Clofibrate - CAS 637-07-0
Catalog number: 637-07-0
Category: Inhibitor
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Molecular Formula:
C12H15ClO3
Molecular Weight:
242.7
COA:
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Targets:
PPAR
Description:
Clofibrate is a fibric acid derivative used in the treatment of hyperlipoproteinemia type III and severe hypertriglyceridemia.
Purity:
>98%
Synonyms:
Atromid-S
MSDS:
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InChIKey:
KNHUKKLJHYUCFP-UHFFFAOYSA-N
InChI:
InChI=1S/C12H15ClO3/c1-4-15-11(14)12(2,3)16-10-7-5-9(13)6-8-10/h5-8H,4H2,1-3H3
Canonical SMILES:
CCOC(=O)C(C)(C)OC1=CC=C(C=C1)Cl
1.Widely used pharmaceuticals present in the environment revealed as in vitro antagonists for human estrogen and androgen receptors.
Ezechiáš M1, Janochová J2, Filipová A2, Křesinová Z1, Cajthaml T3. Chemosphere. 2016 Jun;152:284-91. doi: 10.1016/j.chemosphere.2016.02.067. Epub 2016 Mar 12.
A considerable amount of scientific evidence indicates that a number of pharmaceuticals that could be detected in the environment can contribute towards the development of problems associated with human reproductive systems, as well as those of wildlife. We investigated the estrogenic and androgenic effects of select pharmaceuticals with high production volume and environmental relevance. We examined the receptor-binding activities of these pharmaceuticals in the T47D human cell line using altered secretion of cytokine CXCL12. Functional yeast-luciferase reporter gene assays were also employed to confirm the mechanism of receptor binding by estrogen and androgen. Non-steroidal anti-inflammatory drugs, namely ibuprofen, diclofenac and antiarrhythmic agent amiodarone showed strong anti-estrogenic effects in the T47D cell line. In the yeast-luciferase assay, these anti-inflammatory drugs also demonstrated anti-estrogenic potency and inhibited the E2 response in a concentration-dependent manner.
2.Involvement of Inflammatory Cytokines in Antiarrhythmic Effects of Clofibrate in Ouabain-Induced Arrhythmia in Isolated Rat Atria.
Moradi S1, Nikoui V2, Imran Khan M3, Amiri S4, Jazaeri F1, Bakhtiarian A4. Adv Pharmacol Sci. 2016;2016:9128018. doi: 10.1155/2016/9128018. Epub 2016 Feb 10.
Considering the cardioprotective and anti-inflammatory properties of clofibrate, the aim of the present experiment was to investigate the involvement of local and systemic inflammatory cytokines in possible antiarrhythmic effects of clofibrate in ouabain-induced arrhythmia in rats. Rats were orally treated with clofibrate (300 mg/kg), and ouabain (0.56 mg/kg) was administered to animals intraperitoneally. After induction of anesthesia, the atria were isolated and the onset of arrhythmia and asystole was recorded. The levels of inflammatory cytokines in atria were also measured. Clofibrate significantly postponed the onset of arrhythmia and asystole when compared to control group (P ≤ 0.05 and P ≤ 0.01, resp.). While ouabain significantly increased the atrial beating rate in control group (P ≤ 0.05), same treatment did not show similar effect in clofibrate-treated group (P > 0.05). Injection of ouabain significantly increased the atrial and systemic levels of all studied inflammatory cytokines (P ≤ 0.
3.Effect of clofibrate on fatty acid metabolism in the kidney of puromycin-induced nephrotic rats.
Muroya Y1, Ito O2. Clin Exp Nephrol. 2016 Mar 7. [Epub ahead of print]
BACKGROUND: Proteinuria plays an essential role in the progression of tubulointerstitial damage, which causes end-stage renal disease. An increased load of fatty acids bound to albumin reabsorbed into proximal tubular epithelial cells (PTECs) contributes to tubulointerstitial damage. Fibrates, agonists of peroxisome proliferator-activated receptor α (PPARα), have renoprotective effects against proteinuria whereas the effects of these compounds on fatty acid metabolism in the kidney are still unknown. Therefore, the present study examined whether the renoprotective effects of clofibrate were associated with improvement of fatty acid metabolism in puromycin aminonucleoside (PAN)-induced nephrotic rats.
4.Peroxisome proliferator-activated receptors (PPAR) downregulate the expression of pro-inflammatory molecules in an experimental model of myocardial infarction.
Ibarra-Lara ML1, Sánchez-Aguilar M1, Soria E2, Torres-Narváez JC1, Del Valle-Mondragón L1, Cervantes-Pérez LG1, Pérez-Severiano F3, Ramírez-Ortega MD1, Pastelín-Hernández G1, Oidor-Chan VH1,4, Sánchez-Mendoza A1. Can J Physiol Pharmacol. 2016 Jan 17:1-9. [Epub ahead of print]
Myocardial infarction (MI) has been associated with an inflammatory response and a rise in TNF-α, interleukin (IL)-1β, and IL-6. Peroxisome proliferator-activated receptors (PPARs) promote a decreased expression of inflammatory molecules. We aimed to study whether PPAR stimulation by clofibrate decreases inflammation and reduces infarct size in rats with MI. Male Wistar rats were randomized into 3 groups: control, MI + vehicle, and MI + clofibrate (100 mg/kg). Treatment was administered for 3 consecutive days, previous to 2 h of MI. MI induced an increase in protein expression, mRNA content, and enzymatic activity of inducible nitric oxide synthase (iNOS). Additionally, MI incited an increased expression of matrix metalloproteinase (MMP)-2 and MMP-9, intercellular adhesion molecule (ICAM)-1, and IL-6. MI also elevated the nuclear content of nuclear factor-κB (NF-κB) and decreased IκB, both in myocyte nuclei and cytosol. Clofibrate treatment prevented MI-induced changes in iNOS, MMP-2 and MMP-9, ICAM-1, IL-6, NF-κB, and IκB.
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CAS 637-07-0 Clofibrate

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