Just posted this comment on The Street article...
I just couldn't help it.
Comment:
So let me get this straight, your source feels Iclusig is a "dirty drug" due to similar side effects and no improvement on efficacy. So since all second generation TKI's for CML demonstrate comparable safety and efficacy then Pfizer, Novartis, and Bristol-Meyers must have dirty drugs too, right? Halting the EPIC trial early? Perhaps...but for accelerated approval. Have you seen the MyCR data from the PACE trial for Iclusig in patients previously treated with only one TKI? Here's a recap: Nilotinib 40%, Dasatinib 45%, Bosutinib 36%, Iclusig 84%. Regarding efficacy I suggest relying on leading MD's in CML treatment for assessment of efficacy, not sell side analysts. A few examples below for your convenience.
Dr. Jorge Cortes -
“These results show that ponatinib has outstanding activity regardless of the stage or presence or absence of mutations associated with resistance, and responses are durable. "The side effects are very acceptable, like all the tyrosine kinase inhibitors they all have some side effects."
Dr. Neil Shah -
“This drug has the potential to be a best-in-class agent that may be completely invulnerable to single-kinase-domain mutations,” says Neil Shah, the UCSF hematologist who treated Galliart. “I’m hopeful that it really will remove single-kinase-mutation–mediated resistance out of the picture.”
Dr. Hagop Kantajian-
"The standard of care in refractory or relapsed patients to multiple TKIs doesn't exist. What we have usually is some data on either dasatinib or nilotinib in patients who have failed imatinib and one of the other TKIs. This drug is effective even when those three drugs have failed. So it establishes a new standard of care of highly effective therapy. If you ask if we can anticipate how this drug will compare to the other TKIs in the same setting, I think this drug will be more effective than the second-generation TKIs in the setting of salvage therapy, but that remains to be seen. But this drug is also highly effective against the T315I mutation."
