Unidentified Analyst: And the data presentations for EHA and ASH later on that’s just an encore of the ASCO presentation?
Christian Itin: No, the presentations are — some are related, but there’s not — the abstracts are not identical between the two. They may share some of the data, but in terms of the focus is slightly different.
Unidentified Analyst: Okay. Got it. Thank you so much.
Christian Itin: Thanks a lot, Karina.
Operator: Thank you. Our next question comes from Gil Blum with Needham & Company. Your line is open.
Gil Blum: Hey, good morning and good afternoon. Thanks for taking our questions. So first question kind of focusing on the bridging aspect in the study. This is something that has also recently come up in the advisory committee materials for ABECMA and CARVYKTI. It looked like bridging had a pretty important impact on patient survival even before you got there, treatment. In many ways, maybe the fact that you allowed physicians to pick their bridging may have actually assisted you here. And how can you optimize bridging? Is there like a study to be done here?
Christian Itin: It’s a really good question. I think, first of all, the situation is obviously a bit different between multiple myeloma, adult ALL and multiple myeloma, which is the progression of disease is much less rampant, much less significant in terms of the speed of deterioration as you would have in ALL. ALL obviously can go as you have seen, you have patients go from minimal residual disease to more than 75% tumor burden. I mean, that gives you a sense of the explosiveness of the disease. So, bridging is obviously something that we have to do in these patients. Otherwise, the tumor burden actually gets overwhelming and in of itself becomes a limitation in these patients. But as you could see, obviously, the impact can be that you either have no — see no impact whatsoever and the patient just go straight over, stays about 75%.
These are — certainly, you would call this refractory in the very functional — as a very functional determination. But you also may have patients that actually transiently may actually have a significant decrease in tumor burden between involvement and the actual dosing. And that does have an impact in the sense that the level of tumor burden as lymphodepletion. So right before your dosing, obviously, it seems to actually have quite a significant impact and outcome. And this is the data that we have shown and we just walked through a little earlier. So that is absolutely true. That is what you do see. And it seems better correlated than actually the tumor burden at the time of screening or inclusion because that obviously is somewhat arbitrary.
It just happens to be when you actually see the patient, determine the level of tumor burden and that obviously could be at any level in the relapse. And so, at the time of bridging, obviously, that gives you much more relevant information. It’s part of the therapy. It’s always been part of the therapy in ALL. Even when you look at other therapies at times, if you have excessive tumor burden, you would actually first need to with a short course of chemotherapy to push down tumor burden [indiscernible] before you dose. So one of the things we have done during inside the development and certainly was important to also not only improve or have a chance for outcome in that approach, but also to reduce the risk for very severe adverse events. So, it is an integral part.
And what we certainly will do is over time is probably look at different types of bridging and whether we might actually see differences there. So that’s certainly a part of the analysis we’re also still running through the trial, I think we actually post, I think, opportunities for also potentially investigating sponsored study [eventually] (ph).
Gil Blum: Okay. And switching to autoimmunity, you mentioned that there are a lot of similarities between obe-cel and the German [ISD] (ph) assets. There are a couple of other companies out there who also have very similar programs to the German ISD. What would you say is a differentiator between your program and other programs? And what do you think is your key advantage?
Christian Itin: Well, the first thing, I think, which is interesting is that it’s not — I think, is that we can make a statement to our product as it stands, how that may compare to others, I think, is very difficult because, for the most part, we don’t have data to compare to. But we do have data to compare our product to the product that was used in Erlangen and that is relevant because that gives us a very clear understanding of the features that a product in Erlangen had versus ours and with that the predictability for outcome. I think that is relevant. And I think what we do see also compared to the Erlangen program is that as we have seen prior in the pediatric ALL patients is going to compare the CARPALL study to the ELIANA study from a safety perspective, there’s a very significant difference there.
Where we have none of the cases actual experience high-grade CRS, where compared to 47%. We have patients with high-grade CRS in the ELIANA study, virtualized were conducted within a very short period of time, actually overlapping each other as well. So, the same environment, same way of treating patients and managing safety, et cetera. So, we do know that we have a quite a significant difference there and that difference also was observed and was observable when comparing to the program that was running in Erlangen on the pediatric patients, which obviously was sort of prior to the work that we all know about on the obe-cel side.
Gil Blum: All right. And maybe a last one on this topic. So, most discussions that we’ve had on the use of cell therapy and autoimmune diseases, suggest that only a relatively small window of deep B cell aplasia needed to “reset” the immune system. I mean, I guess that’s one kind of hypothesis that is out there, but I’m sure you have maybe a different view on that.
