Keretsu Seketoulie, Ghosh Suparna, Cho Seung Joo
Department of Biomedical Sciences, College of Medicine, Chosun University, 375 Seosuk-dong, Dong-gu, Gwangju, 501-759, Republic of Korea.
Department of Cellular Molecular Medicine, College of Medicine, Chosun University, Gwangju, 501-759, Republic of Korea.
Sci Rep. 2021 Nov 29;11(1):23051. doi: 10.1038/s41598-021-02364-2.
Janus kinases (JAKs) are a family of non-receptor kinases that play a key role in cytokine signaling and their aberrant activities are associated with the pathogenesis of various immune diseases. The JAK1 isoform plays an essential role in the types 1 and II interferon signaling and elicits signals from the interleukin-2, interleukin-4, gp130, and class 2 receptor families. It is ubiquitously expressed in humans and its overexpression has been linked with autoimmune diseases such as myeloproliferative neoplasm. Although JAK1 inhibitors such as Tofacitinib have been approved for medical use, the low potency and off-target effects of these inhibitors have limited their use and calls for the development of novel JAK1 inhibitors. In this study, we used computational methods on a series of pyrrolopyridine derivatives to design new JAK1 inhibitors. Molecular docking and molecular dynamics simulation methods were used to study the protein-inhibitor interactions. 3D-quantitative structure-activity relationship models were developed and were used to predict the activity of newly designed compounds. Free energy calculation methods were used to study the binding affinity of the inhibitors with JAK1. Of the designed compounds, seventeen of the compounds showed a higher binding energy value than the most active compound in the dataset and at least six of the compounds showed higher binding energy value than the pan JAK inhibitor Tofacitinib. The findings made in this study could be utilized for the further development of JAK1 inhibitors.
Janus激酶(JAKs)是一类非受体激酶家族,在细胞因子信号传导中起关键作用,其异常活性与多种免疫疾病的发病机制相关。JAK1亚型在I型和II型干扰素信号传导中起重要作用,并引发来自白细胞介素-2、白细胞介素-4、gp130和2类受体家族的信号。它在人类中普遍表达,其过表达与骨髓增殖性肿瘤等自身免疫性疾病有关。尽管托法替布等JAK1抑制剂已被批准用于医学用途,但这些抑制剂的低效性和脱靶效应限制了它们的使用,因此需要开发新型JAK1抑制剂。在本研究中,我们对一系列吡咯并吡啶衍生物采用计算方法来设计新的JAK1抑制剂。使用分子对接和分子动力学模拟方法研究蛋白质-抑制剂相互作用。建立了3D定量构效关系模型,并用于预测新设计化合物的活性。使用自由能计算方法研究抑制剂与JAK1的结合亲和力。在设计的化合物中,有17种化合物的结合能值高于数据集中活性最高的化合物,至少有6种化合物的结合能值高于泛JAK抑制剂托法替布。本研究中的发现可用于JAK1抑制剂的进一步开发。