They are just now looking to initiate a preclinical study to find out the MOA?!? They've had a boat full of money, why didn't they start this study a long time ago back when they started claiming CYT387 had an anemia benefit? You would think a potential partner would want to know how/why it works...If you can't even explain how your own product works, not sure they will find a partner. I guess we have to wait for this study to be done before P3....
Someone asked, "Why waste the money in an MOA Study?" Sorry, but dumb question. Differentiation is an imperative in drug marketing and this study will provide marketing a bazooka on Jakafi. These folks so know what they are doing. It's reassuring they are pursuing good science to show they have best in class. Other indications will come, but this MOA study will turn heads. It's the sizzle in the steak.
So you would have had them initiating a study prior to them becoming convinced that there was a lasting anemia benefit? Or should they have intuited that there would be a lasting anemia benefit? It is unfortnate that they don't understand the mechanism but there's no reason to suppose that it will delay Phase III trials. Why would it?
Would you rather have the benefit and be puzzled as to the mechanism or not have the benefit at all...in which case you could call yourself Incyte...or lack of Incyte?
I didn't interpret his words as negative regarding additional studies. I think the point is similar to what atypical antipsychotic companies have done. You want to be able to say empirically that our drugs hits this receptor at this rate and this is why we think we're superior to Jakafi. In other words, it's very important for marketing and perhaps for the targeting of additional diseases. I didn't read this negatively at all. I think they know they're sitting on a winner and common sense tells us that they're going to want to know as much as possible about the mechanism of action. Also, the mechanism could ultimately serve to broaden the label. I'm sure there is a good reason behind their thinking. I am positive that this is what is done with other drugs in competitive spaces. The more information the better.
I agree with everything you've said and I also don't see this having any impact on Phase III studies.
I'd rather have the benefit clarified. Without understanding the mechanism, you're opening yourself up to problems in the future where although the drug can cure a disease or ailment short term, it's effects may effect something else down the line, that may lead to long term problems. Happens with many drugs. Therefore, I am holding for a while, but not for over a year after the drug is released, due to the increased chances for issues, especially since our current testing sample population is so low
First, you don't have to know exactly how a drug works to start phase III or obtain approval. Second, this isn't the only Jak inhibitor that doesn't quite fit the MOA mold. It is well known that inhibiting Jak 1 is likely the basis for the benefit in RA but it also has a negative lipid effect. But there is at least on Jak 1 inhibitor that doesn't seem to result in a negative lipid effect. Likewise, inhibiting Jak 2 appears to worsen anemia but as we all know cyt387 runs counter to that thesis. It's not clear why at this point but several theories exist. If cyt387 continues to provide the anemia benefit while also coming close to providing the other benefits of Incyte's Jakafi, it may have a significant advantage.
He heard it at the annual meeting or in the accompanying slide deck from that meeting which is now posted at YMI's website - see slide 4 which refers to initiating preclinical studies in 2013 to identify MOA for the anemia benefit.