Comparative Pharmacology
Head-to-head clinical analysis: AFATINIB versus SUTENT.
Peer-Reviewed Evidence
Head-to-head clinical analysis: AFATINIB versus SUTENT.
AFATINIB vs SUTENT
Comparing the clinical profiles, pharmacokinetic behaviors, and safety indices of these two therapeutic agents.
Afatinib is an irreversible, covalent-binding inhibitor of the ErbB family of tyrosine kinases, including EGFR (ErbB1), HER2 (ErbB2), ErbB3, and ErbB4. It blocks downstream signaling pathways such as PI3K/AKT and MAPK, leading to inhibition of tumor cell proliferation and survival.
Sunitinib is a multi-targeted receptor tyrosine kinase inhibitor that inhibits platelet-derived growth factor receptors (PDGFR-α and PDGFR-β), vascular endothelial growth factor receptors (VEGFR-1, VEGFR-2, VEGFR-3), stem cell factor receptor (c-KIT), FMS-like tyrosine kinase-3 (FLT3), colony-stimulating factor 1 receptor (CSF-1R), and the glial cell line-derived neurotrophic factor receptor (RET). It inhibits angiogenesis and tumor cell proliferation.
40 mg orally once daily, continuously.
50 mg orally once daily for 4 weeks, followed by 2 weeks off (schedule 4/2).
None Documented
None Documented
Clinical Note
moderateAfatinib + Digitoxin
"Afatinib may decrease the cardiotoxic activities of Digitoxin."
Clinical Note
moderateAfatinib + Deslanoside
"Afatinib may decrease the cardiotoxic activities of Deslanoside."
Clinical Note
moderateAfatinib + Acetyldigitoxin
"Afatinib may decrease the cardiotoxic activities of Acetyldigitoxin."
Clinical Note
moderateAfatinib + Ouabain
"Afatinib may decrease the cardiotoxic activities of Ouabain."
Terminal half-life is approximately 37 hours; supports once-daily dosing with steady-state achieved within 8 days.
Terminal elimination half-life of sunitinib is 40-60 hours; for its primary active metabolite (SU12662) it is 80-110 hours. Steady-state achieved by day 14.
Primarily fecal (85%) as unchanged drug and metabolites; renal excretion accounts for <4% of the dose.
Renal: 16% of total radioactivity; Fecal: ~70% of total radioactivity (primarily as unchanged parent and metabolites).
Category C
Category C
Tyrosine Kinase Inhibitor Antineoplastic
Tyrosine Kinase Inhibitor Antineoplastic