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. Author manuscript; available in PMC: 2015 Aug 1.
Published in final edited form as: Cancer. 2014 Apr 17;120(15):2289–2298. doi: 10.1002/cncr.28723

Figure 3.

Figure 3

Relative potency of different EGFR kinase inhibitors against different EGFR genotypes in vitro. The Y-axis represents the relative IC50 normalized to the IC50 against EGFR sensitizing mutations (L858R or exon 19 deletion).27,57,62 Second-generation EGFR TKIs like afatinib are more potent against T790M than gefitinib, but dosing in the clinic is limited by wildtype inhibition (and toxicity) at a relatively lower dose. Third-generation EGFR TKIs like CO-1686 and AZD9291 selectively inhibit EGFR T790M well below the dose at which wildtype EGFR is inhibited and have the potential to yield reduced toxicity as a result.