Wandel C, Kim R B, Kajiji S, Guengerich P, Wilkinson G R, Wood A J
Division of Clinical Pharmacology, Vanderbilt University, Nashville, Tennessee 37232-6602, USA.
Cancer Res. 1999 Aug 15;59(16):3944-8.
Many P-glycoprotein (P-gp) inhibitors studied in vitro and in vivo are also known or suspected to be substrates and/or inhibitors of cytochrome P-450 3A (CYP3A). Such overlap raises the question of whether CYP3A inhibition is an intrinsic characteristic of P-gp inhibitors, a matter of concern in the development and rational use of such agents. Thus, the purpose of the present study was to determine whether the ability to inhibit P-gp and CYP3A is, in fact, linked and whether specific P-gp inhibitors with limited ability to inhibit CYP3A can be identified. Therefore, the potency of a series of 14 P-gp inhibitors was assessed by measuring their inhibition of the transepithelial flux across Caco-2 cells of digoxin, a prototypical P-gp substrate. CYP3A inhibition was determined from the impairment of nifedipine oxidation by human liver microsomes. Determination of the apparent Ki values for CYP3A inhibition and the IC50s for P-gp and CYP3A inhibition allowed comparison of the relative inhibitory potency of the compounds on the two proteins' function. The IC50s for P-gp inhibition ranged from 0.04 to 3.8 microM. All compounds inhibited CYP3A with apparent Ki values of between 0.3 and 76 microM and IC50s between 1.5 and 50 microM. However, no correlation was found between the extent of P-gp inhibition and CYP3A inhibition, and the ratio of the IC50 for CYP3A inhibition to the IC50 for P-gp inhibition varied from 1.1 to 125. These results demonstrate that, although many P-gp inhibitors are potent inhibitors of CYP3A, a varying degree of selectivity is present. The development and use of P-gp inhibitors with minimal or absent CYP3A inhibitory effects should decrease the impact of drug interactions on the therapeutic use of such compounds.
许多在体外和体内进行研究的P-糖蛋白(P-gp)抑制剂也已知或被怀疑是细胞色素P-450 3A(CYP3A)的底物和/或抑制剂。这种重叠引发了一个问题,即CYP3A抑制是否是P-gp抑制剂的固有特性,这是此类药物开发和合理使用中令人关注的问题。因此,本研究的目的是确定抑制P-gp和CYP3A的能力实际上是否相关,以及是否可以鉴定出抑制CYP3A能力有限的特异性P-gp抑制剂。因此,通过测量一系列14种P-gp抑制剂对典型P-gp底物地高辛跨Caco-2细胞的上皮转运通量的抑制作用,评估了它们的效力。通过人肝微粒体对硝苯地平氧化作用的损害来确定CYP3A抑制作用。确定CYP3A抑制的表观Ki值以及P-gp和CYP3A抑制的IC50值,可以比较这些化合物对这两种蛋白质功能的相对抑制效力。P-gp抑制的IC50值范围为0.04至3.8 microM。所有化合物均抑制CYP3A,其表观Ki值在0.3至76 microM之间,IC50值在1.5至50 microM之间。然而,未发现P-gp抑制程度与CYP3A抑制程度之间存在相关性,CYP3A抑制的IC50与P-gp抑制的IC50之比在1.1至125之间变化。这些结果表明,尽管许多P-gp抑制剂是CYP3A的有效抑制剂,但存在不同程度的选择性。开发和使用对CYP3A抑制作用最小或无抑制作用的P-gp抑制剂应会减少药物相互作用对这类化合物治疗应用的影响。