Key result
A phenotypic switch of P-gp from normal to poor metabolizer increased apixaban and rivaroxaban AUC0−6h by 16% and 25%, respectively (p < 0.001).
Why the study?
Current dose-adjustment recommendations for apixaban and rivaroxaban do not consider CYP3A and P-gp genotype and phenotype, despite safety concerns from drug-drug interactions with CYP3A/P-gp modulators.
Does CYP3A and P-gp genotype and phenotype impact apixaban and rivaroxaban blood exposure in hospitalized patients?
Observational (n=300)
Does CYP3A and P-gp genotype and phenotype impact apixaban and rivaroxaban blood exposure in hospitalized patients?
p-value: p=<0.001
P-gp phenotypic activity, rather than known CYP3A/P-gp polymorphisms, significantly impacts apixaban and rivaroxaban exposure and could be relevant for dose adjustment.
P-gp phenotype may modestly affect apixaban/rivaroxaban exposure; hypothesis-generating and should not yet change dosing practice.
Apixaban and rivaroxaban are the two most prescribed direct factor Xa inhibitors. With the increased use of DOACs in real-world settings, safety and efficacy concerns have emerged, particularly regarding their concomitant use with other drugs. Increasing evidence highlights drug−drug interactions with CYP3A/P-gp modulators leading to adverse events. However, current recommendations for dose adjustment do not consider CYP3A/P-gp genotype and phenotype. We aimed to determine their impact on apixaban and rivaroxaban blood exposure. Three-hundred hospitalized patients were included. CYP3A and P-gp phenotypic activities were assessed by the metabolic ratio of midazolam and AUC0−6h of fexofenadine, respectively. Relevant CYP3A and ABCB1 genetic polymorphisms were also tested. Capillary blood samples collected at four time-points after apixaban or rivaroxaban administration allowed the calculation of pharmacokinetic parameters. According to the developed multivariable linear regression models, P-gp activity (p < 0.001) and creatinine clearance (CrCl) (p = 0.01) significantly affected apixaban AUC0−6h. P-gp activity (p < 0.001) also significantly impacted rivaroxaban AUC0−6h. The phenotypic switch (from normal to poor metabolizer) of P-gp led to an increase of apixaban and rivaroxaban AUC0−6h by 16% and 25%, respectively, equivalent to a decrease of 38 mL/min in CrCl according to the apixaban model. CYP3A phenotype and tested SNPs of CYP3A/P-gp had no significant impact. In conclusion, P-gp phenotypic activity, rather than known CYP3A/P-gp polymorphisms, could be relevant for dose adjustment.
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Lenoir et al. (2022) conducted an observational in Patients taking apixaban or rivaroxaban (n=300). P-gp and CYP3A genotype and phenotype vs. Normal metabolizer phenotype was evaluated on Apixaban and rivaroxaban blood exposure (AUC0−6h) (p=<0.001). A phenotypic switch of P-gp from normal to poor metabolizer increased apixaban and rivaroxaban AUC0−6h by 16% and 25%, respectively (p < 0.001).
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