Autolus Therapeutics plc (AUTL) Earnings Call Transcript & Summary

Hello, ladies and gentlemen, and welcome to the Autolus Therapeutics EHA Data Update Conference Call. As a reminder, this conference call is being recorded. I would now like to turn the conference over to your host, Mr. Andrew Oakley, the company's Chief Financial Officer. Please go ahead.

Thank you, Kevin, and good morning or good afternoon, everyone, and thank you for taking part in today's EHA data update call. I am Andrew Oakley, the Chief Financial Officer. With me today is Dr. Christian Itin, our Chief Executive Officer; and Dr. Martin Pule, our Chief Scientific Officer. Before we begin, I would like to remind you that today -- during today's call, our discussion will contain forward-looking statements. All statements other than statements of historical facts on this call are forward-looking statements. Actual results may differ materially from those indicated by these forward-looking statements as a result of various important factors, including those discussed in the section titled Risk Factors in our annual report on Form 20-F filed with the Securities and Exchange Commission on March 3, 2020, which can be accessed on the EDGAR database at www.sec.gov and in subsequent filings we make with the SEC from time to time. The forward-looking statements on this call reflect the company's views as of today, June 11, 2021, regarding future events and should not be relied upon as representing the speakers or the company's views as of any subsequent date. While the company may elect to update these forward-looking statements at some future point, the company specifically disclaims any obligation to do so even if the company's views change. These forward-looking statements should not be relied upon as representing the company's views as of any date subsequent to today. Please be advised that today's call is being recorded and webcast. On Slide 3, you will see the agenda for today and is as follows. Christian will provide a brief introduction; and that will be followed by Martin summarizing the iNHL data presented at EHA today; after which Christian will give an update on the adult ALL durability data that was also presented. Christian will then conclude with the upcoming milestones and other concluding comments. And of course, we will welcome your questions following our remarks. So with that, I'd now like to turn the call over to Christian. Christian?

Thanks, Andrew, and welcome, everybody, to our EHA update. We've been looking forward to, obviously, sharing with you our newest data on AUTO1 or obe-cel. As you know, we've been obviously very active working in the field of ALL and particularly obviously driving the FELIX study. But we've also obviously continued to observe the data coming from the ALLCAR19 study, and I'll be sharing with you some additional update after Martin's presentation. We're also active in addition -- within the ALLCAR study in additional indications, including a set of non-Hodgkin indications and CLL. And this is where we're going to be focusing on the first part of the presentation, on the first experience that we have in patients with indolent lymphoma. In addition, we're also actually active in patients that have primary CNS lymphoma with the so-called CAROUSEL study. And we're active in an extension of the CARPALL study with the next-generation program called AUTO1/22 that is designed to address the antigen-driven relapses that we've seen in the original CARPALL study with AUTO1. So with that, we're moving to Slide #6. I just would like to remind you of kind of some of the key features that we have seen with obe-cel in ALL in particular. Today's data is coming from a data cutoff that was on May 17 this year. Now what we have seen obviously across the study is a high level of sustained, complete remissions that were achieved without subsequent stem cell transplant. The durability that we're seeing is highly encouraging, and we're obviously providing an update today that actually extends to 24 months. And we do see that indeed, the event-free survival actually is at or slightly above 50%, and it is stabilized at 24 months. What we also do obviously know from the program, what we shared with you in the past, is that the program has a very good safety profile with no patients experiencing high-grade cytokine release syndrome which is grade 3 or higher. And only a small proportion of patients, total of 20%, had experienced ICANS, or neurological adverse events, of any grade. And all of those events swiftly resolved with the administration of steroids. We have a pivotal study ongoing called the FELIX study and expect full data during the course of next year. And finally, I'd just like to remind you of the opportunity in ALL, which is very significant. It's a market that's significantly underserved, and we'll talk briefly about that in a later slide. But it's important that it's a market that is addressable with a very focused commercial footprint. With that, I would like to actually hand over to Martin to give us the update on the indolent non-Hodgkin's lymphoma experience. Martin?

