Biotech Values

[biomaven0]

many—perhaps even most—cases of resistance to Crizotinib stem from reasons other than a mutation in ALK.

That might stem from the fact that Crizotinib isn't a great ALK-inhibitor in the first place (it was not in fact specifically developed as one - it's actually a dual cMET/ALK drug). Resistance develops when you only partially knock down a pathway - that way you have cells mutating under selective pressure - whether by furhter ALK mutations or via new pathways. If you can knock down the pathway better from the outset, there is less chance of resistance developing.

Preclinically, '113 is a way better drug than Crizotinib - more potent by a factor of 10, much more selective against wild-type ALK and having a factor of 10 better therapeutic index.

Peter