Drug Interactions between budesonide / formoterol and glofitamab

MONITOR: Coadministration with glofitamab may increase the plasma concentrations of drugs that are substrates of CYP450 isoenzymes. Initiation of glofitamab treatment causes transient release of cytokines that may suppress CYP450 isoenzymes, although the potential for an interaction has not been studied. According to the manufacturer, the highest drug-drug interaction risk would be from the first dose on day 8 of cycle 1, up to 14 days after the first 30 mg dose on day 1 of cycle 2, as well as during and after cytokine release syndrome.

MANAGEMENT: Caution is advised when glofitamab is administered with drugs that are metabolized by CYP450 isoenzymes, particularly sensitive CYP450 substrates and/or those with a narrow therapeutic range, where minimal changes to concentration may lead to significant adverse reactions, such as carbamazepine, colchicine, cyclosporine, disopyramide, phenytoin, quinidine, theophylline, warfarin, macrolide immunosuppressants, vinca alkaloids, and some narcotic analgesics. Clinical and/or laboratory monitoring are recommended, particularly at the initial phase of treatment with glofitamab as well as during and after cytokine release syndrome, and individual product labeling for the CYP450 substrate(s) should be consulted for specific dosage adjustment recommendations.

Although they are often combined in clinical practice, the concomitant use of beta-2 adrenergic agonists and corticosteroids may result in additive hypokalemic effects. Since beta-2 agonists can sometimes cause QT interval prolongation, the development of hypokalemia may potentiate the risk of ventricular arrhythmias including torsade de pointes. However, clinical data are limited, and the potential significance is unknown. Patients who are receiving systemic or nebulized formulations of beta-2 agonists, high dosages of inhaled beta-2 agonists, or systemic corticosteroid therapy may be at a greater risk of developing hypokalemia.