Thank you very much, Christian. Hello, everybody. And Julia, could you please go to Slide 8? So on Slide 8 then. We're just really describing what we've done with the ALLCAR19 study. So Christian briefly mentioned the ALLCAR19 study, and many of you will be familiar with it. This is our Phase I study, testing obe-cel in relapsed/refractory B-ALL. We initially aimed to recruit 20 patients to this study, to treat 20 patients on the study, which we did do by the end of last year. And because the data was so encouraging, we amended the study to turn it into a kind of a basket study. So -- and this is described here, so with cohort B, where we would treat some 10 DLBCL patients; cohort C, where we would treat 10 B-CLL patients; and cohort D, where we would treat some B-NHL patients. And the aim of this was to see if the same safety profile and high levels of long-term engraftment of obe-cel was the same across all these different subtypes. We've initially focused on cohort B because for many reasons, this is -- this should be quite interesting, and this is really what I'm going to talk about next. So Julia, if you can go to Slide 9, please. So here, we're talking -- so here is an update on that cohort and indolent B-NHL cohorts. And we've treated 9 patients, 7 of these patients with follicular lymphoma and 2 with mantle cell lymphoma. And in terms of the patient characteristics, they're pretty much what we would expect for relapsed/refractory indolent and B-NHL with the median previous -- with median of 3 previous lines of treatment. 4 out of 9 had a previous autologous hematopoietic stem cell transplant, and 1 had a previous allogeneic hematopoietic stem cell transplant. All of the patients were either Stage III or IV by PET-CT. So that's the patient characteristic. So if you remember, there are 2 main characteristics of obe-cel due to the design of receptor having a fast off-rate interacting with its target. So we hope that we'll get less exhaustion and, hence, better engraftment and persistence. And then at the same time, because each contraction with the targets that will result in less inflammation, we hope to see low levels of toxicity. So we know that this is what we get in pediatric and adult ALL. So this is what we get in indolent B-NHL. So on the top right of the slide, you can see the marking levels done by flow. And you can see, indeed, we do see very nice high levels of expansion of CAR T cells in most patients in a nice plateau. So this is really very similar to what we see in B-ALL. And then do we see the same thing, same low levels of toxicity. And I think you can see that indeed, we do. We have seen CRS of any grade in 5 out of 9 patients. However, only one of these was grade 2 CRS, and we did not see any grade 3 CRS in any of these patients. So that is really quite a promising safety profile. In terms of CAR-mediated neurotoxicity, we have not seen that in any of these patients. So I think that's very nice to see that we have really now the same safety profile in indolent B-NHL as we do in pediatric and adult B-NHL. So what happened to these patients' response [ lives ]? So Julia, if you can go to Slide 10. So this is just a swim plot of all these patients. So all of these patients or all 9 patients went into a metabolic remission by PET-CT, and 8 of -- out of 9 are disease-free at the last follow-up. Sadly, we lost one patient due to COVID infection, and one patient relapsed with small volume subcutaneous CD19-positive disease, the salvaged, and with localized radiotherapy, all right? So as we go on to Slide 11, these are small patient numbers, obviously. This is really just to get our feet wet, just to see what the performance of our receptor was in this setting. But we just put a slide together here just comparing obe-cel with Tecartus and Kymriah, just really for your information to get a sense of how our receptor -- our product compares with the competition. And as you can see, we have -- well, in this very small group of patients, 100% metabolic CR. And we have very -- we have no severe CRS, and we have no neurotoxicity. And I think this compares favorably with both Tecartus and Kymriah. And then if we go on to Slide 12, really, which is my summary. So this initial obe-cel efficacy data in indolent NHL is really quite encouraging. It's very nice to see the same, consistent safety profile across increasing numbers of indications. And it's also nice to see the engraftment and persistence profile also reproduced in another disease subgroup. We're adding these additional -- we're exploring -- the additional cohorts, as explored. And further data, we should have by Q4 of this year. And Christian mentioned the CAROUSEL study, which is actually separate to the ALLCAR study. So it's not part of the ALLCAR19 basket study. This is a separate study in primary CNS lymphoma, which is now currently open, and we hope to have some initial data at the end of this year. And as Christian also mentioned, the 19/22 version of obe-cel is now open and recruiting patients in pediatric ALL, again with the data expected at the end of this year. So with that, I'd like to hand back over to Christian. Thank you very much for your attention.

