25 °C(SRC), determined from a fragment constant method(2), will exist in both the vapor and particulate phases in the ambient atmosphere. Vapor-phase fenofibrate is degraded in the atmosphere by reaction with photochemically-produced hydroxyl radicals(SRC)the half-life for this reaction in air is estimated to be 15 hours(SRC), calculated from its rate constant of 2.5X10-11 cu cm/molecule-sec at 25 °C(SRC) that was derived using a structure estimation method(3). Particulate-phase fenofibrate may be removed from the air by wet or dry deposition(SRC). Fenofibrate contains chromophores that absorb at wavelengths >290 nm(4) and therefore may be susceptible to direct photolysis by sunlight(SRC).
Unerwünschte WirkungenSome of the most common adverse effects of fibrates include headaches, dizziness, back pain, joint pain, asthenia, diarrhea, nausea, constipation, dyspepsia, cough, wheezing, nasopharyngitis, and flu-like symptoms. Some potentially serious adverse effects that may require dose adjustment or discontinuation may include elevated liver enzymes, elevated creatine phosphokinase, cholelithiasis development, arrhythmia exacerbation, pulmonary embolism, pancreatitis, agranulocytosis, and myocardial infarction.
ExpositionspfadeFenofibrate is well absorbed from the gastrointestinal tract. After absorption, fenofibrate is mainly excreted in the urine in the form of metabolites, primarily fenofibric acid and fenofibric acid glucuronide
ToxizitätsübersichtThe most common toxicity associated with fenofibrate is myopathy when given with statin medicines concurrently. If rhabdomyolysis is excluded and other muscle-related diseases are suspected, the statin-associated muscle symptoms clinical index (SAMS-CI) should be evaluated to determine if muscle symptoms are due to statin therapy. Discontinuing fenofibrate, administering vitamin D replacement (for low vitamin D levels), and switching the medication are all possible options depending on the cause of myopathy.Fenofibrate exerts its therapeutic effects through activation of peroxisome proliferator activated receptor a (PPARa). This increases lipolysis and elimination of triglyceride-rich particles from plasma by activating lipoprotein lipase and reducing production of apoprotein C-III. The resulting fall in triglycerides produces an alteration in the size and composition of LDL from small, dense particles, to large buoyant particles. These larger particles have a greater affinity for cholesterol receptors and are catabolized rapidly.
Ökotoxizitätsauszüge/AQUATIC SPECIES/ Pharmaceuticals are found in the aquatic environment but their potential effects on non-target species like fish remain unknown. This in vitro study is a first approach in the toxicity assessment of human drugs on fish. Nine pharmaceuticals were tested on two fish hepatocyte models: primary cultures of rainbow trout hepatocytes (PRTH) and PLHC-1 fish cell line. Cell viability, interaction with cytochrome P450 1A (CYP1A) enzyme and oxidative stress were assessed by using 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrasodium bromide tetrazolium (MTT), 7-ethoxyresorufin-o-deethylase (EROD) and dichlorofluorescein (DCFH-DA) assays, respectively. The tested drugs were clofibrate (CF), fenofibrate (FF), carbamazepine (CBZ), fluoxetine (FX), diclofenac (DiCF), propranolol (POH), sulfamethoxazole (SFX), amoxicillin (AMX) and gadolinium chloride (GdCl3). All substances were cytotoxic, except AMX at concentration up to 500 uM. The calculated MTT EC50 values ranged from 2 uM (CF) to 651 uM (CBZ) in PLHC-1, and from 53 uM (FF) to 962 uM (GdCl3) in PRTH. CF, FF, and FX were the most cytotoxic drugs and induced oxidative stress before being cytotoxic. Compared to hepatocytes from human and dog, fish hepatocytes seemed to be more susceptible to the peroxisome proliferators (PPs) CF and FF. In PLHC-1 cells none of the tested drugs induced the EROD activity whereas POH appeared as a weak EROD inducer in PRTH. Moreover, in PRTH, SFX, DiCF, CBZ and to a lesser extend, FF and CF inhibited the basal EROD activity at clearly sublethal concentrations which may be of concern at the biological and chemical levels in a multipollution context./ENDOCRINE MODULATION/ In the last years pharmaceuticals have /increased/ interest as environmental pollutants for their toxic effects towards non target organisms. This study /draws/ attention to a further adverse effect of drugs, the endocrine interference. The most representative drugs of the widespread classes in environment were investigated. The /Yeast Estrogen System/ (YES)-test and the E-screen assay were performed to detect the capability of these substances to bind the human estrogenic receptor a (hERa) in comparison with 17beta-estradiol. Out of 14 tested pharmaceuticals, 9 were positive to YES-assay and 11 were positive to E-screen assayin particular, Furosemide and the fibrates (Bezafibrate, Fenofibrate and Gemfibrozil) gave the maximal estrogenic response. Tamoxifen showed its dual activity as agonist and antagonist of hERa.
