Kandeel Mahmoud, Yamamoto Mizuki, Tani Hideki, Kobayashi Ayako, Gohda Jin, Kawaguchi Yasushi, Park Byoung Kwon, Kwon Hyung-Joo, Inoue Jun-Ichiro, Alkattan Abdallah
Department of Biomedical Sciences, College of Veterinary Medicine, King Faisal University, Al-Ahsa 31982, Saudi Arabia.
Department of Pharmacology, Faculty of Veterinary Medicine, Kafrelsheikh University, Kafrelsheikh 33516, Egypt.
Biomol Ther (Seoul). 2021 May 1;29(3):282-289. doi: 10.4062/biomolther.2020.201.
A novel coronavirus, severe acute respiratory syndrome coronavirus-2 (SARS-CoV-2), caused a worldwide pandemic. Our aim in this study is to produce new fusion inhibitors against SARS-CoV-2, which can be the basis for developing new antiviral drugs. The fusion core comprising the heptad repeat domains (HR1 and HR2) of SARS-CoV-2 spike (S) were used to design the peptides. A total of twelve peptides were generated, comprising a short or truncated 24-mer (peptide #1), a long 36-mer peptide (peptide #2), and ten peptide #2 analogs. In contrast to SARS-CoV, SARS-CoV-2 S-mediated cell-cell fusion cannot be inhibited with a minimal length, 24-mer peptide. Peptide #2 demonstrated potent inhibition of SARS-CoV-2 S-mediated cell-cell fusion at 1 µM concentration. Three peptide #2 analogs showed IC50 values in the low micromolar range (4.7-9.8 µM). Peptide #2 inhibited the SARS-CoV-2 pseudovirus assay at IC50=1.49 µM. Given their potent inhibition of viral activity and safety and lack of cytotoxicity, these peptides provide an attractive avenue for the development of new prophylactic and therapeutic agents against SARS-CoV-2.
一种新型冠状病毒,即严重急性呼吸综合征冠状病毒2(SARS-CoV-2),引发了全球大流行。我们在本研究中的目标是生产针对SARS-CoV-2的新型融合抑制剂,这可为开发新型抗病毒药物奠定基础。利用包含SARS-CoV-2刺突蛋白(S)七肽重复结构域(HR1和HR2)的融合核心来设计肽段。共生成了12种肽段,包括一种短的或截短的24肽(肽段#1)、一种长的36肽(肽段#2)以及10种肽段#2类似物。与SARS-CoV不同,SARS-CoV-2 S介导的细胞-细胞融合不能被最短长度的24肽所抑制。肽段#2在1 µM浓度下对SARS-CoV-2 S介导的细胞-细胞融合表现出强效抑制作用。三种肽段#2类似物的IC50值在低微摩尔范围内(4.7 - 9.8 µM)。肽段#2在IC50 = 1.49 µM时抑制了SARS-CoV-2假病毒试验。鉴于它们对病毒活性的强效抑制作用、安全性以及缺乏细胞毒性,这些肽段为开发针对SARS-CoV-2的新型预防和治疗药物提供了一条有吸引力的途径。