Institute for Drug Research and Development, S.E. Bogoro Center, Afe Babalola University, Ado-Ekiti, Nigeria; Department of Pharmacology and Toxicology, College of Pharmacy, Afe Babalola University, Ado-Ekiti, Nigeria; Bio-Computing & Drug Research Unit, Mols and Sims, Ado Ekiti, Ekiti State, Nigeria.
Department of Pharmacology and Toxicology, College of Pharmacy, Afe Babalola University, Ado-Ekiti, Nigeria.
Microb Pathog. 2023 Mar;176:105994. doi: 10.1016/j.micpath.2023.105994. Epub 2023 Jan 20.
The development of clinically actionable pharmaceuticals against coronavirus disease (COVID-19); an infectious disease caused by the SARS-CoV-2 virus is very important for ending the pandemic. Coronavirus spike glycoprotein (GP)-Receptor Binding Domain (RBD) and its interaction with host receptor angiotensin converting enzyme 2 (ACE2) is one of the most structurally understood but therapeutically untapped aspect of COVID-19 pathogenesis. Binding interface based on previous x-ray structure of RBD/ACE2 were virtually screened to identify fragments with high-binding score from 12,000 chemical building blocks. The hit compound was subjected to fingerprint-based similarity search to identify compounds within the FDA-approved drug library containing the same core scaffold. Identified compounds were then re-docked into of RBD/ACE2. The best ranked compound was validated for RBD/ACE2 inhibition using commercial kit. Molecular dynamics simulation was conducted to provide further insight into the mechanism of inhibition. From the original 12000 chemical building blocks, benzimidazole (BAZ) scaffold was identified. Fingerprint-based similarity search of the FDA-approved drug library for BAZ-containing compounds identified 12 drugs with the benzimidazole-like substructure. When these compounds were re-docked into GP/ACE2 interface, the consensus docking identified bazedoxifene as the hit. In vitro RBD/ACE2 inhibition kinetics showed micromolar IC50 value (1.237 μM) in the presence of bazedoxifene. Molecular dynamics simulation of RBD/ACE2 in the presence BAZ resulted in loss of contact and specific hydrogen-bond interaction required for RBD/ACE2 stability. Taken together, these findings identified benzimidazole scaffold as a building block for developing novel RBD/ACE2 complex inhibitor and provided mechanistic basis for the use of bazedoxifene as a repurposable drug for the treatment of COVID-19 acting at RBD/ACE2 interface.
针对由 SARS-CoV-2 病毒引起的传染性疾病 COVID-19 开发具有临床应用潜力的药物对于结束大流行非常重要。冠状病毒刺突糖蛋白(GP)-受体结合域(RBD)及其与宿主受体血管紧张素转换酶 2(ACE2)的相互作用是 COVID-19 发病机制中结构研究最透彻但治疗尚未开发的方面之一。基于以前 RBD/ACE2 的 X 射线结构,对结合界面进行虚拟筛选,从 12000 个化学构建块中鉴定出具有高结合评分的片段。对命中化合物进行基于指纹的相似性搜索,以鉴定 FDA 批准药物库中含有相同核心支架的化合物。然后将鉴定出的化合物重新对接至 RBD/ACE2。使用商业试剂盒对最佳排名的化合物进行 RBD/ACE2 抑制验证。进行分子动力学模拟以提供对抑制机制的进一步了解。从最初的 12000 个化学构建块中,鉴定出苯并咪唑(BAZ)支架。对 FDA 批准药物库中含有 BAZ 化合物的基于指纹的相似性搜索确定了 12 种具有苯并咪唑类似结构的药物。当这些化合物重新对接至 GP/ACE2 界面时,共识对接确定巴泽多昔芬为命中化合物。体外 RBD/ACE2 抑制动力学显示,在存在巴泽多昔芬的情况下,IC50 值为微摩尔级(1.237μM)。在存在 BAZ 的情况下,RBD/ACE2 的分子动力学模拟导致 RBD/ACE2 稳定性所需的接触和特定氢键相互作用丧失。总之,这些发现确定了苯并咪唑支架作为开发新型 RBD/ACE2 复合物抑制剂的构建块,并为使用巴泽多昔芬作为作用于 RBD/ACE2 界面的 COVID-19 再利用药物提供了机制基础。