Thanks a lot, Martin, and we're moving to the update on the ALL side on Slide 14. As you remember, the medical need in ALL, particularly adult ALL, remains very high. We start the therapy once the patients are diagnosed with a high-dose combination chemotherapy regimen. We get about 90% of the patients in complete remissions. However, only between 30% and 40% has a chance of long-term remissions. When we look at the median overall survival of the relapsed/refractory part of the population, it is less than 1 year. And at this point, obviously we do not have an approved CAR T therapy in the space. The only redirected T cell therapy that is on the market is blinatumomab. Now we do know from the original experiences in the space obviously that CAR T therapies can be highly active but obviously often had challenges either on durability or on safety. When we look in terms of the opportunity more broadly, we believe that in addition to the last-line setting, there are significant opportunities for the products to move up the line and into the earlier settings. Obe-cel has been granted orphan drug designation by the FDA for ALL, and we also received earlier this year a prime designation by EMA for adult patients with ALL. Next slide. What we're looking at on Slide 15 is really the updated swim plot of our patients. And this is one of those cases where actually, no change is good news. In fact, we had no event between the data cut that we had for ASH at the end of last year and the data cut now in May 17 this year. All the patients that were in remission continue in remission, which is obviously very good news. I'm just pointing out that we have now patients that, without any subsequent therapies, have crossed 30 months in molecular complete remission. Slide 16. What we're looking at here is the updated event-free survival curve, which is really kind of the most sensitive way of looking at how the patients are faring. In blue, we're looking at the morphological EFS curve. Remember, the way we're assessing responses in ALL is by actually measuring the number of blasts in the marrow. If the patient has less than 5% blasts in the marrow, the patient is in morphological complete remission. But then we also measure with a much more sensitive methodology, either by flow or by PCR, whether it is actually presence of much lower levels of leukemic cells in the marrow, and that is usually referred to as minimal residual disease at that state where that disease is measurable with those methodologies. And what we also put on here is -- in the light green curve, is actually the molecular EFS curve, in other words all of the patients that are still in molecular complete remission. It has no sign whatsoever of any disease in the marrow. You see the curves are slightly apart. There is one patient difference, and this is literally a patient that was in -- had an MRD relapse that was still in morphological CR and was then moved on to a stem cell transplant. And that's the difference between the 2 curves. The important part, however, is that as you're looking from 12 months onwards, that both curves are going horizontal. So when we look at the molecular -- or the morphological EFS at 12 months and at 24 months, we do see that we get to 50.2%, which is sustained over time. Now as we go on Slide 17, what we are looking at here is actually our experience in the ALLCAR19 study, and we're also including as a point of reference the now published Phase II data from ZUMA-3. This is the Tecartus data in adult ALL that was published in Lancet and also presented literally a week ago at ASCO. I think when we look at the baseline characteristics of the patients, we see that they're overall very comparable. The -- on the ALLCAR side, we have obviously some patients that have an ECOG Status 2, which is obviously patients that do a bit worse. And we also seem to have a higher number of patients that have gone through a stem cell transplant and failed after the stem cell transplant. Overall, however, the patient populations are very comparable. Going to Slide #18. When we look at the key markers for the activity, we can see that the -- we're having with obe-cel obviously a very robust complete remission rate and molecular complete remission rate at 85%, which obviously are numerically higher than what was reported for ZUMA-3 in the Phase II study, which were reported at around 71% and 69%, respectively. When we look at the event-free survival and we look at the median, which was not reached obviously for ALLCAR but then look at 12 months, 18 months and 24 months, obviously the numbers are all 50.2%. They're identical. However, what we're seeing with the -- with Tecartus and ZUMA-3 is that while at 12 months that number was still around 45%, it dropped to 25% at around 18 months. And there is no data reported for 20 -- 24 months' time point. So -- while the activity obviously as we see on obe-cel is a consistent high level of complete remissions and a stabilization of the responses after 12 months. Going to Slide 19. What we're looking at, at Slide 19 on the top is obviously, again, the morphological event-free survival curve for obe-cel, and we have plotted at the bottom with the same time axis the corresponding data from the Lancet paper with Tecartus from ZUMA-3. And as you can see, the -- clearly, the data for Tecartus continues to fall and does not stabilize and clearly highlights that difference -- fundamental difference in terms of the longer-term outlook that the 2 therapies appear to be offering to patients. When we go on Slide 20, when we look at the actual behavior of the CAR T cells themselves, there seems to be quite a stark difference. I'd like to point out that what we're looking at here on the Y-axis is a logarithmic scale. And what you can see is actually that in terms of the peak expansion, the maximal amount of CAR T cells formed in the patients, we see about a tenfold increase or higher number of CAR T cells with obe-cel compared to Tecartus. We then see obviously, as we go to 3 months, that difference going to about 1,000-fold, very few cells, CAR T cells left in circulation with Tecartus. And they're all gone by month 6. On the other hand, with obe-cel, you see that the persisting CAR T cells are stabilizing, and they're stabilizing throughout the full 24-month observation period that we now have with these patients. So it's a stark difference in terms of behavior of the product both in terms of maximal activity in the sense of actually available CAR T cells at peak, which is tenfold, but then obviously a massive difference in terms of the presence -- continued presence of the CAR T cells. So when we then look on the safety slide -- side on Slide 21, obviously you do remember that we have overall a very good safety profile with no high-grade CRS, limited neurotoxicity compared to obviously the published data for Tecartus. I think what is quite telling is we actually look at the treatment for CRS or ICANS, which obviously gives you a very good view of the intensity of patient management required to actually ensure that it can keep the patients safe during the therapy. As you can see for obe-cel, there is limited use of tocilizumab and steroids and there's no vasopressors that were required, which is indicative, in fact, of none of the patients having required access to intensive care. Now if you compare that to obviously the data from ZUMA-3, you see extensive use of tocilizumab, extensive use of steroids. But still, although this extensive use was put in place, 40% of the patients received vasopressors, which tell you that those patients have required intensive care. So there's a stark difference obviously in terms of the safety profile between the approved products as well. So we believe that we have a potentially differentiated product on efficacy, on durability and on safety. We obviously have seen a very high level of molecular CRs, of MRD-negative CRs at a level of 85%. We've seen a stabilization of morphological EFS at around 50%. We have seen exceptional long-term CAR T persistence, which clearly correlate with long-term benefit. And we have seen a favorable safety profile with the product in these difficult-to-treat patients. So with that, I'd like to actually summarize kind of where we are with the program, and we're going to Slide 24. Obviously, building on the positive experience that we're having both in the adult as well as the pediatric ALL population, we're obviously conducting now the pivotal study in adult patients, the FELIX study. But we're also, as Martin pointed out and walked you through, are exploring and evaluating the activity in the broader range of non-Hodgkin's indications as well as taking the next-generation program, AUTO1/22, into pediatric patients. And for all of those subindications, we expect data by the end of this year. So with that, I would like to actually close the formal part of the presentation, and we'd be happy to take questions.

