A common structural feature shared by the representative nucleoside analogues active against HIV is the lack of hydroxyl substituents at the positions C -2′ and C-3′ of the furanose ring.1 These analogues which include AZT, ddI, D4T, ddC, 3′Fddt, are first converted to their 5′-0- triphosphates, which then exert their biological effect either as reverse transcriptase (RT) inhibitors or chain tetminators or both.2
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Sterzycki et al. (1991) studied this question.
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