Etomoxir (Na salt)

Catalog No.S8244

Etomoxir (Na salt) Chemical Structure

Molecular Weight(MW): 320.74

Etomoxir is an irreversible inhibitor of carnitine palmitoyltransferase-1 (CPT-1) on the outer face of the inner mitochondrial membrane.

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Cited by 4 Publications

4 Customer Reviews

  • Immunoblot analysis of CyclinD1, PCNA, γ-H2AX, cleaved-PRAP and -caspase3 (F) in normal saline or ETO-treated groups were determined at 10 weeks after HFD treatment (n = 10 mice/group).

    Cancer Lett, 2018, 442:40-52. Etomoxir (Na salt) purchased from Selleck.

    CPT1A inhibitor counteracted the protective effect of BBR against PA-induced lipid accumulation and apoptosis in HK-2 cells. HK-2 cells were pretreated with or without 40 μmol/L Etomoxir for 24 h, and then treated with 12.5 μmol/L BBR in the presence or absence of 450 μmol/L PA for 24 h. Intracellular lipid content was detected by Oil Red O staining (400×). The lower panels showed enlarged views of the boxed areas in the upper panels.

    Med Sci Monit, 2018, 24:1484-1492. Etomoxir (Na salt) purchased from Selleck.

  • CPT1A inhibitor counteracted the protective effect of BBR against PA-induced lipid accumulation and apoptosis in HK-2 cells. HK-2 cells were pretreated with or without 40 μmol/L Etomoxir for 24 h, and then treated with 12.5 μmol/L BBR in the presence or absence of 450 μmol/L PA for 24 h. Intracellular lipid content was detected by Oil Red O staining (400×) (A) .

    Med Sci Monit, 2018, 24: 1484-1492. Etomoxir (Na salt) purchased from Selleck.

    Inflammatory gene expression in lipid stressed LECs. Inflammatory gene expression in control LECs was determined by qRT-PCR following a 24-hour exposure to factors that perturbed lipid homeostasis or cellular metabolism (A). Results presented are from three independentexperiments performed in triplicate. Expression is normalized to LECs grown in EGM-2MV.

    Lymphatic Research and BiologyVol, 2018, 16(1). https://doi.org/10.1089/lrb.2017.0033. Etomoxir (Na salt) purchased from Selleck.

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Biological Activity

Description Etomoxir is an irreversible inhibitor of carnitine palmitoyltransferase-1 (CPT-1) on the outer face of the inner mitochondrial membrane.
Targets
CPT-1 [1] PPARα [1]
In vitro

Etomoxir has also been identified as a direct agonist of PPARα. Etomoxir is a compound that binds irreversibly to the catalytic site of CPT-1 inhibiting its activity, but also upregulates fatty acid oxidation enzymes. Transcriptional effects of etomoxir could be due to 1. shift in energy metabolism with increased glucose utilization and 2. PPARalpha activation[1]. Etomoxir reduces pro-inflammatory cyokine production and increases apoptosis of MOG specific T cells[2]. Etomoxir has been shown to decrease oxygen consumption rates (OCRs) and impair ATP and NADPH production in the pediatric glioblastoma cell line SF188[3].

Cell Data
Cell Lines Assay Type Concentration Incubation Time Formulation Activity Description PMID
KB cells NEf4dmVEgXSxdH;4bYNqfHliYYPzZZk> M3:0WmN6fG:2b4jpZ4l1gSCrbjDoeY1idiCNQjDj[YxteyxiSVO1NF0zNjd4IN88US=> MXOyNVUxPDF3Nh?=
U251 M{XKeWdzd3e2aDDpcohq[mm2b36gZZN{[Xl? NEPjRXg2OCEQvF2= NEj0NpU4Oi2qIITy[YF1dWWwdIOgbIF3\SC|bHnnbJQh\3Kxd4ToJIlvcGmkaYTvdpkh\W[oZXP0dy=> Mnv6N|A2PzRyMkC=
U87 M3yyemdzd3e2aDDpcohq[mm2b36gZZN{[Xl? NH6yWng2OCEQvF2= MYm3Nk1pKHS{ZXH0cYVvfHNiaHH2[UB{dGmpaISg[5Jwf3SqIHnubIljcXSxcomg[YZn\WO2cx?= M1zMe|MxPTd2MEKw
U373-U MlTyS5Jwf3SqIHnubIljcXSxbjDhd5NigQ>? M{HIZlUxKM7:TR?= M2robFczNWhidILlZZRu\W62czDoZZZmKHOuaXfoeEBoem:5dHigbY5pcWKrdH;yfUBm\m[nY4Tz M12zPFMxPTd2MEKw
MCF-7 cells Mm\lSpVv[3Srb36gZZN{[Xl? Ml[3NQKBmzJyMPMAs:69VQ>? MX60JIg> M3LNSIlvKGSkLXPBUXAu\Xiyb4Pl[EBk\WyuczDFWG8h[2G3c3XkJIEhdWW2YXLvcIlkKGmvYnHsZY5k\Q>? MVGzNFk5OTd2MB?=
HepG2 cells MYHGeY5kfGmxbjDhd5NigQ>? MXKyOEBp MU\FeI9ud3ircjDzbYdvcW[rY3HueIx6KGmwaHnibZR{KHCjbH3peIF1\SCvZYThZo9tcXOvIIfpeIgh[W5iSVO1NEBqdiC2aHWgcoFvd22xbHHyJJJidmenLh?= NEfwb20zQTd2MEOxOC=>

