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SARS\u2010CoV\u20102 replication is closely linked to the metabolism of cytosine\u2010containing nucleotides, especially cytidine\u20105\u2032\u2010triphosphate (CTP), such that the integrity of the viral genome is highly sensitive to intracellular CTP levels. CTP synthase (CTPS) catalyzes the rate\u2010limiting step for the <jats:italic>de novo<\/jats:italic> biosynthesis of CTP. Hence, it is of interest to know the effects of the 5\u2032\u2010triphosphate (TP) metabolites of repurposed antiviral agents on CTPS activity. Using <jats:italic>E. coli<\/jats:italic> CTPS as a model enzyme, we show that ribavirin\u20105\u2032\u2010TP is a weak allosteric activator of CTPS, while sofosbuvir\u20105\u2032\u2010TP and adenine\u2212arabinofuranoside\u20105\u2032\u2010TP are both substrates. \u03b2\u2010<jats:sc>d<\/jats:sc>\u2010<jats:italic>N<\/jats:italic><jats:sup>4<\/jats:sup>\u2010Hydroxycytidine\u20105\u2032\u2010TP is a weak competitive inhibitor relative to CTP, but induces filament formation by CTPS. Alternatively, sofosbuvir\u20105\u2032\u2010TP prevented CTP\u2010induced filament formation. 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