Farag Marc, Guedeney Nicolas, Schwalen Florian, Zadoroznyj Aymeric, Barczyk Amélie, Giret Martin, Antraygues Kevin, Wang Alice, Cornu Marie, Suzanne Peggy, Since Marc, Sophie Voisin-Chiret Anne, Dubrez Laurence, Leleu-Chavain Natascha, Kieffer Charline, Sopkova-de Oliveira Santos Jana
Department, Normandie Univ, UNICAEN, CERMN, bd Becquerel, F-14000, Caen, Cedex, France.
Institut National de la Santé et de la Recherche Médicale (Inserm), LNC UMR1231, Dijon, France.
ChemMedChem. 2025 Jan 14;20(2):e202400567. doi: 10.1002/cmdc.202400567. Epub 2024 Nov 12.
The X-chromosome-linked inhibitor of apoptosis protein (XIAP) plays a crucial role in controlling cell survival across multiple regulated cell death pathways and coordinating a range of inflammatory signalling events. The discovery of selective inhibitors for XIAP-BIR2, able to disrupt the direct physical interaction between XIAP and RIPK2, offer promising therapeutic options for NOD2-mediated diseases like Crohn's disease, sarcoidosis, and Blau syndrome. The objective of this study was to design, synthesize, and evaluate small synthetic molecules with binding selectivity to XIAP-BIR2 domain. To achieve this, we applied an interdisciplinary drug design approach and firstly we have synthesized an initial fragment library to achieve a first XIAP inhibition activity. Then using a growing strategy, larger compounds were synthesized and one of them presents a good selectivity for XIAP-BIR2 versus XIAP-BIR3 domain, compound 20 c. The ability of compound 20 c to block the NOD1/2 pathway was confirmed in cell models. These data show that we have synthesized molecules capable of blocking NOD1/2 signalling pathways in cellulo, and ultimately leading to new anti-inflammatory compounds.
X染色体连锁凋亡抑制蛋白(XIAP)在控制多种程序性细胞死亡途径中的细胞存活以及协调一系列炎症信号事件方面发挥着关键作用。能够破坏XIAP与RIPK2之间直接物理相互作用的XIAP-BIR2选择性抑制剂的发现,为克罗恩病、结节病和布劳综合征等NOD2介导的疾病提供了有前景的治疗选择。本研究的目的是设计、合成并评估对XIAP-BIR2结构域具有结合选择性的小分子合成化合物。为实现这一目标,我们采用了跨学科药物设计方法,首先合成了一个初始片段库以获得首个XIAP抑制活性。然后采用逐步增长策略合成更大的化合物,其中一种对XIAP-BIR2结构域相对于XIAP-BIR3结构域具有良好的选择性,即化合物20 c。在细胞模型中证实了化合物20 c阻断NOD1/2途径的能力。这些数据表明,我们已经合成了能够在细胞内阻断NOD1/2信号通路的分子,并最终产生新的抗炎化合物。