Bebernitz G R, Aicher T D, Stanton J L, Gao J, Shetty S S, Knorr D C, Strohschein R J, Tan J, Brand L J, Liu C, Wang W H, Vinluan C C, Kaplan E L, Dragland C J, DelGrande D, Islam A, Lozito R J, Liu X, Maniara W M, Mann W R
Metabolic and Cardiovascular Disease Research, Novartis Institute for Biomedical Research, Summit, New Jersey 07901, USA.
J Med Chem. 2000 Jun 1;43(11):2248-57. doi: 10.1021/jm0000923.
The optimization of a series of anilide derivatives of (R)-3,3, 3-trifluoro-2-hydroxy-2-methylpropionic acid as inhibitors of pyruvate dehydrogenase kinase (PDHK) is described that started from N-phenyl-3,3,3-trifluoro-2-hydroxy-2-methylpropanamide 1 (IC(50) = 35 +/- 1.4 microM). It was found that small electron-withdrawing groups on the ortho position of the anilide, i.e., chloro, acetyl, or bromo, increased potency 20-40-fold. The oral bioavailability of the compounds in this series is optimal (as measured by AUC) when the anilide is substituted at the 4-position with an electron-withdrawing group (i.e., carboxyl, carboxyamide, and sulfoxyamide). N-(2-Chloro-4-isobutylsulfamoylphenyl)-(R)-3,3, 3-trifluoro-2-hydroxy-2-methylpropionamide (10a) inhibits PDHK in the primary enzymatic assay with an IC(50) of 13 +/- 1.5 nM, enhances the oxidation of [(14)C]lactate into (14)CO(2) in human fibroblasts, lowers blood lactate levels significantly 2.5 and 5 h after oral doses as low as 30 micromol/kg, and increases the ex vivo activity of PDH in muscle, kidney, liver, and heart tissues. However, in contrast to sodium dichloroacetate (DCA), these PDHK inhibitors did not lower blood glucose levels. Nevertheless, they are effective at increasing the utilization and disposal of lactate and could be of utility to ameliorate conditions of inappropriate blood lactate elevation.
本文描述了一系列(R)-3,3,3-三氟-2-羟基-2-甲基丙酸的酰苯胺衍生物作为丙酮酸脱氢酶激酶(PDHK)抑制剂的优化过程,该过程始于N-苯基-3,3,3-三氟-2-羟基-2-甲基丙酰胺1(IC50 = 35±1.4μM)。研究发现,酰苯胺邻位上的小吸电子基团,即氯、乙酰基或溴,可使活性提高20-40倍。当酰苯胺在4-位被吸电子基团(即羧基、羧酰胺和磺氧基酰胺)取代时,该系列化合物的口服生物利用度最佳(通过AUC测量)。N-(2-氯-4-异丁基氨磺酰基苯基)-(R)-3,3,3-三氟-2-羟基-2-甲基丙酰胺(10a)在初级酶学测定中抑制PDHK,IC50为13±1.5 nM,可增强人成纤维细胞中[(14)C]乳酸氧化为(14)CO2的能力,口服低至30μmol/kg剂量后2.5小时和5小时可显著降低血乳酸水平,并增加肌肉、肾脏、肝脏和心脏组织中PDH的体外活性。然而,与二氯乙酸钠(DCA)不同,这些PDHK抑制剂不会降低血糖水平。尽管如此,它们在增加乳酸的利用和清除方面是有效的,可能有助于改善血乳酸异常升高的情况。