The Ph.D. Program of Biotechnology and Biomedical Industry, China Medical University, Taichung, 40403, Taiwan.
Department of Medical Laboratory Science and Biotechnology, China Medical University, Taichung, 40403, Taiwan.
Sci Rep. 2022 Jan 7;12(1):303. doi: 10.1038/s41598-021-03590-4.
Targeting the programmed cell death protein 1/programmed cell death ligand 1 (PD-1/PD-L1) axis with monoclonal antibodies (mAbs) represents a crucial breakthrough in anticancer therapy, but mAbs are limited by their poor oral bioavailability, adverse events in multiple organ systems, and primary, adaptive, and acquired resistance, amongst other issues. More recently, the advent of small molecule inhibitors that target the PD-1/PD-L1 axis have shown promising cellular inhibitory activity and the potential to counteract the disadvantages of mAbs. In this study, structure-based virtual screening identified small molecule inhibitors that effectively inhibited the PD-1/PD-L1 interaction. Six of those small molecule inhibitors were applied to cell-based experiments targeting PD-1: CH-1, CH-2, CH-3, CH-4, CH-5, and CH-6. Of all 6, CH-4 displayed the lowest cytotoxicity and strongest inhibitory activity towards the PD-1/PD-L1 interaction. The experiments revealed that CH-4 inhibited the interaction of soluble form PD-L1 (sPD-L1) with PD-1 surface protein expressed by KG-1 cells. Investigations into CH-4 analogs revealed that CH-4.7 effectively blocked the PD-1/sPD-L1 interaction, but sustained the secretion of interleukin-2 and interferon-γ by Jurkat cells. Our experiments revealed a novel small molecule inhibitor that blocks the interaction of PD-1/sPD-L1 and potentially offers an alternative PD-1 target for immune checkpoint therapy.
靶向程序性细胞死亡蛋白 1/程序性细胞死亡配体 1(PD-1/PD-L1)轴的单克隆抗体(mAbs)代表了癌症治疗的一个重要突破,但 mAbs 受到其较差的口服生物利用度、多器官系统的不良反应以及原发性、适应性和获得性耐药性等问题的限制。最近,靶向 PD-1/PD-L1 轴的小分子抑制剂的出现显示出有希望的细胞抑制活性,并有可能克服 mAbs 的缺点。在这项研究中,基于结构的虚拟筛选确定了有效抑制 PD-1/PD-L1 相互作用的小分子抑制剂。其中 6 种小分子抑制剂被应用于针对 PD-1 的基于细胞的实验:CH-1、CH-2、CH-3、CH-4、CH-5 和 CH-6。在所有 6 种抑制剂中,CH-4 的细胞毒性最低,对 PD-1/PD-L1 相互作用的抑制活性最强。实验表明,CH-4 抑制可溶性 PD-L1(sPD-L1)与 KG-1 细胞表达的 PD-1 表面蛋白的相互作用。对 CH-4 类似物的研究表明,CH-4.7 有效地阻断了 PD-1/sPD-L1 相互作用,但维持了 Jurkat 细胞中白细胞介素-2 和干扰素-γ的分泌。我们的实验揭示了一种新型小分子抑制剂,可阻断 PD-1/sPD-L1 的相互作用,并可能为免疫检查点治疗提供替代的 PD-1 靶点。