This indicates that the situation with resistance to the first-generation ALK inhibitor is more complex than with CML. In CML most resistance involves a mutation in the main BCR/ABL pathway that is susceptible to the later generation drugs. In these ALK patients by contrast, only a minority of the patients have mutations that say '113 could (in theory) deal with.
If this work holds up in practice, it means the majority of the patients that fail crizotinib will not be rescued by '113. Instead they will likely need some sort of combination therapy, perhaps an EGFR drug or perhaps an HSP90 drug.
It may be that if you started the patients on a more potent drug like '113 in the first place you wouldn't see the same resistance developing. But unfortunately it will likely be a while before you see naive ALK patients on the drug.
So at least for the ALK subset of patients, this likely isn't good news for either the patients or for the ultra-quick development of '113.
Peter
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