Operator: Next, we’ll move to Gil Blum at Needham & Company.
Ethan Markowski: Hi. This is Ethan Markowski on for Gil. Thank you for taking our questions. So just two quick ones from our side. First one, maybe a little bit of a follow up from one of the previous questions. And I did try to look quickly, but I was unable to find it. Could you give any color on the rux dosing that was used in improving that? I know you’ve mentioned imetelstat those things. And then the other question, I’m looking at Slide 10 of the presentation. So the ASH abstract regarding mutations, and you can definitely see a pretty clear efficacy across the various mutations. I was just wondering if there’s any biologic rationale why, in particular, ASXL-1 appeared to have a little bit lower effect than the others or if you think it’s just small numbers. Thank you for taking the question.
John Scarlett: Yes. Ethan, thanks very much. Both really interesting and good questions. I will invite Faye to comment on the rux dosing first and then riff a bit on the efficacy across the different mutations and how our old friend ASXL-1 appears to be a difficult patients with that mutation appear to be particularly difficult to treat. Faye?
Faye Feller: Thanks. Sure, Chip. And thanks for the question, Ethan. Regarding the start with ASXL-1 first. Regarding ASXL-1, yes, I do believe that, it appears to be a smaller magnitude of benefits, and that’s mostly due to a low number of patients with the ASXL-1 mutation. That mutation in particular portents a very poor prognosis and a quick transformation to higher risk disease or AML. So it was even a bit surprising that we had patients with these mutations in the lower risk population that speaks further to the relevance of the IPSS-M classification. And the results that we are showing it ASH regarding that abstract as well. So it all fits together that because of the mechanism of imetelstat that’s directed at telomerase and telomerase is overexpressed in malignant cells and drives the malignant phenotype by targeting the disease itself, we have activity across the broad mutations, regardless of what prognosis they portend for patients.
To address your second question, or if it was actually your first. To address your first question about ruxolitinib dosing, the aim of the study is to assess safety and make a sense of safety in the context of real-world use. So patients enter the study on ruxolitinib at whatever dose was most beneficial and tolerable for that. And so the ruxolitinib dose varies per patient.
Operator: We’ll call next to Joel Beatty at Baird.
Joel Beatty: In considering the market research data that shows a larger market share for imetelstat than luspatercept. Do you expect that upon launch there could be some moving from luspatercept to imetelstat some switching or what would use upon launch mainly being patients who are either like newly diagnosed or failing their previous therapy?
John Scarlett: Thanks. Again, I think this is Anil’s area to comment on whether there’s possibility for at least switching et cetera at launch. Anil?
Anil Kapur: Sure. Joel, thank you for the question. I think, Joel, just one fact to keep in mind as I answer the question is, there are very few treatment options and low risk MDS. As Chip spoke to earlier, I think the words he used was competitively less intense. In practice physicians only have a handful of choices. So what we feel is, while we may expect or want a patient, I think the key need here is for patient to really be best treated with whatever option the physician thinks for them till they no longer see benefit. So if it’s the case of a patient not seeing benefit, and there is a more effective option, I think physicians will consider switching the patient over but if the patient is responding, our belief and typically clinical practices to allow that patient to benefit fully through that disease through that treatment choice.
And then, consider other choices for that patient for where they are. But so hopefully that answers that part of the question. The last remark I’ll make here is to have a completely new novel mechanism of action with the level of durability and all the clinical effectiveness that we have shown, I think will become a really important tool in armamentarium for physicians to consider and continue to optimize a patient therapy. So I’ll stop here, and Faye, is there are any clinical remarks from your side, that might be good.
John Scarlett: Okay. Thank you. Any further questions, Joel or did that?
Joel Beatty: Great. Thank you.
Operator: And there are no further questions at this time. I would like to turn the conference back over to Aron Feingold for closing remarks.
Aron Feingold: Thanks so much, operator. Thank you, everyone so much for your participation today. We look forward to keeping you updated on our progress. Thanks so much.
Operator: And this concludes today’s conference call. Thank you for your participation. You may now disconnect.
