(R)-(+)-etomoxir sodium salt is inhibitor of carnitine palmitoyltransferase I (CPT1) and can reduce β-oxidation in mitochondria. It shows inhibition of cardiolipin biosynthesis.
Oxidation of long-chain fatty acids inside of the mitochondrial matrix provides an essential source of energy for some cells. Since long-chain fatty acids cannot freely pass into the mitochondrial matrix, they rely on a protein called carnitine palmitoyltransferase I (CPT1) for transport. CPT1 has been identified as a potential therapeutic target for a growing list of cancers that include breast cancer, prostate cancer, glioblastoma, colon cancer, gastric cancer, myeloma, and others[3]. (R)-(+)-etomoxir sodium salt is an inhibitor of carnitine palmitoyltransferase I (CPT1). Etomoxir at 10-6 M prevented the palmitate-induced depression of function in heart but did not decrease myocardial long chain acylcarnitine or long chain acyl-CoA levels, and oxygen consumption per unit work was decreased during reperfusion recovery, and ATP and creatine-phosphate levels were significantly higher after reperfusion[4]. 200 μM of etomoxir caused a significant reduction in cellular proliferation rate in BT549 cells, while 10 μM did not. 200 μM etomoxir treatment, however, significantly impaired mitochondrial respiration in BT549 cells, and a 65% decrease in basal respiration and a 65% decrease in maximal respiratory capacity after treating cells with 200 μM etomoxir was measured[3]. Non-insulin-dependent diabetes mellitus (NIDDM) patients who received oral etomoxir treatment twice daily at the dose of 25 mg to 100 mg showed dose-dependent decrease in fasting blood glucose[5].
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