(R)-(+)-Etomoxir sodium salt
(R)-(+)-Etomoxir sodium salt is an irreversible inhibitor of carnitine palmitoyltransferase 1(CPT-1)[1].
Etomoxir (100 μM) has no effect on T cells cultured in high glucose. In contrast, there is a significant increase in apoptosis in etomoxir-treated cultures stimulated with antigen under low glucose conditions[2].
C57BL/6 mice treated with Etomoxir (15 mg/kg, i.p) reduce the infiltration of immune cells in the central nervous system. Only a small number of macrophages, activated microglia or T cells are present, while reducing the inflammatory response and Demyelinating reaction[2].
References:
[1]. Rupp H, Zarain-Herzberg A, Maisch B. The Use of Partial Fatty Acid Oxidation Inhibitors for Metabolic Therapy of Angina Pectoris and Heart Failure. Herz, 2002, 27(7): 621-636.
[2]. Shriver L P, Manchester M. Inhibition of fatty acid metabolism ameliorates disease activity in an animal model of multiple sclerosis. Scientific Reports, 2011, 1.
Physical Appearance | A solid |
Storage | Store at -20°C |
M.Wt | 320.74 |
Cas No. | 828934-41-4 |
Formula | C15H18ClNaO4 |
Solubility | insoluble in H2O; insoluble in EtOH; ≥12 mg/mL in DMSO |
Chemical Name | sodium (R)-2-(6-(4-chlorophenoxy)hexyl)oxirane-2-carboxylate |
SDF | Download SDF |
Canonical SMILES | ClC1=CC=C(C=C1)OCCCCCC[C@@]2(C([O-])=O)OC2.[Na+] |
Shipping Condition | Small Molecules with Blue Ice, Modified Nucleotides with Dry Ice. |
General tips | We do not recommend long-term storage for the solution, please use it up soon. |
Cell experiment:[1] | |
Cell lines |
Splenocytes isolated from C57BL/6 mice immunized with myelin oligodendrocyte glycoprotein (MOG35-55) peptide |
Reaction Conditions |
100 μM etomoxir for 72 h incubation |
Applications |
Etomoxir exhibited no effect on MOG35-55-specific T cells cultured in high glucose conditions in terms of pro-inflammatory cyokine production and apoptosis. In contrast, there were a significant reduction in IFN-γ production and a substantial increase in apoptosis in etomoxir-treated cultures stimulated with antigen under low glucose conditions. |
Animal experiment:[1] | |
Animal models |
A mouse model of multiple sclerosis |
Dosage form |
15 mg/kg Injected intraperitoneally on days 8 and 15 after experimental autoimmune encephalomyelitis (EAE) induction |
Applications |
Etomoxir-treated mice displayed a reduced immune cell infiltration in the central nervous system with few macrophages, activated microglia, or T cells present. Etomoxir treatment also alleviated inflammation and prevented myelin destruction in spinal cords. |
Note |
The technical data provided above is for reference only. |
References: 1. Shriver LP, Manchester M. Inhibition of fatty acid metabolism ameliorates disease activity in an animal model of multiple sclerosis. Scientific Reports, 2011, 1: 79. |
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