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I was called to answer some important questions to
discuss potential interactions, the effect of polymorphism of P-
glycoprotein and the effect of absence of Cremophor, an inhibitor of P-
glycoprotein, on the pharmacokinetics and pharmacodynamics of
paclitaxel and I am in trouble.
It is well known that CrEL, the common vehicle used in clinical for
taxol , is a P-gp inhibitor and as such may facilitate the penetration
of the drug within cell, overcoming MDR of paclitaxel which is
substrate for P-gp. On the other hands, it is also known that CrEl
does affect the disposition of paclitaxel , heavily influencing the
PK and PD characteristics of the drug, with the consequent known
toxicity. Based on this consideration and according to what reported
in the literature the absence of CrEl should give an improvement on
the PK/PD of paclitaxel and in some cases have been demonstrated. My
question is: how can change the role of P-gp polymorphism in the
presence or absence of CrEL on paclitaxel PK/PD?
I know that it is a complicated answer
thanks so much
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