(R)-(+)-Etomoxir sodium salt

Carnitine palmitoyltransferase I (CPT1) inhibitor CAS# 828934-41-4

(R)-(+)-Etomoxir sodium salt

Catalog No. BCC7946----Order now to get a substantial discount!

Product Name & Size Price Stock
(R)-(+)-Etomoxir sodium salt:10mg $165.00 In stock
(R)-(+)-Etomoxir sodium salt:20mg $281.00 In stock
(R)-(+)-Etomoxir sodium salt:50mg $660.00 In stock
(R)-(+)-Etomoxir sodium salt:100mg $1155.00 In stock
Related Products

Quality Control of (R)-(+)-Etomoxir sodium salt

Number of papers citing our products

Chemical structure

(R)-(+)-Etomoxir sodium salt

3D structure

Chemical Properties of (R)-(+)-Etomoxir sodium salt

Cas No. 828934-41-4 SDF Download SDF
PubChem ID 57345784 Appearance Powder
Formula C15H18ClNaO4 M.Wt 320.74
Type of Compound N/A Storage Desiccate at -20°C
Synonyms (+)-Etomoxir sodium salt
Solubility DMSO : 100 mg/mL (311.78 mM; Need ultrasonic)
H2O : 5 mg/mL (15.59 mM; Need ultrasonic)
Chemical Name sodium;(2R)-2-[6-(4-chlorophenoxy)hexyl]oxirane-2-carboxylate
SMILES C1C(O1)(CCCCCCOC2=CC=C(C=C2)Cl)C(=O)[O-].[Na+]
Standard InChIKey RPACBEVZENYWOL-XFULWGLBSA-M
Standard InChI InChI=1S/C15H19ClO4.Na/c16-12-5-7-13(8-6-12)19-10-4-2-1-3-9-15(11-20-15)14(17)18;/h5-8H,1-4,9-11H2,(H,17,18);/q;+1/p-1/t15-;/m1./s1
General tips For obtaining a higher solubility , please warm the tube at 37 ℃ and shake it in the ultrasonic bath for a while.Stock solution can be stored below -20℃ for several months.
We recommend that you prepare and use the solution on the same day. However, if the test schedule requires, the stock solutions can be prepared in advance, and the stock solution must be sealed and stored below -20℃. In general, the stock solution can be kept for several months.
Before use, we recommend that you leave the vial at room temperature for at least an hour before opening it.
About Packaging 1. The packaging of the product may be reversed during transportation, cause the high purity compounds to adhere to the neck or cap of the vial.Take the vail out of its packaging and shake gently until the compounds fall to the bottom of the vial.
2. For liquid products, please centrifuge at 500xg to gather the liquid to the bottom of the vial.
3. Try to avoid loss or contamination during the experiment.
Shipping Condition Packaging according to customer requirements(5mg, 10mg, 20mg and more). Ship via FedEx, DHL, UPS, EMS or other couriers with RT, or blue ice upon request.

Biological Activity of (R)-(+)-Etomoxir sodium salt

DescriptionInhibitor of carnitine palmitoyltransferase I (CPT1); inhibits β-oxidation in mitochondria. Shown to inhibit cardiolipin biosynthesis from exogenous fatty acid in H9c2 cells.

Protocol

Cell Assay [2]
Rat heart H9c2 myoblastic cells are incubated in DMEM containing 10% fetal bovine serum until near confluence. In some experiments, cells are preincubated for 2 h with DMEM (serum-free) in the absence or presence of 1-80 μM Etomoxir and then incubated for 2 h with 0.1 mM [1-14C]oleic acid (10 μCi/dish, binds to BSA in a 1:1 molar ratio). In other experiments, cells are preincubated for 2 h plus or minus 40 μM Etomoxir and then incubated for 2 h with 0.1 μM or 0.1 mM [1,3-3H]glycerol (10 μCi/dish), 0.1 mM [1-14C]oleic acid (2 μCi/dish, binds to BSA in a 1:1 molar ratio), 0.1 mM [1-14C]palmitic acid (2 μCi/dish, binds to BSA in a 1:1 molar ratio), 28 μM [3H]ethanolamine (2 μCi/dish), 28 μM [methyl-3H]choline (2 μCi/dish), 0.4 mM [3H]serine (20 μCi/dish), or 40 μM myo-[3H]inositol (10 μCi/dish). The medium is removed and the cells washed twice with ice-cold saline and then harvested from the dish with 2 mL methanol-water (1:1, v/v) for lipid extraction. An aliquot of the homogenate is taken for the determination of total uptake of radioactivity into cells. Phospholipids are then isolated and radioactivity in these determined[2].

