ErbB Family Blockade and Afatinib Infographic

Boehringer Ingelheim

Afatinib*, a Boehringer Ingelheim investigational compound, is an irreversible blocker of the ErbB-Family.¹

How does ErbB-Family signalling work?
Signals from receptors of the ErbB-Family inform cells to perform normal cell functions such as multiply or differentiate as shown below with the ErbB1 receptor.²

Disregulated activation of ErbB-signalling in cancer cells
Cancer cells can mutate and therefore dysregulate normal signalling processes leading to an abnormal continuous signaling, resulting in a higher rate of cell division and tumour growth.³

ErbB-Family receptors are frequently overexpressed on cancer cell surfaces. Overexpression of ErbB-Family receptors such as EGFR and HER2 has been associated with a variety of tumour types and is associated with
poor prognosis and advanced-stage cancer.^2-4

Mode of action of afatinib* – targeting the ErbB-Family¹
Since ErbB-receptor family signalling can be initiated by a variety of homo- and heterodimers, an irreversible inhibition of all ErbB-Family members may provide a more successful blockade of the ErbB-Family signalling. Afatinib* acts on all ErbB-Family receptors, therefore blocking the key pathways involved in cell growth.

1. BI Data on File.
2. Hynes NE, et al. Nat Rev Cancer 2005;5:341–54.
3. Hanahan D, Weinberg RA. Cell. 2000;100(1):57–70.
4. Normanno N, et al. Cur Drug Targets 2005;6(3):243-47.

Source for healthcare professionals: www.inoncology.com
* Nintedanib (BIBF 1120), afatinib (BIBW 2992) and volasertib (BI 6727) are investigational compounds. Their safety and efficacy have not yet been fully established.

† Not an official event of the 2012 ASCO Annual Meeting. Not sponsored or endorsed by ASCO or the Conquer Cancer Foundation.

Boehringer Ingelheim on

ErbB Family Blockade and Afatinib Infographic

1. BI Data on File.2. Hynes NE, et al. Nat Rev Cancer 2005;5:341–54. 3. Hanahan D, Weinberg RA. Cell. 2000;100(1):57–70. 4. Normanno N, et al. Cur Drug Targets 2005;6(3):243-47.

1. BI Data on File.
2. Hynes NE, et al. Nat Rev Cancer 2005;5:341–54.
3. Hanahan D, Weinberg RA. Cell. 2000;100(1):57–70.
4. Normanno N, et al. Cur Drug Targets 2005;6(3):243-47.