GIOTRIF® is the first approved irreversible ErbB family blocker6
- The ErbB family of receptors is composed of 4 members: EGFR (ErbB1), HER2 (ErbB2), ErbB3 and ErbB45
- ErbB family members dimerise with other ErbB family members to signal5
- EGFR mutations trigger aberrant ErbB family signalling, a key driver in the growth and spread of EGFR M+ NSCLC5
- Whereas first-generation TKIs, such as gefitinib, reversibly inhibit EGFR, second-generation GIOTRIF® irreversibly blocks signalling from all ErbB family receptors5,7,8
EGFR M+= epidermal growth factor receptor mutation positive; NSCLC=non-small cell lung cancer.
GIOTRIF® has demonstrated consistent efficacy across multiple trials1-4
- Consistent efficacy demonstrated in 3 separate trials1-3
EGFR M+= epidermal growth factor receptor mutation positive; PFS=progression-free survival.
GIOTRIF® mechanism of action in NSCLC
GIOTRIF®, an irreversible ErbB family blocker, inhibits signal transduction and blocks key pathways involved in cell growth and division. Since ErbB Family signalling can be initiated by a variety of homo- and heterodimers, a combined inhibition of more than one ErbB Family member may provide a more successful blockade of ErbB Family signalling.9
ErbB blockade mechanism of action
GIOTRIF® (afatinib) is a potent, oral, once-daily, highly selective, irreversible ErbB family blocker designed to covalently bind to and irreversibly block signaling from all homo- and heterodimers formed by ErbB Family receptors.5,10 Whereas reversible EGFR tyrosine kinase inhibitors (TKIs) only target EGFR, GIOTRIF® demonstrates activity against all the kinase-active members of the ErbB Family: EGFR, HER2 and ErbB4; and indirectly against ErbB3 by inhibiting its transphosphorylation by heterodimerisation partners. GIOTRIF® not only provides potent signal blockade of mutated EGFR, but also silences aberrant ErbB network activity and displays a long duration of action.5