it's a question of semantics - it is simply a more potent version in the sense that the final common pathway is the same. by requiring only 2 versus 3 phospholylation steps to achieve the active triphosphate enables it to be dosed in such a way to achieve greater levels of the active moiety since there is lower toal drug exposure and off target toxicity when bypassing the first phosphorylation step, but the ultimate MOA in vivo is really the same (i.e. it does not act via a distinct binding pocket on the polymerase like non-nukes, and so could never be paired as complementary agents)
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