Table 2. Cancer-therapy–specific... | American Society of Hematology

Table 2.

Cancer-therapy–specific inhibitors and inducers of CYP3A4 and P-glycoprotein

Cancer-related therapies	Cytochrome p450 CYP3A4	P-glycoprotein
Anthracyclines
Doxorubicin	↓	↑
Idarubicin	↓
Antimycotic agents
Vinblastine	↓	↑
Vincristine	↓
Vinorelbine	↓
Paclitaxel	↑
Topoisomerase inhibitors
Topotecan	↓
Etoposide	↓	↑
Alkylating agents
Cyclophosphamide	↓
Ifosfamide	↓
Lomustine	↓
Tyrosine kinase inhibitors
Afatinib		↓
Alectinib		↓
Ceritinib	↓
Crizotinib	↓	↓
Dasatinib	↓
Ibrutinib		↓
Idelalisib	↓	↓
Imatinib	↓	↓
Lapatinib	↓	↓
Nilotinib	↓	↓
Osimertinib	↓
Vemurafenib	↑	↓
Lenvatinib	↑	↑
Sunitinib		↓
Vandetanib		↓
Immune-modulating agents
Cyclosporine	↓	↓
Sirolimus	↓
Temsirolimus	↓
Tacrolimus	↓	↓
Methylprednisolone	↑
Dexamethasone	↑	↑
Hormonal agents
Tamoxifen	↓	↓
Anastrozole	↓
Bicalutamide	↓
Enzalutamide	↑	↓
Abiraterone	↓	↓
Mitotane	↑
Supportive care
Aprepitant	↑↓
Fosaprepitant	↑↓
Fentanyl	↓
Methadone	↓
Acetaminophen	↓
Other
Bortezomib	↓
Bexarotene	↑
Venetoclax		↓

Cancer-related therapies	Cytochrome p450 CYP3A4	P-glycoprotein
Anthracyclines
Doxorubicin	↓	↑
Idarubicin	↓
Antimycotic agents
Vinblastine	↓	↑
Vincristine	↓
Vinorelbine	↓
Paclitaxel	↑
Topoisomerase inhibitors
Topotecan	↓
Etoposide	↓	↑
Alkylating agents
Cyclophosphamide	↓
Ifosfamide	↓
Lomustine	↓
Tyrosine kinase inhibitors
Afatinib		↓
Alectinib		↓
Ceritinib	↓
Crizotinib	↓	↓
Dasatinib	↓
Ibrutinib		↓
Idelalisib	↓	↓
Imatinib	↓	↓
Lapatinib	↓	↓
Nilotinib	↓	↓
Osimertinib	↓
Vemurafenib	↑	↓
Lenvatinib	↑	↑
Sunitinib		↓
Vandetanib		↓
Immune-modulating agents
Cyclosporine	↓	↓
Sirolimus	↓
Temsirolimus	↓
Tacrolimus	↓	↓
Methylprednisolone	↑
Dexamethasone	↑	↑
Hormonal agents
Tamoxifen	↓	↓
Anastrozole	↓
Bicalutamide	↓
Enzalutamide	↑	↓
Abiraterone	↓	↓
Mitotane	↑
Supportive care
Aprepitant	↑↓
Fosaprepitant	↑↓
Fentanyl	↓
Methadone	↓
Acetaminophen	↓
Other
Bortezomib	↓
Bexarotene	↑
Venetoclax		↓

Adapted from Short and Connors.¹⁹ Cancer-treatment specific inducers (↑) and inhibitors (↓) of cytochrome p450 CYP3A4 and P-glycoprotein are shown. DOACs are substrates to CYP3A4 and P-glycoprotein enzymes. Inducers of these enzymes may potentially increase metabolization of DOACs thereby leading to lower plasma concentrations, and inhibitors may decrease metabolization leading to higher plasma concentrations. Edoxaban, rivaroxaban, and apixaban are reported to have major interactions with the P-glycoprotein pathway. Rivaroxaban and apixaban are reported to have major interactions with the CYP3A4 pathway whereas edoxaban has been reported to have minor interactions. Dabigatran has moderate interactions with the P-glycoprotein pathway. The extent to which plasma concentrations of DOACs are influenced by inducers or inhibitors of CYP3A4 and P-glycoprotein is unknown.

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