... Click to View More Cell Line Experimental Data

Assay
Methods Test Index PMID
Western blot
p-ERK / p-p38 / p-JNK / p-FoxO4; 

PubMed: 26716645     


Ovarian cancer cell lines were treated with etomoxir (0.3 mM) for the indicated periods of time (hours).  Immunoblotting analyses were performed to assess phosphorylation of Erk, p38, JNK and FoxO4 T451 (JNK specific phosphorylation site).

p21 / FoxO1 / FoxO3a; 

PubMed: 26716645     


The effects of shRNA knockdown of FoxO1-sh or FoxO3a-sh on induction of p21 by etomoxir (0.3 mM, 24 hours) were examined.

p-mTOR(S2448) / mTOR / p-S6K(T389) / p-4EBP1 / p-BAD(S112) / cleaved PARP; 

PubMed: 25122071     


Expression of mTOR-S6K-BAD-Caspase3 axis after metabolic treatments for 16 hours in LNCaP cells. 

p-ACC2 / p-AMPK / AMPK; 

PubMed: 25122071     


Blot of AMPK activation and ACC2 inactivation of LNCaP lysates.

26716645 25122071
In vivo Etomoxir has a protective action on the ischemia/reperfusion injury of the kidney similarly to an established PPARalpha agonist. It has been developed for treating non-insulindependent diabetes mellitus. Etomoxir increases the functional recovery of fatty acid perfused ischemic rat hearts which is unrelated to changes in levels of long-chain acylcarnitines and is attributed to an increased glucose use. A chronic treatment of rats with etomoxir increases the SR Ca2+-ATPase activity, the Ca2+ uptake rate, the number of active Ca2+ pumps E~P, the SERCA2 protein and the SERCA2 mRNA abundance of the heart. At a low dosage, etomoxir has a selective influence on the rate of contraction and relaxation of overloaded hearts. Etomoxir, in the liver can act as peroxisomal proliferator, increasing DNA synthesis and liver growth[1]. Etomoxir-treated mice displays a reduced immune cell infiltration in the CNS with few macrophages, activated microglia, or T cells present. Etomoxir reduces inflammation and demyelination in the CNS of treated mice[2]. Inhibition of fatty acid oxidation by etomoxir prolongs survival time in a syngeneic mouse model of malignant glioma and slow tumor growth. Emergence and progression of glioma are delayed upon treatment with the investigational drug etomoxir. Etomoxir has already been tested in phase I/II clinical trials for treating moderate congestive heart failure; this trial is discontinued because 4 patients (of 226 taking the drug) developed unacceptably high liver transaminase levels upon treatment, and the risk of such drastic side effects is deemed sufficient to negate the potential benefit of this drug for these patients[3].

Protocol

Cell Research:

[2]

+ Expand
  • Cell lines: Splenocytes
  • Concentrations: 100 μM
  • Incubation Time: 72 h
  • Method:

    C57BL/6 mice are immunized with 200 μg MOG35-55 peptide s.c., and 14 days later splenocytes are isolated and cultured at a concentration of 6×106 cells/ml in DMEM containing high (4.5 g/L) or low (1 g/L) glucose, 10% FBS 50 μg/ml MOG peptide, and 25 ng/ml IL-12 (R&D systems, Minneapolis, MN) in the presence of vehicle or 100 μM etomoxir. 72 hours later cells are harvested for APO-BrdU staining and supernatants collected for IL-4, IL-17 and IFN-γ ELISA. (MOG:myelin oligodendrocyte glycoprotein)


    (Only for Reference)
Animal Research:

[2]

+ Expand
  • Animal Models: C57BL6/J mice
  • Formulation: Sterile water
  • Dosages: 15 mg/kg
  • Administration: i.p.
    (Only for Reference)

Solubility (25°C)

In vitro DMSO 64 mg/mL (199.53 mM)
Water 64 mg/mL warmed (199.53 mM)
Ethanol 13 mg/mL (40.53 mM)

* Please note that Selleck tests the solubility of all compounds in-house, and the actual solubility may differ slightly from published values. This is normal and is due to slight batch-to-batch variations.

Chemical Information

Molecular Weight 320.74
Formula

C15H18ClO4.Na

CAS No. 828934-41-4
Storage powder
in solvent
Synonyms N/A

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Transferase Signaling Pathway Map

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Cell Lines Assay Type Concentration Incubation Time Formulation Activity Description PMID