Tesaglitazar - CAS 251565-85-2
Category: Inhibitor
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Tesaglitazar is a dual-acting agonist of PPARα/γ (IC50 = 0.35 and 3.8 μM for PPARγ and PPARα, respectively). It reduces insulin resistance in obese Zucker rats that has the potential for the treatment of type 2 diabetes. Tesaglitazar also prevents atherosclerosis progression in E3L.CETP transgenic mice.
Brife Description:
PPARα/γ agonist
≥98% by HPLC
White Solid
(S)-2-Ethoxy-3-[4-[2-(4-methanesulfonyloxyphenyl)ethoxy]phenyl]propanoic acid; Tesaglitazar; AR-H-039242XX; AZ-242; AZ242; AZ 242; ARH-039242XX; Galida.
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1.[Peroxisome proliferator-activated receptor α/γ agonist tesaglitazar stabilizes atherosclerotic plaque in diabetic low density lipoprotein receptor knockout mice].
Zhang BC1, Li XK, Che WL, Li WM, Hou L, Wei YD, Xu YW. Zhonghua Xin Xue Guan Bing Za Zhi. 2013 Feb;41(2):143-9.
OBJECTIVE: To investigate the effects of peroxisome proliferator-activated receptor (PPAR) α/γ agonist on atherosclerotic plaque stabilization in diabetic LDL receptor knockout (LDLr-/-) mice.
2.The PPAR α / γ Agonist, Tesaglitazar, Improves Insulin Mediated Switching of Tissue Glucose and Free Fatty Acid Utilization In Vivo in the Obese Zucker Rat.
Wallenius K1, Kjellstedt A, Thalén P, Löfgren L, Oakes ND. PPAR Res. 2013;2013:305347. doi: 10.1155/2013/305347. Epub 2013 Oct 27.
METABOLIC FLEXIBILITY WAS ASSESSED IN MALE ZUCKER RATS: lean controls, obese controls, and obese rats treated with the dual peroxisome proliferator activated receptor (PPAR) α/γ agonist, tesaglitazar, 3  μ mol/kg/day for 3 weeks. Whole body glucose disposal rate (R d ) and hepatic glucose output (HGO) were assessed under basal fasting and hyperinsulinemic isoglycemic clamp conditions using [3,(3)H]glucose. Indices of tissue specific glucose utilization (R g ') were measured at basal, physiological, and supraphysiological levels of insulinemia using 2-deoxy-D-[2,6-(3)H]glucose. Finally, whole body and tissue specific FFA and glucose utilization and metabolic fate were evaluated under basal and hyperinsulinemic conditions using a combination of [U-(13)C]glucose, 2-deoxy-D-[U-(14)C]glucose, [U-(14)C]palmitate, and [9,10-(3)H]-(R)-bromopalmitate. Tesaglitazar improved whole body insulin action by greater suppression of HGO and stimulation of R d compared to obese controls.
3.Dual PPAR α / γ Agonism Normalizes Lipoprotein Profile of Renal Dyslipidemia.
Samuelsson O1, Attman PO, Gause-Nilsson I, Svensson MK, Alaupovic P. PPAR Res. 2013;2013:391628. doi: 10.1155/2013/391628. Epub 2013 Mar 28.
Chronic kidney disease (CKD) is characterised by specific lipoprotein abnormalities and insulin resistance. Dual activation of the peroxisome proliferators-activated receptors (PPAR) α and γ can significantly improve insulin sensitivity. The aim of the study was to investigate the effects of a dual PPAR α / γ agonist on lipoprotein abnormalities in patients with CKD. One mg of the dual PPAR α / γ agonist tesaglitazar was given once daily during six weeks to CKD patients, and to healthy subjects. Plasma lipids, apolipoproteins (apo) and discrete lipoprotein subclasses were measured at baseline and end of treatment. In the CKD patients apoA-I increased significantly by 9%, and apoB decreased by 18%. There was an increase of apoC-III in HDL by 30%, and a parallel decrease of apoC-III in VLDL + LDL by 13%. Both the apoB-containing cholesterol-rich and the triglyceride-rich subclasses decreased significantly. With the exception of ApoC-III,all plasma lipids apolipoproteins and lipoprotein subclasses were reduced by treatment down to similar levels as the baseline levels of a healthy group of reference subjects.
4.PPAR agonists regulate brain gene expression: relationship to their effects on ethanol consumption.
Ferguson LB1, Most D2, Blednov YA3, Harris RA3. Neuropharmacology. 2014 Nov;86:397-407. doi: 10.1016/j.neuropharm.2014.06.024. Epub 2014 Jul 15.
Peroxisome proliferator-activated receptors (PPARs) are nuclear hormone receptors that act as ligand-activated transcription factors. Although prescribed for dyslipidemia and type-II diabetes, PPAR agonists also possess anti-addictive characteristics. PPAR agonists decrease ethanol consumption and reduce withdrawal severity and susceptibility to stress-induced relapse in rodents. However, the cellular and molecular mechanisms facilitating these properties have yet to be investigated. We tested three PPAR agonists in a continuous access two-bottle choice (2BC) drinking paradigm and found that tesaglitazar (PPARα/γ; 1.5 mg/kg) and fenofibrate (PPARα; 150 mg/kg) decreased ethanol consumption in male C57BL/6J mice while bezafibrate (PPARα/γ/β; 75 mg/kg) did not. We hypothesized that changes in brain gene expression following fenofibrate and tesaglitazar treatment lead to reduced ethanol drinking. We studied unbiased genomic profiles in areas of the brain known to be important for ethanol dependence, the prefrontal cortex (PFC) and amygdala, and also profiled gene expression in liver.
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CAS 251565-85-2 Tesaglitazar

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