TABLE 1.

Summary of safety and the enzymes involved in the metabolism and CYP induction of strong CYP3A inducers

	Therapeutic class	Metabolizing enzymes a	CYP induction			Mechanism of induction a	Safety
			Strong	Moderate	Weak
Apalutamide	Antiandrogen	CYP2C8 CYP3A4	CYP2C19 CYP3A		CYP2C9	PXR	QT prolongation
Avasimibe	Antilipemic	NA	CYP3A	CYP2C9		PXR
Carbamazepine	Anticonvulsant	CYP3A4 CYP2C8 UGT2B7	CYP2B6 CYP3A	CYP2C8 CYP2C9	CYP1A2 CYP2C19	CAR/PXR	NTR
Enzalutamide	Antiandrogen	CYP2C8 CYP3A	CYP3A	CYP2C9 CYP2C19		PXR/CAR
Ivosidenib b	Anticancer	CYP3A4 CYP2B6 CYP2C8	CYP3A		CYP2C8		QT prolongation
Lumacaftor	Cystic Fibrosis Treatment	CYP3A4 (minor)	CYP3A	CYP2B6 c ; CYP2C8 c ; CYP2C9 c ; CYP2C19 c		PXR
Mitotane	Antineoplastic	NA	CYP3A				NTR
Phenytoin	Anticonvulsant	CYP2C9 CYP2C19	CYP3A	CYP1A CYP2C19		CAR/PXR	NTR
Rifampicin d	Antibiotic	AADAC UGT e	CYP2C19 CYP3A	CYP1A2 CYP2B6 CYP2C8 CYP2C9		PXR
Rifapentine	Antibiotic	AADAC	CYP3A	CYP2C8 c CYP2C9 c		PXR
St. John’s wort extract	Herbal Medication	CYP3A4 f CYP2C8/9/19	CYP3A		CYP2C9 CYP2C19	PXR

Note: Gray boxes: None.

Abbreviations: NA, not available; NTR, narrow therapeutic range.

^a Bolded refers to primary pathway.

^b Physiologically‐based pharmacokinetic (PBPK) modeling was used to assess drug‐drug interaction potential.

^c Possible DDIs were assessed at clinically relevant concentration from in vitro data.

^d No definitive information on CYP3A involvement in metabolism of rifampicin.

^e Asaumi et al. assigned fm (0.76) through UGTs in PBPK modeling. ⁹⁶

^f Enzyme responsible for hyperforin metabolism. Hyperforin, a constituent of St. John’s Wart, responsible for CYP3A induction.