Animal Administration [3][4]
Mice[3] 80 male C57BLKS/J lar-Leprdb/db mice and 20 wild type littermates (8 week) are used. db/db mice are randomly divided into four groups: db/db group, Etomoxir group, MitoQ group, and PFT-α group. In the Etomoxir group, mice are intraperitoneally injected with 1 mg/kg Etomoxir twice every week. In the MitoQ group, 50 μM MitoQ is given to the mice in water. Water bottles, containing either MitoQ, are covered with aluminum foil, and all bottles are refilled every 3 days. In the PFT-α group, mice are intraperitoneally injected with 1 mg/kg PFT-α twice every week. WT mice are administrated with vehicle instead. The experimental period is 8 weeks. At the end, peripheral blood samples and bone marrow cells are harvested for the assays. Rats[4] Male Lewis rats, weighing 150-200 g, are used in the present study. Animals are kept on a 12 h:12 h light/dark cycle and fed a Purina Chow diet and water ad libitum. The rats are divided into two groups: (1) control and (2) Etomoxir. Etomoxir (20 mg/kg of body weight) is dissolved in 0.9% (w/v) NaCl and administered intraperitoneally for 8 days. Control rats receive saline. The last injection is given 24 h before the experiment. Animals are anaesthetized with an intraperitoneal injection of a nembutal and heparin (3:1) mixture. Subsequently, the heart is removed for LCFA uptake studies and for analyses of transporter protein contents.

References:
[1]. Rupp H, et al. The use of partial fatty acid oxidation inhibitors for metabolic therapy of angina pectoris and heart failure. Herz. 2002 Nov;27(7):621-36. [2]. Xu FY, et al. Etomoxir mediates differential metabolic channeling of fatty acid and glycerol precursors into cardiolipin in H9c2 cells. J Lipid Res. 2003 Feb;44(2):415-23. [3]. Li J, et al. FFA-ROS-P53-mediated mitochondrial apoptosis contributes to reduction of osteoblastogenesis and bone mass in type 2 diabetes mellitus. Sci Rep. 2015 Jul 31;5:12724. [4]. Luiken JJ, et al. Etomoxir-induced partial carnitine palmitoyltransferase-I (CPT-I) inhibition in vivo does not alter cardiac long-chain fatty acid uptake and oxidation rates. Biochem J. 2009 Apr 15;419(2):447-55.

(R)-(+)-Etomoxir sodium salt Dilution Calculator

Concentration (start)
x
Volume (start)
=
Concentration (final)
x
Volume (final)
 
 
 
C1
V1
C2
V2

calculate

(R)-(+)-Etomoxir sodium salt Molarity Calculator

Mass
=
Concentration
x
Volume
x
MW*
 
 
 
g/mol

calculate

Preparing Stock Solutions of (R)-(+)-Etomoxir sodium salt

1 mg 5 mg 10 mg 20 mg 25 mg
1 mM 3.1178 mL 15.589 mL 31.1779 mL 62.3558 mL 77.9448 mL
5 mM 0.6236 mL 3.1178 mL 6.2356 mL 12.4712 mL 15.589 mL
10 mM 0.3118 mL 1.5589 mL 3.1178 mL 6.2356 mL 7.7945 mL
50 mM 0.0624 mL 0.3118 mL 0.6236 mL 1.2471 mL 1.5589 mL
100 mM 0.0312 mL 0.1559 mL 0.3118 mL 0.6236 mL 0.7794 mL
* Note: If you are in the process of experiment, it's necessary to make the dilution ratios of the samples. The dilution data above is only for reference. Normally, it's can get a better solubility within lower of Concentrations.

Organizitions Citing Our Products recently

 
 
 

Calcutta University

University of Minnesota

University of Maryland School of Medicine

University of Illinois at Chicago

The Ohio State University

University of Zurich

Harvard University

Colorado State University

Auburn University

Yale University

Worcester Polytechnic Institute

Washington State University

Stanford University

University of Leipzig

Universidade da Beira Interior

The Institute of Cancer Research

Heidelberg University

University of Amsterdam

University of Auckland
TsingHua University
TsingHua University
The University of Michigan
The University of Michigan
Miami University
Miami University
DRURY University
DRURY University
Jilin University
Jilin University
Fudan University
Fudan University
Wuhan University
Wuhan University
Sun Yat-sen University
Sun Yat-sen University
Universite de Paris
Universite de Paris
Deemed University
Deemed University
Auckland University
Auckland University
The University of Tokyo
The University of Tokyo
Korea University
Korea University

Background on (R)-(+)-Etomoxir sodium salt

(R)-(+)-Etomoxir sodium salt is R-form of Etomoxir sodium salt. Etomoxir is a potent inhibitor of carnitine palmitoyltransferase-I (CPT-1).

