ReviewFrontiers in pharmacology2026
Cellular pharmacology of fludarabine: molecular determinants of transport and metabolism.
Review in Frontiers in pharmacology, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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7 authors.
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Abstract
Fludarabine monophosphate is an antimetabolite and a cornerstone of hematology and oncology treatments, with expanding clinical applications in hematological malignancies, stem cell transplantation conditioning, and chimeric antigen receptor T-cell (CAR-T) therapy. Despite widespread clinical use, there is substantial interpatient pharmacokinetic variability with up to 14.5-fold differences in drug exposure. Suboptimal exposures (both under- and overexposure) correlate directly with both treatment failure and non-relapse mortality, emphasizing the critical need for personalized dosing strategies. The therapeutic efficacy of fludarabine is determined by complex transport and metabolic processes. Cellular uptake is mediated primarily by human equilibrative (hENT1, hENT2) and concentrative nucleoside transporters (hCNT2, hCNT3). Once intracellular, deoxycytidine kinase catalyzes the rate-limiting phosphorylation step, converting fludarabine to its pharmacologically active triphosphate, which inhibits DNA synthesis and repair, ultimately driving cytotoxicity. The elimination mechanisms of fludarabine involve multiple pathways: cytoplasmic 5'-nucleotidase II and CD73-mediated dephosphorylation, while UDP-glucuronosyltransferases (particularly UGT2B17) catalyze glucuronidation-based elimination. The breast cancer resistance protein (BCRP/
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