Scannevin Robert H, Alexander Richard, Haarlander Tara Mezzasalma, Burke Sharon L, Singer Monica, Huo Cuifen, Zhang Yue-Mei, Maguire Diane, Spurlino John, Deckman Ingrid, Carroll Karen I, Lewandowski Frank, Devine Eric, Dzordzorme Keli, Tounge Brett, Milligan Cindy, Bayoumy Shariff, Williams Robyn, Schalk-Hihi Celine, Leonard Kristi, Jackson Paul, Todd Matthew, Kuo Lawrence C, Rhodes Kenneth J
From Janssen Research and Development, LLC, Spring House, Pennsylvania 19477
From Janssen Research and Development, LLC, Spring House, Pennsylvania 19477.
J Biol Chem. 2017 Oct 27;292(43):17963-17974. doi: 10.1074/jbc.M117.806075. Epub 2017 Aug 31.
Aberrant activation of matrix metalloproteinases (MMPs) is a common feature of pathological cascades observed in diverse disorders, such as cancer, fibrosis, immune dysregulation, and neurodegenerative diseases. MMP-9, in particular, is highly dynamically regulated in several pathological processes. Development of MMP inhibitors has therefore been an attractive strategy for therapeutic intervention. However, a long history of failed clinical trials has demonstrated that broad-spectrum MMP inhibitors have limited clinical utility, which has spurred the development of inhibitors selective for individual MMPs. Attaining selectivity has been technically challenging because of sequence and structural conservation across the various MMPs. Here, through a biochemical and structural screening paradigm, we have identified JNJ0966, a highly selective compound that inhibited activation of MMP-9 zymogen and subsequent generation of catalytically active enzyme. JNJ0966 had no effect on MMP-1, MMP-2, MMP-3, MMP-9, or MMP-14 catalytic activity and did not inhibit activation of the highly related MMP-2 zymogen. The molecular basis for this activity was characterized as an interaction of JNJ0966 with a structural pocket in proximity to the MMP-9 zymogen cleavage site near Arg-106, which is distinct from the catalytic domain. JNJ0966 was efficacious in reducing disease severity in a mouse experimental autoimmune encephalomyelitis model, demonstrating the viability of this therapeutic approach. This discovery reveals an unprecedented pharmacological approach to MMP inhibition, providing an opportunity to improve selectivity of future clinical drug candidates. Targeting zymogen activation in this manner may also allow for pharmaceutical exploration of other enzymes previously viewed as intractable drug targets.
基质金属蛋白酶(MMPs)的异常激活是在多种疾病(如癌症、纤维化、免疫失调和神经退行性疾病)中观察到的病理级联反应的一个共同特征。特别是MMP-9,在几个病理过程中受到高度动态调节。因此,开发MMP抑制剂一直是一种有吸引力的治疗干预策略。然而,长期以来临床试验失败的历史表明,广谱MMP抑制剂的临床效用有限,这促使了对单个MMP具有选择性的抑制剂的开发。由于各种MMP之间的序列和结构保守性,实现选择性在技术上具有挑战性。在这里,通过生化和结构筛选范式,我们鉴定出了JNJ0966,一种高度选择性的化合物,它抑制MMP-9酶原的激活以及随后催化活性酶的产生。JNJ0966对MMP-1、MMP-2、MMP-3、MMP-9或MMP-14的催化活性没有影响,也不抑制高度相关的MMP-2酶原的激活。这种活性的分子基础被确定为JNJ0966与靠近Arg-106附近MMP-9酶原切割位点的一个结构口袋相互作用,该口袋与催化结构域不同。JNJ0966在小鼠实验性自身免疫性脑脊髓炎模型中有效降低了疾病严重程度,证明了这种治疗方法的可行性。这一发现揭示了一种前所未有的MMP抑制药理学方法,为提高未来临床候选药物的选择性提供了机会。以这种方式靶向酶原激活也可能允许对其他以前被视为难以处理的药物靶点的酶进行药物探索。