No formal clinical drug interaction studies with decitabine have been reported.
There is the potential for a drug-drug interaction with other agents which are also activated by sequential phosphorylation (via intracellular phosphokinase activities) and/or metabolized by enzymes implicated in the inactivation of decitabine (e.g., cytidine deaminase). Therefore, caution should be exercised if these drugs are combined with decitabine.
Impact of co-administered drugs on decitabine: CYP450-mediated metabolic drug interactions are not anticipated as decitabine metabolism is not mediated by this system but by oxidative deamination. Displacement of decitabine from its plasma protein binding by co-administered drugs is unlikely given the negligible in vitro plasma protein binding (<1%) of decitabine. In vitro reported data indicated that decitabine is a poor P-glycoprotein (P-gp) substrate and is therefore not prone to interaction with P-gp inhibitors.
Impact of decitabine on co-administered drugs: Given its low in vitro plasma protein binding (<1%), decitabine is unlikely to displace co-administered drugs from their plasma protein binding. In vitro reported studies show that decitabine does not inhibit nor induce CYP450 enzymes up to more than 20-fold of the therapeutic maximum observed plasma concentration (Cmax). Thus, CYP-mediated metabolic drug interactions are not anticipated and is unlikely to interact with agents metabolized through these pathways. Decitabine has been reported to be a weak inhibitor of P-gp mediated transport in vitro and is therefore also not expected to affect P-gp mediated transport of co-administered drugs (see Pharmacology: Pharmacokinetics under Actions).
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