This is an early stage study in animal models of induced fibrosis, not IPF. You are jumping to unfound conclusions. The ITMN and Japanese studies clearly show a decreased in progression and severity of IPF when perfinidone in 2400mg/day doses are used. UP to 72 weeks possible longer. These patients die a horrible death and there is nothing right now to help them. Perfinidone with its low risk profile and shown benefits will be a welcome relief to many of these patients. The FDA knows this (read the FDA advisory panel report; google it). It is only a matter of time before an understanding is worked out. GLTA
Nice factless spin. I don't need to google the FDA Advisory panel report, I was here when it occurred. The members were looking for more data even then. ITMN still did not produce it.
The Japanese and ITMN studies showed very little - thus the letter. You can make stats do whatever you want them to - just like your 72 weeks longer. I can also say perfinidone allowed some to live shorter lives because it killed them.
Of course the animal models had induced fibrosis but they found the scars had healed. This early indication shows a lot more promise than perfinidone (i.e possible cure vs. possible days/weeks of extention of life). By the time InterMune gets their act together and does another phase III, this newcomer might just beat them to market. At a minimum, ITMN doesn't have the market cornered like some pumpers have been trying to suggest.
The FDA and ITMN will come to an understanding after ITMN performs the required phase III on the FDA's term, not their own made up endpoints.
"You can make stats do whatever you want them to - just like your 72 weeks longer. I can also say perfinidone allowed some to live shorter lives because it killed them." - not really, not if you have the full data sets.
And perhaps you can show us WHERE the pifenidone toxicity shortened the lives of IPF patients... otherwise don't invent your own clinical findings.
While the FibroGen data is compelling stuff, it is also hardly fair to directly compare treatment of a known experimental injury in mice to clinical treatment of an idiopathic (i.e. unknown origin) lung disease. So interesting? Yes. Comparable? Not at all.
And even if they've started to enroll for phase II, they would be a good 3-5 years away from filing an NDA, given one year + for the phase II and 2 years + for the phase III.
No ITMN does not have the market cornered on possible IPF therapies, but given the lack of clinical success in treating IPF (steroids, NAC, Bosentan, etc) prior to the Shionogi Phase II & III results, you must admit it looked very positive for ITMN leading up to the CAPACITY trials.
Please tell me which member wanted more data. I have talked to most of them and they seemed like more data was not necessary. (hence the approval) Are you at the ATS today. If so were having lunch with some of the presenters; Univ of Washington group.
Ok I take offense at that. Look at page 68-80, fig 22,table 26, etc and the statistical analysis of the pooled data. It clearly show that there is statisticaly significant difference in outcome with primary and most secondary outcomes. IPF has a lot of intra individual variablity and most of my patients don't act the same as others. That is why these pt's are difficult to study. (they don't act in a similar linear fashion) Also, look at the placebo pooled data the strange skewing that confirms this. So far, this drug has had the most potential success for this disease. Statistical analysis is an exact science so you can't just make things up, even if you want certain results.