rakara schreef op 17 mei 2018 08:16:
So, what do you think on the key differentiation for filgotinib as the market compared to the other JAK inhibitors for RA?
John McHutchison
Thank you. Good question, which I spent a lot of time thinking about. Look, there are three ways program, not just the molecule differentiator. Firstly, in terms of execution and the overall status of the program, having read what's gone on in the field recently,
and we are ahead of schedule. All our Phase 3 RA trials are enrolled now way ahead of schedule. So, that’s great news.We’re in all different populations, naïve, and methotrexate inadequate responders, biologic non-responders. And we have two doses in all studies. And we have those doses continuing on in the long-term expansions, which is an important difference, but there is no crossover. We can continue to look at safely at 100 and 200 milligrams going forward, which is an important point in the field as was recently discussed in an advisory committee. So that's the way the program's differentiated.
There's no doubt that god knows this is the most JAK1 specific drug, independent academic investigators have recently have shown. We don't hit JAK2, the selectivity index is much less, for god knows and we don’t hit JAK3. Because we don’t hit JAK2, we don't see this decline in hemoglobin. In fact, we see 0.3 to 0.4-gram increase in hemoglobin, which is what you see in somebody with rheumatoid arthritis you give them a TNF inhibitor and you control their disease and control their inflammation.
When you hit JAK2 you see increase in platelets, other the drugs in the class 2 there as well. We do not do that. In fact, we see a small decrease in platelet counts.
This might be associated with thrombo embolic phenomena that have been observed with some of the drugs being developed.Uit het artikel van seekingalpha. Het nieuws van de dag, vind ik. Uitermate positief!