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1 of a fluorine atom at C3 of 3DUrd shifts its antimetabolic action to inhibition of the orotidylate de
3 ity allows pathogens to evolve resistance to antimetabolic drugs by acquiring new metabolic pathways
4 = 23.3 muM) coupled with the absence of any antimetabolic effect (CC50 > 224 muM; SI > 28) in a cell
6 on of hindbrain catecholamine neurons by the antimetabolic glucose analogue, 2-deoxy-D-glucose (2DG;
7 volumes of 5-thio-D-glucose (5TG), a potent antimetabolic glucose analogue, were studied at 142 hind
8 ility to monitor biomarkers for responses to antimetabolic therapy in real-time, paving the way for c
9 results offer a rationale to evaluate novel antimetabolic treatment strategies being developed in ot
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