(R)-(+)-Etomoxir sodium salt

CAS No. : 828934-41-4

(R)-(+)-Etomoxir sodium salt,828934-41-4
Product Details
For research use only. Not Intended for Therapeutic Use!
Cat No:I004996
Synonyms:sodium (R)-2-(6-(4-chlorophenoxy)hexyl)oxirane-2-carboxylate
Molecular Formula:C15H18ClO4 • Na
Molecular Weight:320.7
Target:Histone Acetyltransferases
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Appearance:A crystalline solid
Cat No:I004996
Cas No:828934-41-4
Product-Name:(R)-(+)-Etomoxir sodium salt
IUPAC Name:sodium;(2R)-2-[6-(4-chlorophenoxy)hexyl]oxirane-2-carboxylate

(R)-(+)-Etomoxir sodium salt(cas 828934-41-4) is a potent inhibitor of carnitine palmitoyltransferase I (CPT1); inhibits β-oxidation in mitochondria; shown to inhibit cardiolipin biosynthesis from exogenous fatty acid in H9c2 cells.

1. FASEB J. 2002 Oct;16(12):1688-90. Epub 2002 Aug 21.
Etomoxir-induced increase in UCP3 supports a role of uncoupling protein 3 as a mitochondrial fatty acid anion exporter.
Schrauwen P(1), Hinderling V, Hesselink MK, Schaart G, Kornips E, Saris WH, Westerterp-Plantenga M, Langhans W.
Author information:
(1)Nutrition and Toxicology Research Institute Maastricht, Department of Human Biology, Maastricht University, 6200 MD Maastricht, The Netherlands. p.schrauwen@hb.unimaas.nl
The physiological function of human uncoupling protein-3 is still unknown. Uncoupling protein-3 is increased during fasting and high-fat feeding. In these situations the availability of fatty acids to the mitochondria exceeds the capacity to metabolize fatty acids, suggesting a role for uncoupling protein-3 in handling of non-metabolizable fatty acids. To test the hypothesis that uncoupling protein-3 acts as a mitochondrial exporter of non-metabolizable fatty acids from the mitochondrial matrix, we gave human subjects Etomoxir (which blocks mitochondrial entry of fatty acids) or placebo in a cross-over design during a 36-h stay in a respiration chamber. Etomoxir inhibited 24-h fat oxidation and fat oxidation during exercise by approximately 14-19%. Surprisingly, uncoupling protein-3 content in human vastus lateralis muscle was markedly up-regulated within 36 h of Etomoxir administration. Up-regulation of uncoupling protein-3 was accompanied by lowered fasting blood glucose and increased translocation of glucose transporter-4. These data support the hypothesis that the physiological function of uncoupling protein-3 is to facilitate the outward transport of non-metabolizable fatty acids from the mitochondrial matrix and thus prevents mitochondria from the potential deleterious effects of high fatty acid levels. In addition our data show that up-regulation of uncoupling protein-3 can be beneficial in the treatment of type 2 diabetes.

2. Toxicol Sci. 2002 Jul;68(1):93-101.
Etomoxir-induced oxidative stress in HepG2 cells detected by differential gene expression is confirmed biochemically.
Merrill CL(1), Ni H, Yoon LW, Tirmenstein MA, Narayanan P, Benavides GR, Easton MJ, Creech DR, Hu CX, McFarland DC, Hahn LM, Thomas HC, Morgan KT.
Author information:
(1)Department of Microbiology, Pathology and Parasitology, North Carolina State University, Raleigh 27606, USA. clm70753@gsk.com
Although they are known to be effective antidiabetic agents, little is published about the toxic effects of carnitine palmitoyltransferase-1 (CPT-1) inhibitors, such as etomoxir (ET). These compounds inhibit mitochondrial fatty acid beta-oxidation by irreversibly binding to CPT-1 and preventing entry of long chain fatty acids into the mitochondrial matrix. Treatment of HepG2 cells with 1 mM etomoxir for 6 h caused significant modulations in the expression of several redox-related and cell cycle mRNAs as measured by microarray analysis. Upregulated mRNAs included heme oxygenase 1 (HO1), 8-oxoguanine DNA glycosylase 1 (OGG1), glutathione reductase (GSR), cyclin-dependent kinase inhibitor 1A (CDKN1 [p21(waf1)]) and Mn+ superoxide dismutase precursor (SOD2); while cytochrome P450 1A1 (CYP1A1) and heat shock 70kD protein 1 (HSPA1A) were downregulated. Real time quantitative PCR (RT-PCR) confirmed the significant changes in 4 of 4 mRNAs assayed (CYP1A1, HO1, GSR, CDKN1), and identified 3 additional mRNA changes; 2 redox-related genes, gamma-glutamate-cysteine ligase modifier subunit (GCLM) and thioredoxin reductase (TXNRD1) and 1 DNA replication gene, topoisomerase IIalpha (TOP2A). Temporal changes in selected mRNA levels were examined by RT-PCR over 11 time points from 15 min to 24 h postdosing. CYP1A1 exhibited a 38-fold decrease by 4 h, which rebounded to a 39-fold increase by 20 h. GCLM and TXNRD1 exhibited 13- and 9-fold increases, respectively at 24 h. Etomoxir-induced oxidative stress and impaired mitochondrial energy metabolism were confirmed by a significant decrease in reduced glutathione (GSH), reduced/oxidized glutathione ratio (GSH/GSSG), mitochondrial membrane potential (MMP), and ATP levels, and by concurrent increase in oxidized glutathione (GSSG) and superoxide generation. This is the first report of oxidative stress caused by etomoxir.

3. Mol Cell Biochem. 2002 Mar;232(1-2):57-62.
Differential effects of etomoxir treatment on cardiac Na+-K+ ATPase subunits in diabetic rats.
Kato K(1), Lukas A, Chapman DC, Rupp H, Dhalla NS.
Author information:
(1)Institute of Cardiovascular Sciences, St Boniface General Hospital Research Centre and Department of Physiology, Faculty of Medicine, University of Manitoba, Winnipeg, Canada.
Etomoxir, an inhibitor of mitochondrial carnitine palmitoyltransferase-1, is known to attenuate the changes in myosin isoforms and sarcoplasmic reticular function that occur in diabetic rat hearts. In the present study, we tested the hypothesis that etomoxir also prevents the diabetes-induced depression of sarcolemmal (SL) Na+-K+ATPase activity by differentially affecting its alpha and beta-subunit levels. Streptozotocin-induced diabetes was associated with a decreased in alpha2-, alpha3-subunit levels, whereas the alpha1-and beta1-subunits were unchanged. Treatment of diabetic rats for 4 weeks with etomoxir (8 mg/kg/day) increased the alpha1-subunit levels, but failed to prevent the decrease in alpha2- and alpha3-subunit levels. In euglycemic control rats, etomoxir increased the alpha1-subunit protein level per g heart weight, but did not alter the alpha2-, alpha3- and beta1-subunit levels. The large decrease in Na+-K+ ATPase activity per g heart weight in diabetic rats was prevented by etomoxir, which suggests that the increased alpha1-subunit levels seen with this drug compensated for the decreased alpha2- and alpha3-subunit levels. The SL yield was also increased by etomoxir in euglycemic rats in proportion to the higher alpha1-subunit level, which resulted in an unchanged alpha1-content when expressed per mg SL protein; however, the alpha2- and beta1-subunit levels were reduced (p < 0.05). The depressed alpha2- and beta3 subunit levels of diabetic rats were associated with reduced mRNA abundance. However, no increase in alpha1-subunit mRNA abundance was seen in the etomoxir treated rats, which suggests that possibly post-transcriptional mechanisms are occurring in these hearts.
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