If you can knock down the pathway 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.
That’s all well and good, but it doesn’t speak to the point I’m discussing about the size of the addressable market for 113 in the second-line setting, specifically.
“The efficient-market hypothesis may be the foremost piece of B.S. ever promulgated in any area of human knowledge!”