And in our case, the normal total hemoglobin for female was 12 to 16 grams per deciliter. And for male it’s 13.8 to 18 grams per deciliter, and we’re pleased to see our patients going to the normal range. And we are pleased to share more data during the ASH and webinar presentation later next month.
Gilmore O’Neill: Yes. I think the only other thing is we do note that we’ve had very successful engraftment timelines. It’s too early to say more than that in the space. And I think we’re also very happy with where our hemolytic markers are.
Operator: Our next question is from the line of Greg Harrison with Bank of America. Pleased proceed with your question.
Greg Harrison: Hey, good morning. Thanks for taking the question. Just thinking, when should we expect an update on the in vivo editing efforts? How do you think the commercial opportunity is there relative to ex vivo in sickle cell? And then, what other indications or tissues do you think are attractive candidates for your in vivo technology?
Gilmore O’Neill: Thanks very much, Greg. With regard to future updates, this is a company who philosophically wants to make promises and make discussions that we believe that we can absolutely deliver on. We have been doing work over the last year. Linda has only been here about three months, and we want to ensure that she has the time to again engaging with our medical and commercial team now led by our new Chief Commercial and Strategy Officer, the ability to make sure that we choose and progress against high conviction targets based on our selection criteria. With regard to your second question, let’s just remind again —
Greg Harrison: Targets and tissues.
Gilmore O’Neill: Targets and tissues. Yes, forgive me. So we have actually advanced for — in fact, Linda, might actually talk about target and tissues.
Linda Burkly: Yes. Thank you. Yes. Thank you for the question. So, of course, we’re very excited to develop an in vivo HSC program based on the success of the — our targeting approach for sickle cell disease and TDT, and so moving the targeting of the HBG12 low just to an in vivo approach. And so we’re very well-positioned for that, considering the emerging success that we’re seeing in the clinic that Baisong has described. And so we’re working very hard to come up with the delivery strategy for in vivo HSC. And we’re doing that both internally and through potential external partners. And so that’s a — I’m very excited about that avenue. And then in terms of other tissues of interest, we’ll be talking about those in the future. We are interested in deliver, but I’ll be talking about other tissues as well in the future. Thank you.
Gilmore O’Neill: Thanks very much, Linda. And then, with regard to the third part of your question, you asked about the commercial opportunity for in vivo. Essentially, what you can actually see is a strategy that we’re driving, which progressively expands the number of patients and a fraction or proportion of the patient population that can actually use the tissue or use these treatments allogeneic opened a door to therapeutics. But the substantial issue there was finding matched donors where about only about one-tenth of patients can find a matched donor. By going to autologous ex vivo, we’ve increased that tenfold. By going to in vivo and thus eliminating the risks and burdens of conditioning, we can actually further expand the patient population and address the unmet need that extends into patients who while not described as severe, it’s worth remembering that the median survival for this disease in a developed healthcare system like that of the United States is about 45 to 50.
As again was impressed upon us at the AdCom by those incredibly moving testimonies from patients and their parents and family members. And indeed, in economies with no healthcare system, it’s an 80% mortality by five years of age. So there is a substantial unmet need and in vivo will massively increase the commercial the eligible patient population.
Greg Harrison: Great. That’s helpful. Thanks again, and looking forward to the update.
Operator: Our next question is from the line of Gena Wang with Barclays. Please proceed with your question.
Gena Wang: My questions, I think a lot of questions asked about the differentiating profile for the EDIT-101. So maybe I wanted to ask in a way actually it was surprising we saw VOE event happen so early during exa-cel AdCom. I’m wondering what is your thoughts there and then for your efficacy clinical profile, what kind of say factors you can pay attention to in order to monitor this event and try to develop differentiate profile versus exa-cel.
Gilmore O’Neill: Thank you very much, Gena. So doesn’t want to just recapitulate your questions to be sure I get it all. You want to talk about the differentiation of our EDIT-301 product for as we’re focusing on severe sickle cell disease. You were interested in or surprised to see VOEs reported in some patients post-treatment at the AdCom. And I think you’re interested in also understanding what are the elements that we’re monitoring for differentiation in our efficacy profile. What I will start and then pass, I can start and then I’ll have Baisong on comment on the differentiation of our efficacy profile. With regard to the VOEs, I think understanding a full explanation will be hard for us at this point. There were many elements of the data that were not presented, which is not surprising in a very truncated presentation.
But obviously looking at the correlation of fetal hemoglobin expression, the other factors that can drive VOEs, et cetera, is something that we obviously afford to get with more data being able to understand. I think what does stand and remains true is that the upregulation of fetal hemoglobin actually has a substantive impact on controlling VOEs. Now, as we look to differentiation for EDIT-301, we’re looking beyond not just the control of the VOEs, but actually correcting other elements of the disease. And with that and with a particular focus on the correction of anemia to normal physiologic range and its impact, and I’d say Baisong to talk more about that.
Baisong Mei: Yes. Thanks, Gilmore. Gena, yes, absolutely. We are still very confident that we believe that EDIT-301 is a differentiated molecule, given that what we’ve seen so far, we have to see that we can actually have correction of thalassemia to physiological range of total hemoglobin. And with that, we look into that not only hematological parameter, but an organ function and as well as patient report outcomes. So we continue to believe that direction will allow us to demonstrate differentiation.
