Johns Hopkins Drug Discovery, The Johns Hopkins University School of Medicine, Baltimore, MD, United States; Department of Pharmacology and Molecular Sciences, The Johns Hopkins University School of Medicine, Baltimore, MD, United States.
Adv Pharmacol. 2024;101:265-285. doi: 10.1016/bs.apha.2024.10.001. Epub 2024 Oct 15.
Over the past decade, the zinc metalloenzyme glutamate carboxypeptidase (GCPII) has emerged as a novel therapeutic target for IBD. This enzyme is minimally expressed in healthy ileum or colon, but is profoundly upregulated in multiple IBD subtypes including: adult and pediatric Crohn's disease (CD), adult and pediatric ulcerative colitis (UC), and UC pouchitis. Encouragingly, small molecule GCPII inhibitors display promising efficacy in chemical and genetic preclinical colitis models. In this chapter we will: (1) review GCPII biology, (2) present the data confirming its upregulation in IBD patients at gene and protein levels, (3) discuss foundational pre-clinical studies that established the anti-colitis efficacy of small molecule GCPII inhibitors, and (4) introduce the rationale and development of a novel class of GCPII inhibitors, including lead compound (S)-IBD3540, which hold therapeutic promise for IBD.
在过去的十年中,锌金属酶谷氨酸羧肽酶(GCPII)已成为炎症性肠病(IBD)的一个新的治疗靶点。这种酶在健康的回肠或结肠中表达很少,但在多种 IBD 亚型中显著上调,包括:成人和儿童克罗恩病(CD)、成人和儿童溃疡性结肠炎(UC)和 UC pouchitis。令人鼓舞的是,小分子 GCPII 抑制剂在化学和遗传结肠炎模型中显示出有希望的疗效。在本章中,我们将:(1)回顾 GCPII 的生物学特性,(2)介绍其在 IBD 患者基因和蛋白水平上调的证据,(3)讨论确立小分子 GCPII 抑制剂抗结肠炎疗效的基础临床前研究,以及(4)介绍一类新型 GCPII 抑制剂的原理和开发,包括先导化合物(S)-IBD3540,它们为 IBD 提供了治疗希望。