| 包装 | 价格(元) |
| 10mM (in 1mL DMSO) | 电议 |
| 5mg | 电议 |
| 10mg | 电议 |
| 50mg | 电议 |
Etomoxir ((R)-(+)-Etomoxir) 是肉碱棕榈酰转移酶 1a (CPT-1a) 的不可逆抑制剂，通过 CPT-1a 抑制脂肪酸氧化 (FAO) 并抑制人、大鼠中的棕榈酸酯 β-氧化和豚鼠。
Cell lines | Rat heart H9c2 myoblastic cells |
Preparation method | This compound is soluble in DMSO. General tips for obtaining a higher concentration: Please warm the tube at 37℃ for 10 minutes and/or shake it in the ultrasonic bath for a while. Stock solution can be stored below -20℃ for several months. |
Reacting condition | 1-80 μM; 2 h |
Applications | In rat heart H9c2 myoblastic cells, Etomoxir concentration-dependently reduced [1-14C]oleic acid incorporation into phosphatidylglycerol (PtdGro) and cardiolipin (CL). In contrast, etomoxir increased [1,3-3H]glycerol incorporation into CL. |
Animal models | Experimental autoimmune encephalomyelitis (EAE) mice model |
Dosage form | 15 mg/kg i.p.; days 8 and 15 |
Application | In experimental autoimmune encephalomyelitis (EAE) mice, Etomoxir reduced disease severity and the inflammatory response. Etomoxir-treated mice displayed a reduced immune cell infiltration in the CNS with few macrophages, activated microglia, or T cells present. Etomoxir also reduced inflammation and demyelination in the CNS. |
Other notes | Please test the solubility of all compounds indoor, and the actual solubility may slightly differ with the theoretical value. This is caused by an experimental system error and it is normal. |
| 文献引用 | |
| 产品描述 | Etomoxir ((R)-(+)-Etomoxir) 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. 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]. 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: |
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