Effluent ConcentrationsFenofibrate was detected in sewage treatment plant effluents at concentrations of 0.12 and 0.02 ug/L (France), 0.16, 0.1, and 0.16 ug/L (Italy), and not detected (Sweden)(1). The concentration in effluent from 2 of 20 German municipal sewage treatment plants sampled was 0.03 ug/L, detection limit = 0.05 ug/L(2). The compound was not detected in sewage influent samples collected at the 26th Ward municipal waste water treatment plant in Brooklyn, NY(3).
Soil Adsorption/MobilityUsing a structure estimation method based on molecular connectivity indices(1), the Koc of fenofibrate can be estimated to be 3,800(SRC). According to a classification scheme(2), this estimated Koc value suggests that fenofibrate is expected to have slight mobility in soil.
Human Toxicity Excerpts/SIGNS AND SYMPTOMS/ Severe rashes requiring hospitalization and corticosteroid therapy, including Stevens-Johnson syndrome and toxic epidermal necrolysis, have been reported rarely with fenofibrate in clinical studies. Urticaria and rash also have been reported in approximately 1% of patients receiving fenofibrate therapy in controlled trials./CASE REPORTS/ Lipid disorders have been treated with fibrates for many years. Rhabdomyolysis is one of the side effects of these drugs. ... A case of a septic-toxic shock due to rhabdomyolysis in a 75-year old patient, who had been treated with fenofibrate for 2 years /is reported/. This case shows necessity of the standard monitoring of aminotransferase, phosphocreatine kinase and creatinine levels during treatment with fibrates./CASE REPORTS/ A 56-year-old white hypercholesterolemic man was treated with fenofibrate 160 mg/day for 1 year. During the course of treatment, he developed gynecomastia on the left side, which resolved after the drug was stopped and replaced with alpha tocopherol acetate. Sixteen months after fenofibrate discontinuation, the patient was rechallenged and subsequently developed gynecomastia symptoms on the right side. The usual etiologies of gynecomastia were excluded by careful assessment of the patient's medical history, physical examination, and results of diagnostic tests such as chest X-ray, mammography, scrotal ultrasonography, routine blood chemistry, and extensive hormonal panel. Gynecomastia again resolved after discontinuation of fenofibrate.In this case, the resolution of gynecomastia on discontinuation of fenofibrate and recurrence after rechallenge highly suggest the role of fenofibrate. Use of the Naranjo probability scale registered causality as probable. .../CASE REPORTS/ Fenofibrate therapy was initiated for a 60-year old Hispanic man with stage 4 chronic kidney disease (CKD) for the treatment of hypertriglyceridemia. Two weeks after taking 48 mg of fenofibrate daily, the patient's SCr and blood urea nitrogen concentrations increased from 3.0 and 25 mg/dL, respectively, to 3.5 and 30 mg/dL, respectively. His estimated glomerular filtration rate (eGFR) had decreased from 24.8 to 17.9 mL/min/1.73 sq m. One month after initiating fenofibrate, his SCr concentration had increased to 3.7 mg/dL, a 32% increase from baseline. Because of persistently high triglyceride concentrations (e.g., 402 mg/dL), the fenofibrate dosage was increased to 145 mg daily. The patient's SCr concentration rose to 4.7 mg/dL (a 62% increase from baseline), and his eGFR was calculated as 13 mL/min/1.73 sq m. The patient was referred by the nephrology service for vascular-access placement in preparation for hemodialysis. Four days after discontinuation of fenofibrate, the patient's SCr concentration dropped to 3.3 mg/dL and returned to baseline approximately six weeks later, with an eGFR of 20.5 mL/min/1.73 sq m. Preparation for hemodialysis was terminated, and the patient's eGFR remained stable at 20.2 mL/min/1.73 sq m for the 12 months after fenofibrate discontinuation. A score of 4 on the Naranjo et al. probability scale indicated that there was a possible association between fenofibrate and renal dysfunction in this patient. A 60-year-old patient developed renal impairment after receiving fenofibrate for the treatment of hypertriglyceridemia.
Artificial Pollution SourcesFenofibrate's production and use as an antilipemic(1) may result in its release to the environment through various waste streams(SRC).
Wassergefährdungsklasse (WGK)3
Zollcode29189900
RTECS-Nr.UA2453400
R-Sätze (R)22-36/37/38
ToxizitätLD50 in mice: 1600 mg/kg orally (Sornay)
GefahrensymboleXn,Xi
Sicherheitshinweise (S)36-26-24/25
Lagerklasse11 - Combustible Solids
Gefahrstoffdaten49562-28-9(Hazardous Substances Data)
GefahrenklasseSTOT RE 2 Oral