I thought the expectation was 534 was good enough on its own
EXACTLY!
That approach the doctor was talking about makes no sense to me considering what Clackson and other doctors in the trial (as well as Berger) have been pumping on conference calls for the past year. "A pan BCR-ABL inhibitor" as Berger continues to call it...
What would be the point of taking a drug (Sprycel) and then effectively "stacking" '534 on top of it, just to possibly negate a possible mutation. Mutations don't occur in everyone, and most patients go their entire lives on Gleevec without a mutation occuring. So, why would a patient (or an insurance company for that matter) allow a higher cost to the patient and possible toxicity, by stacking two TKIs, just for the possibility that a mutation might occur??
Oh, and, by the way, in JP Morgan's model, they have a 60% chance of ridaforolimus success in SUCCEED trial, and a 35% chance (yes, 35%) of success in the '534. Obviously, they understand that final data is WAY off and you cannot base approval on a trial of only 50 patients (as in the Phase 1 trial). I, myself, believe it's higher, but a 50 patient trial is HARDLY enough overwhelming evidence for the FDA (which sucks in my opinion for the patients it clearly works with).