Abstract
Despite being a common viral disease, influenza has very negative consequences, causing the death of around half a million people each year. A neuraminidase located on the surface of the virus plays an important role in viral reproduction by contributing to the release of viruses from infected host cells. The treatment of influenza is mainly based on the administration of neuraminidase inhibitors. The neuraminidase inhibitors zanamivir, laninamivir, oseltamivir and peramivir have been commercialized and have been demonstrated to be potent influenza viral neuraminidase inhibitors against most influenza strains. In order to create more potent neuraminidase inhibitors and fight against the surge in resistance resulting from naturally-occurring mutations, these anti-influenza drugs have been used as templates for the development of new neuraminidase inhibitors through structure-activity relationship studies. Here, we review the synthetic routes to these commercial drugs, the modifications which have been performed on these structures and the effects of these modifications on their inhibitory activity.
Highlights
Influenza is a serious viral illness which can lead to hospitalization and death, especially in the elderly [1,2,3]
[53], which predict that zanamivir sulfonate, oseltamivir sulfonate and acidcarboxylic moiety [53], which predict that zanamivir sulfonate, oseltamivir sulfonate and peramivir sulfonate peramivir sulfonate should all exhibit stronger binding to avian influenza neuraminidase
Wulff and coworkers carried out a study on the inhibitory activity of de-guanidinylated peramivir analogue [139], with the results suggesting that the lack of the guanidine group in the peramivir structure had no effect on the inhibitory activity against H1N1 neuraminidases
Summary
Influenza is a serious viral illness which can lead to hospitalization and death, especially in the elderly [1,2,3]. It has been shown inshown tissue culture that neuraminidase activity is required destroy viral receptors by [13,14,15,16,17]. It has been in tissue culture that neuraminidase activity to is required to destroy viral removing the sialic acid of the hemagglutinin-sialic acid linkage, thereby contributing to the release of receptors by removing the sialic acid of the hemagglutinin-sialic acid linkage, thereby contributing progeny viruses from infected cells [18,19,20]. The RNA is released into the cytoplasm; (D) Viral proteins are synthetized and directed to the membrane for for virus assembly. DANA has never been commercialized, its first influenza neuraminidase inhibitor reported (Figure 2) [27]. The following synthetic routes to produce zanamivir have been reported
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