Bhat B Ganesh, Hosea Natilie, Fanjul Andrea, Herrera Jocelyn, Chapman Justin, Thalacker Fred, Stewart Paul M, Rejto Paul A
Diabetes and Metabolism Pharmacology, Genomics Institute of the Novartis Foundation, 10675 John Jay Hopkins Dr., San Diego, CA 92121, USA.
J Pharmacol Exp Ther. 2008 Jan;324(1):299-305. doi: 10.1124/jpet.107.128280. Epub 2007 Oct 5.
Glucocorticoids, through activation of the glucocorticoid receptor (GR), regulate hepatic gluconeogenesis. Elevated hepatic expression and activity of 11beta-hydroxysteroid dehydrogenase type 1 (11betaHSD1) play a key role in ligand-induced activation of the GR through the production of cortisol. Evidence from genetically modified mice suggests that inhibition of 11betaHSD1 might be a therapeutic approach to treat the metabolic syndrome. We have identified a potent 11betaHSD1 inhibitor, 4'-cyano-biphenyl-4-sulfonic acid (6-amino-pyridin-2-yl)-amide (PF-915275), that is selective for the primate and human enzymes. The objective of this study was to demonstrate target inhibition with PF-915275 and to quantify the relationship between target inhibition and drug exposure in monkeys. We characterized the ability of PF-915275 to inhibit the conversion of prednisone, a synthetic cortisone analog that can be distinguished from the endogenous substrate cortisone, enabling a direct measure of substrate to product conversion without the complication of feedback. Adult cynomolgus monkeys were administered either vehicle or various doses of PF-915275 followed by a 10-mg/kg dose of prednisone. Prednisone conversion to prednisolone and the concentrations of PF-915275 were measured by liquid chromatography/tandem mass spectrometry. PF-915275 dose-dependently inhibited 11betaHSD1-mediated conversion of prednisone to prednisolone, with a maximum of 87% inhibition at a 3-mg/kg dose. An exposure-response relationship was demonstrated, with an estimated EC(50) of 391 nM (total) and 17 nM (free). Insulin levels were also reduced in a dose-related manner. These results should enable the development of a biomarker for evaluating target modulation in humans that will aid in identifying 11betaHSD1 inhibitors to treat diabetes and other related metabolic diseases.
糖皮质激素通过激活糖皮质激素受体(GR)来调节肝脏糖异生。11β-羟基类固醇脱氢酶1型(11βHSD1)在肝脏中的表达和活性升高,通过产生皮质醇在配体诱导的GR激活中起关键作用。基因改造小鼠的证据表明,抑制11βHSD1可能是治疗代谢综合征的一种治疗方法。我们已经鉴定出一种有效的11βHSD1抑制剂,4'-氰基-联苯-4-磺酸(6-氨基-吡啶-2-基)-酰胺(PF-915275),它对灵长类和人类酶具有选择性。本研究的目的是证明PF-915275对靶点的抑制作用,并量化猴子体内靶点抑制与药物暴露之间的关系。我们表征了PF-915275抑制泼尼松转化的能力,泼尼松是一种合成的可的松类似物,可与内源性底物可的松区分开来,从而能够直接测量底物到产物的转化,而不会出现反馈的复杂性。给成年食蟹猴给予载体或不同剂量的PF-915275,然后给予10mg/kg剂量的泼尼松。通过液相色谱/串联质谱法测量泼尼松向泼尼松龙的转化以及PF-915275的浓度。PF-915275剂量依赖性地抑制11βHSD1介导的泼尼松向泼尼松龙的转化,在3mg/kg剂量时最大抑制率为87%。证明了暴露-反应关系,估计的EC(50)为391 nM(总浓度)和17 nM(游离浓度)。胰岛素水平也以剂量相关的方式降低。这些结果应该能够开发出一种用于评估人类靶点调节的生物标志物,这将有助于识别治疗糖尿病和其他相关代谢疾病的11βHSD1抑制剂。