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XOVOLTIB® 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 XOVOLTIB® irreversibly blocks signalling from all ErbB family receptors5,7,8

EGFR M+= epidermal growth factor receptor mutation positive; NSCLC=non-small cell lung cancer.

XOVOLTIB® has demonstrated consistent efficacy across multiple trials1-4

LUX-LUNG 3, 6 and 7 PFS results for XOVOLTIB® in patients with common mutations (del19 or L858R)

  • Consistent efficacy demonstrated in 3 separate trials1-3

EGFR M+= epidermal growth factor receptor mutation positive; PFS=progression-free survival.

XOVOLTIB®, 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.11

ErbB blockade mechanism of action

ErbB blockade mechanism of action

XOVOLTIB® (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.5,12 Whereas reversible EGFR tyrosine kinase inhibitors (TKIs) only target EGFR, XOVOLTIB® 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. XOVOLTIB® not only provides potent signal blockade of mutated EGFR, but also silences aberrant ErbB network activity and displays a long duration of action.5

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References

  1. Sequist LV et al. J Clin Oncol. 2013;31(27):3327-3334.
  2. Wu YL et al. Lancet Oncol. 2014;15(2):213-222.
  3. Park K et al. Lancet Oncol. 2016;17(5):577-589.
  4. Soria JC et al. Lancet Oncol. 2015;16(8):897-907.
  5. Solca F et al. J Pharmacol Exp Ther. 2012;343(2):342-350.
  6. BI press release. www.boehringer-ingelheim.com. Accessed 19 December 2016.
  7. IRESSA® (gefitinib) Summary of Product Characteristics, 2018.
  8. TARCEVA® (erlotinib) Summary of Product Characteristics, 2018.
  9. Yang JC et al. Lancet Oncol. 2015;16(2):141-151
  10. Paz-Arez L et al. Ann Oncol. 2017; 28(2):270-277
  11. Reid A et al. Eur J Cancer. 2007;43:481–9.
  12. Li D et al. Oncogene. 2008;27:4702–11.
  1. [1] Sequist LV et al. J Clin Oncol. 2013;31(27):3327-3334.

  2. [2] Wu YL et al. Lancet Oncol. 2014;15(2):213-222.

  3. [3] Yang JC et al. Lancet Oncol. 2015;16(2):141-151.

  4. [4] Park K et al. Lancet Oncol. 2016;17(5):577-589.

  5. [5] Soria JC et al. Lancet Oncol. 2015;16(8):897-907.

  6. [6] Solca F et al. J Pharmacol Exp Ther. 2012;343(2):342-350.

  7. [7] Yang JC et al. J Clin Oncol. 2013;31(27):3342-3350.

  8. [8] Hirsch V et al. Poster #369 presented at: American Society of Clinical Oncology (ASCO) Annual Meeting; Chicago, IL, USA; 3-7 June 2016.

  9. [9] Yang JCH et al. Ann Oncol. 2016;27(11):2103-2110.

  10. [10] Schuler M et al. J Thorac Oncol. 2016;11(3):380-390.

  11. [11] Paz-Arez L et al. Ann Oncol. 2017; 28(2):270-277

  12. [12] XOVOLTIB® Local pack insert version dated 21st July 2017

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