Institute of Biological Psychiatry, Mental Health Centre Sct. Hans, DK-4000 Roskilde, Denmark.
Department of Science and Environment, Roskilde University Center, DK-4000 Roskilde, Denmark.
Viruses. 2021 Jul 14;13(7):1369. doi: 10.3390/v13071369.
GS-441524 is an adenosine analog and the parent nucleoside of the prodrug remdesivir, which has received emergency approval for treatment of COVID-19. Recently, GS-441524 has been proposed to be effective in the treatment of COVID-19, perhaps even being superior to remdesivir for treatment of this disease. Evaluation of the clinical effectiveness of GS-441524 requires understanding of its uptake and intracellular conversion to GS-441524 triphosphate, the active antiviral substance. We here discuss the potential impact of these pharmacokinetic steps of GS-441524 on the formation of its active antiviral substance and effectiveness for treatment of COVID-19. Available protein expression data suggest that several adenosine transporters are expressed at only low levels in the epithelial cells lining the alveoli in the lungs, i.e., the alveolar cells or pneumocytes from healthy lungs. This may limit uptake of GS-441524. Importantly, cellular uptake of GS-441524 may be reduced during hypoxia and inflammation due to decreased expression of adenosine transporters. Similarly, hypoxia and inflammation may lead to reduced expression of adenosine kinase, which is believed to convert GS-441524 to GS-441524 monophosphate, the perceived rate-limiting step in the intracellular formation of GS-441524 triphosphate. Moreover, increases in extracellular and intracellular levels of adenosine, which may occur during critical illnesses, has the potential to competitively decrease cellular uptake and phosphorylation of GS-441524. Taken together, tissue hypoxia and severe inflammation in COVID-19 may lead to reduced uptake and phosphorylation of GS-441524 with lowered therapeutic effectiveness as a potential outcome. Hypoxia may be particularly critical to the ability of GS-441524 to eliminate SARS-CoV-2 from tissues with low basal expression of adenosine transporters, such as alveolar cells. This knowledge may also be relevant to treatments with other antiviral adenosine analogs and anticancer adenosine analogs as well.
GS-441524 是一种腺苷类似物,也是前药瑞德西韦的核苷,瑞德西韦已获得治疗 COVID-19 的紧急批准。最近,GS-441524 被提议可有效治疗 COVID-19,其疗效甚至可能优于瑞德西韦。评估 GS-441524 的临床疗效需要了解其摄取和细胞内转化为 GS-441524 三磷酸,即活性抗病毒物质。我们在这里讨论 GS-441524 的这些药代动力学步骤对其活性抗病毒物质的形成及其治疗 COVID-19 的有效性的潜在影响。现有的蛋白质表达数据表明,几种腺苷转运蛋白仅在肺部肺泡衬里的上皮细胞中低水平表达,即健康肺的肺泡细胞或肺细胞。这可能会限制 GS-441524 的摄取。重要的是,由于腺苷转运蛋白的表达减少,GS-441524 的细胞摄取可能在缺氧和炎症期间减少。同样,缺氧和炎症可能导致腺苷激酶表达减少,据信腺苷激酶将 GS-441524 转化为 GS-441524 一磷酸,这被认为是细胞内 GS-441524 三磷酸形成的限速步骤。此外,在危重病期间,细胞外和细胞内腺苷水平的增加可能会竞争性地降低 GS-441524 的细胞摄取和磷酸化。综上所述,COVID-19 中的组织缺氧和严重炎症可能导致 GS-441524 的摄取和磷酸化减少,从而降低治疗效果。缺氧可能对 GS-441524 从腺苷转运蛋白基础表达低的组织中消除 SARS-CoV-2 的能力特别关键,如肺泡细胞。这一知识可能也与其他抗病毒腺苷类似物和抗癌腺苷类似物的治疗有关。