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Post# of 252302
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Alias Born 11/10/2009

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Tuesday, 04/06/2010 2:28:01 PM

Tuesday, April 06, 2010 2:28:01 PM

Post# of 252302
Ariad's near term price is going to be largely driven by the upcoming second interim analysis for ridaforolimus but I suspect that most of the future upside will actually be driven by their second drug candidate AP534.

The Phase 1 data shows AP534 has real promise as a pan bcr-abl inhibitor. In a patient population that had failed 2 and sometimes 3 tki's, the cytogenetic response rates were much higher than tasigna and equaled that of sprycel. With Gleevec coming off patent in 2015, it's clear that Novartis is going to position tasigna as the new first line treatment. http://www.novartis.com/newsroom/media-releases/en/2009/1359764.shtml

One of the reasons I'm invested in ariad is that I believe they'll move quickly to become the standard second line option and, if they find the right partner, potentially first line. If 15 to 20% of CML patients become resistant due to mutations and AP534 works equally well in CP CML as well as in patients whose disease has mutated then I think there a good chance they may very well succeed. But here's my question, has anyone come across any pre-clinical data that may indicate that AP534 actually inhibits the oncogene from mutating at all? Why wait until you become resistant to the first line treatment if you can achieve the same or better CyR and prevent the mutation from occurring in the first place? I have no idea whether this is the case but I just thought I'd put it out there for discussion.

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