In Vitro:(R)-(+)-Etomoxir sodium salt is R-form of Etomoxir sodium salt. Etomoxir binds irreversibly to the catalytic site of CPT-1 inhibiting its activity, but also upregulates fatty acid oxidation enzymes. Etomoxir is developed as an inhibitor of the mitochondrial carnitine palmitoyltransferase-1 (CPT-1) located on the outer mitochondrial membrane. Etomoxir, in the liver can act as peroxisomal proliferator, increasing DNA synthesis and liver growth. Thus, etomoxir, in addition of being a CPT1 inhibitor could be considered as a PPARalpha agonist[1]. Etomoxir is a member of the oxirane carboxylic acid carnitine palmitoyl transferase I inhibitors and has been suggested as a therapeutic agent for the treatment of heart failure. Acute Etomoxir treatment irreversibly inhibits the activity of carnitine palmitoyltransferase I. As a result, fatty acid import into the mitochondria and β-oxidation is reduced, whereas cytosolic fatty acid accumulates and glucose oxidation is elevated. Prolonged incubation (24 h) with Etomoxir produces diverse effects on the expression of several metabolic enzyme[2].

In Vivo:(R)-(+)-Etomoxir sodium salt is R-form of Etomoxir sodium salt. Etomoxir is an inhibitor of free fatty acid (FFA) oxidation-related key enzyme CPT1. P53 interacts directly with Bax, which is inhibited by Etomoxir, further confirming the direct interaction of P53 and Bax, and the involvement of FAO-mediated mitochondrial ROS generation in db/db mice[3]. Rats are injected daily with Etomoxir, a specific CPT-I inhibitor, for 8 days at 20 mg/kg of body mass. Etomoxir-treated rats display a 44% reduced cardiac CPT-I activity. The treatment of Lewis rats for 8 days with 20 mg/kg Etomoxir does not alter blood glucose, which is in line with comparable etomoxir-feeding studies. Similarly, Etomoxir feeding does not affect general growth characteristics such as gain in body mass, nor does it affect hindlimb muscle mass. However, heart mass and liver mass are both significantly increased by 11% in Etomoxir-treated rats[4].

References:
[1]. Rupp H, et al. The use of partial fatty acid oxidation inhibitors for metabolic therapy of angina pectoris and heart failure. Herz. 2002 Nov;27(7):621-36. [2]. Xu FY, et al. Etomoxir mediates differential metabolic channeling of fatty acid and glycerol precursors into cardiolipin in H9c2 cells. J Lipid Res. 2003 Feb;44(2):415-23. [3]. Li J, et al. FFA-ROS-P53-mediated mitochondrial apoptosis contributes to reduction of osteoblastogenesis and bone mass in type 2 diabetes mellitus. Sci Rep. 2015 Jul 31;5:12724. [4]. Luiken JJ, et al. Etomoxir-induced partial carnitine palmitoyltransferase-I (CPT-I) inhibition in vivo does not alter cardiac long-chain fatty acid uptake and oxidation rates. Biochem J. 2009 Apr 15;419(2):447-55.

Featured Products
New Products
 

References on (R)-(+)-Etomoxir sodium salt

Etomoxir mediates differential metabolic channeling of fatty acid and glycerol precursors into cardiolipin in H9c2 cells.[Pubmed:12576524]

J Lipid Res. 2003 Feb;44(2):415-23.

