Comparative Pharmacology
Head-to-head clinical analysis: GILOTRIF versus NINTEDANIB.
Peer-Reviewed Evidence
Head-to-head clinical analysis: GILOTRIF versus NINTEDANIB.
GILOTRIF vs NINTEDANIB
Comparing the clinical profiles, pharmacokinetic behaviors, and safety indices of these two therapeutic agents.
GILOTRIF (afatinib) is an irreversible inhibitor of the ErbB family of tyrosine kinases, including EGFR (ErbB1), HER2 (ErbB2), ErbB3, and ErbB4. It binds covalently to the ATP-binding pocket of the kinase domain, blocking downstream signaling pathways involved in cell proliferation, survival, and angiogenesis.
Nintedanib is a small molecule tyrosine kinase inhibitor that inhibits multiple receptor tyrosine kinases, including vascular endothelial growth factor receptors (VEGFR-1, VEGFR-2, VEGFR-3), platelet-derived growth factor receptors (PDGFR-α, PDGFR-β), and fibroblast growth factor receptors (FGFR-1, FGFR-2, FGFR-3). It also inhibits RET, FLT3, and Src family kinases. These receptors are involved in angiogenesis, proliferation, and fibrosis.
40 mg orally once daily for first-line treatment of EGFR mutation-positive non-small cell lung cancer; may be increased to 50 mg if tolerated.
150 mg orally twice daily approximately 12 hours apart, taken with food.
None Documented
None Documented
Clinical Note
moderateNintedanib + Digoxin
"Nintedanib may decrease the cardiotoxic activities of Digoxin."
Clinical Note
moderateNintedanib + Digitoxin
"Nintedanib may decrease the cardiotoxic activities of Digitoxin."
Clinical Note
moderateNintedanib + Deslanoside
"Nintedanib may decrease the cardiotoxic activities of Deslanoside."
Clinical Note
moderateNintedanib + Acetyldigitoxin
"Nintedanib may decrease the cardiotoxic activities of Acetyldigitoxin."
Terminal elimination half-life is approximately 41 hours, supporting once-daily dosing. Steady-state is reached within 8 days.
Terminal half-life: 9.5 hours (range 6-14 hours) in patients with IPF; supports twice-daily dosing.
Approximately 88% of the administered dose is eliminated via feces (with 85% as unchanged parent drug), and 8% via urine (with <5% as unchanged drug). Biliary excretion is the primary route for unchanged drug.
Primarily fecal (85%) as unchanged drug; renal excretion accounts for <1%.
Category C
Category C
Tyrosine Kinase Inhibitor
Tyrosine Kinase Inhibitor