John Scarlett: Sure. So I think you were referring, just to be clear, to IMproveMF and on the AML study, did I get your question right about that?
Stephen Willey: Yeah, correct. So the Rux combo study and just some of the other…
John Scarlett: Sure. So I think it’s incumbent on every company developing a drug, regardless of kind of whatever the nuances of the IP positions are. I think we study new combinations and study different utilities of drugs. And I’m sorry for being unpleasant about this. I don’t mean to be, but we have to move it at kind of a high level. I think we do that on the basis that we think — if we think that there is benefit to be derived for patients, that’s when we become really interested. The [Rux] (ph) is a really good example, as you know and have written about, to these people know. There were a whole series of pre-clinical experiments done a number of years ago now. And they were a very good lab of scientists that looked at the question of whether or not there were different ways to exploit some of the intrinsic activity in telomerase inhibitor against some of the cells that are malignancy transformed and ultimately cause myelofibrosis in clinical outcomes.
And what we see is that if you end up treating with [indiscernible] you see any damage. And then if you sort of chase that, if you come after that, which you can do [indiscernible] with a telomerase inhibitor, in this case, in a [indiscernible] you actually get a higher proportion of animals surviving longer and also see a depletion of the living and athletic stem cells. So that was the key for us to start ultimately, to do all the work necessary to start this study. And it’s because, a, we can go up front with this into frontline patients. B, we hope to be able to actually have ultimately improved efficacy, although this study is predominantly a safety study. C, I guess that some people are going to do this. If we don’t do it, some people somewhere in the world will start to do it on their own, and we would, we think we know the drug, we’ve helped that better than anybody else and we have control of that.
So sorry to be, again, kind of [indiscernible] that, but I think that that’s the rationale. The same with AML. AML is a terrible disease and we’ll actually cross the patients have very few options. There are other drugs in the horizon that I hope for these patients also are [indiscernible]. Our goal is really patients and actually if you do something reasonably innovative, which I think these are innovative, ultimately you file for intellectual property protection. That plays out as a completely separate story in one that’s not as interesting.
Stephen Willey: Okay, makes sense. I appreciate the comments, thanks.
John Scarlett: Sure, thanks.
Operator: [Operator Instructions] Your next question comes from the line of Gil Blum from Needham & Company. Your line is open.
Ethan Markowski: Yeah, hi. This is Ethan Markowski on for Gil. Thank you for taking our question. First one would be how much — I know you’ve touched on this before, but how much extra effort do you think you’ll have to spend on educating community physicians on managing cytopenias versus academic ones assuming approval? And then, do you have any thoughts on how the recent data from morphosis at ASH could impact the myelofibrosis landscape and any future development in the space? Thank you.
John Scarlett: I think that’s a killer name Anil Kapur. Anil?
Anil Kapur: Sure. So we have had extensive discussions with both community and academic providers. And just as a reminder for everyone, low risk MDS is predominantly treated within the community setting. Physicians tell us they have deep experiences with drugs such as len HMAs and are very adept at managing heme-related side effects for patients. And for them, they point to prolonged myelosuppression with HMAs, et cetera, as areas which they have managed successfully for a long period of time. With imetelstat in particular, what is really important is, which they receive really favorably, is the predictability of the cytopenias, the fact that the cytopenias typically are of finite duration and tend to go away in by cycles two and cycle three.
And also importantly, there are no clinical consequences associated with these cytopenias in terms of infections and hospitalizations and bleeding events. And when we also provide context on the mechanism of action, this is something that’s received very favorably by the practicing hematologists. So we do not see much differences between the community versus the academic hematologist in terms of their perceptions and management of heme toxicities. They are adept with their training and also their practice experiences. With regards to the question on myelofibrosis, I think this is also an area which is fast moving. We will obviously wait to see what happens with the BCL-2 and the BET inhibitors in terms of entering the landscape. But a reminder for myelofibrosis is that we are the only Phase 3 study, the largest effort to the best of my knowledge in the world, which is looking at survival in a patient population that’s relapsed and refractory to JAKis.
This patient population is extremely underserved and every feedback from physicians, academic experts, leading KOLs, is that if our myelofibrosis study is positive, it is going to be transformative for patients with myelofibrosis and really will be rapidly well adopted within the space. So I’ll just stop here.
Ethan Markowski: Thank you.
Operator: Your next question comes from the line of Joel Beatty From Baird. Your line is open.
Joel Beatty: Hi, Thanks for taking the questions. For the early access program, can you provide any updates or quantify how many patients are a part of that?
Anil Kapur: Chip, do you want me to take that?
John Scarlett: Sorry, yeah, go ahead.