We examined the effect of etomoxir treatment on de novo cardiolipin (CL) biosynthesis in H9c2 cardiac myoblast cells. Etomoxir treatment did not affect the activities of the CL biosynthetic and remodeling enzymes but caused a reduction in [1-14C]palmitic acid or [1-14C]oleic acid incorporation into CL. The mechanism was a decrease in fatty acid flux through the de novo pathway of CL biosynthesis via a redirection of lipid synthesis toward 1,2-diacyl-sn-glycerol utilizing reactions mediated by a 35% increase (P < 0.05) in membrane phosphatidate phosphohydrolase activity. In contrast, etomoxir treatment increased [1,3-3H]glycerol incorporation into CL. The mechanism was a 33% increase (P < 0.05) in glycerol kinase activity, which produced an increased glycerol flux through the de novo pathway of CL biosynthesis. Etomoxir treatment inhibited 1,2-diacyl-sn-glycerol acyltransferase activity by 81% (P < 0.05), thereby channeling both glycerol and fatty acid away from 1,2,3-triacyl-sn-glycerol utilization toward phosphatidylcholine and phosphatidylethanolamine biosynthesis. In contrast, etomoxir inhibited myo-[3H]inositol incorporation into phosphatidylinositol and the mechanism was an inhibition in inositol uptake. Etomoxir did not affect [3H]serine uptake but resulted in an increased formation of phosphatidylethanolamine derived from phosphatidylserine. The results indicate that etomoxir treatment has diverse effects on de novo glycerolipid biosynthesis from various metabolic precursors. In addition, etomoxir mediates a distinct and differential metabolic channeling of glycerol and fatty acid precursors into CL.

Modification of subcellular organelles in pressure-overloaded heart by etomoxir, a carnitine palmitoyltransferase I inhibitor.[Pubmed:1531968]

FASEB J. 1992 Mar;6(6):2349-53.

To examine the signals regulating cardiac growth and molecular structure of subcellular organelles, cardiac hypertrophy was induced in rats by constriction of the abdominal aorta for 12-13 wk or by treatment with a carnitine palmitoyltransferase I inhibitor, etomoxir (12-15 mg/kg body wt) for 12-13 wk. In contrast to pressure overload, etomoxir redistributed the myosin isozyme population from V3 to V1 and increased the sarcoplasmic reticulum (SR) Ca(2+)-stimulated ATPase activity. When rats with pressure-overloaded hearts were treated with etomoxir, the cardiac hypertrophy was increased whereas the shift in myosin isozymes from V1 to V3 was prevented and the depression in SR Ca(2+)-stimulated ATPase activity was reversed. Plasma thyroid hormone and insulin concentrations were not altered but triglyceride concentrations were reduced in etomoxir-treated rats with pressure overload. The data demonstrate a dissociation between cardiac muscle growth and changes in subcellular organelles and indicate that a shift in myocardial substrate utilization may represent an important signal for molecular remodeling of the heart.

Stereospecificity of the inhibition by etomoxir of fatty acid and cholesterol synthesis in isolated rat hepatocytes.[Pubmed:1930298]

Biochem Pharmacol. 1991 Oct 9;42(9):1717-20.

The racemates of substituted 2-oxiranecarboxylates are potent inhibitors of fatty acid oxidation and fatty acid and cholesterol synthesis. We show in the accompanying paper [Agius L, Peak M and Sherratt HSA, Biochem Pharmacol 42: 1711-1715, 1991] that only the R-enantiomer of etomoxir, a potent hypoglycaemic compound, inhibits fatty acid oxidation in hepatocytes. We demonstrate in this paper that although the R-enantiomer of etomoxir is esterified to its CoA-ester more readily than the S-enantiomer, both the R- and S-enantiomers are equally potent inhibitors of fatty acid and cholesterol synthesis from acetate in rat hepatocytes. The inhibition of fatty acid synthesis is not due to direct inhibition of fatty acid synthetase and the inhibition of cholesterol synthesis occurs at a site proximal to formation of mevalonate. Since the S-enantiomer inhibits fatty acid and cholesterol synthesis but not fatty acid oxidation the inhibition of the biosynthetic pathways is not coupled to inhibition of fatty acid oxidation.

Description

Etomoxir sodium salt ((R)-(+)-Etomoxir sodium salt) is an irreversible inhibitor of carnitine palmitoyltransferase 1a (CPT-1a), inhibits fatty acid oxidation (FAO) through CPT-1a and inhibits palmitate β-oxidation in human, rat and guinea pig.

Keywords:

(R)-(+)-Etomoxir sodium salt,828934-41-4,(+)-Etomoxir sodium salt,Natural Products,Histone Acetyltransferases, buy (R)-(+)-Etomoxir sodium salt , (R)-(+)-Etomoxir sodium salt supplier , purchase (R)-(+)-Etomoxir sodium salt , (R)-(+)-Etomoxir sodium salt cost , (R)-(+)-Etomoxir sodium salt manufacturer , order (R)-(+)-Etomoxir sodium salt , high purity (R)-(+)-Etomoxir sodium salt

Online Inquiry for:

      Fill out the information below

      • Size:Qty: - +

      * Required Fields

                                      Result: