Key result
Quinoxaline derivatives disrupt the base stacking of Hepatitis C virus internal ribosome entry site RNA, leading to the inhibition of viral translation and RNA replication.
Quinoxaline derivatives demonstrate potential as antiviral agents by targeting the HCV IRES RNA structure to inhibit translation and replication.
May support RNA-targeted HCV antivirals in preclinical models; leaves open clinical translation.
RNA-biased small molecules with a monoquinoxaline core target the L-shaped structure of subdomain IIa of Hepatitis C virus internal ribosome entry site (IRES) RNA in proximity to the Mg2+ binding site. The binding event leads to the destacking of RNA bases, resulting in the inhibition of IRES-mediated translation and HCV RNA replication.
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Chakraborty et al. (2019) studied this question. Quinoxaline derivatives disrupt the base stacking of Hepatitis C virus internal ribosome entry site RNA, leading to the inhibition of viral translation and RNA replication.
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