Question-and-Answer Session
Operator
(Operator Instructions) Our first question comes from Cory Kasimov - J.P. Morgan.
Cory Kasimov - J.P. Morgan
Two questions here, both relating to the JAK II program. Could you please discuss the difference if any in the burden of proof between the MF indication and PV and ET in terms of most relevant clinical outcomes? And then the second question relates to the developments yesterday in acknowledging that, it’s obviously early but discuss what you learned from the FDA panel meeting for Actemra for the RA indications?
Paul A. Friedman
The PV and ET patients that we are enrolling are those who are farther along in their disease and these are people who have the same issues that myelofibrosis patients have but they still have a hyperproliferative marrow and with one of the blood cell types predominating in its elevation. With PV it being the red cell and with ET it being the platelet. So what we’re hoping to be able to do, and I actually have a reasonable amount of confidence we’re going to be able to do this - I know we will shrink the spleens and I know we will improve the constitutional symptoms in the same manner that we’ve seen with myelofibrosis. That in its own right would be of huge benefit to these patients because they suffer from the same kind of debilitating issues that the myelofibrosis patients have. But beyond that, in these patients we should be able to take advantage of the myelosuppressive properties of the JAK II inhibitory mechanism to bring back to normal or toward normal the elevated counts that these patients have. That in a nutshell is what we’re trying to do in this study that we’ve just started in PV and ET patients which will involve about 100 patients.
With respect to the Actemra FDA advisory meeting yesterday we were very, very encouraged by that because it means that both the FDA, based on the comments that they made, and the vote and the discussion that went on amongst the physicians that people are open to these types of mechanisms having an important role in systemic inflammatory diseases with RA being one but there obviously are quite a few others. The really encouraging thing is that when you look at what Actemra does and you look at the PK of a monoclonal antibody, with something like the 8 milligrams that they give, they’re taking the Interleukin 6 receptor out all day long completely.
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