[Operator Instructions] Our first question comes from Gil Blum with Needham & Company.

Congratulations on the impressive data update. So maybe one for Martin. It looks like patients with indolent lymphoma, when treated with cellular therapeutics, appear to have lower rates of immunological toxicity. We saw that with other CAR Ts and some of these allogeneic cell programs. Is there any underlying biology that might be explaining this?

Thanks for the question. Well, I mean, I think the -- what causes immunotoxicity is really the amount of antigen that the T cells encounter over a period of time. I'm not sure that it's been formally studied, but I would suspect that these indolent cells are probably a little bit smaller. They probably have a little bit less antigen. And probably also, they're slightly less inflammatory. And so overall, the amount of sort of signal -- CAR T signal you get over a short period of time might be a little bit smaller than from, say, something like ALL. I mean having said that, Tecartus -- the Tecartus study in mantle cell lymphoma did show a fair amount of toxicity. I mean it wasn't really that well-tolerated. So that illustrates that it depends on the chimeric antigen receptor you're using as well and the type of costimulatory signal it transmits.

All right. Maybe kind of veering to the ALL program. We've seen really long-term responses there. Is there a historical measure or length of time in which we can see that patients have achieved a cure? I mean another program at the past 2 years, for example, do these usually last like after 5?

So Gil, it's an excellent question. And typically, what you would look at is you -- like in many actually lymphomas and then also potentially other leukemias, you look typically at a 5-year time window. As sort of a point of reference, the work that was done with Blincyto in the early line setting actually did show a -- still although the data looked reasonably positive at 3 years, actually, there was a continued drop to 5 years in some of those patients. So typically, a 5-year time window is what you would look at to sort of believe that the patient is kind of out in the woods. But I think getting to a place where the event-free survival actually starts to stabilize as we've seen now, I think, is obviously very good news and indicative of a high chance of a long-term benefit.

Okay. And kind of a last one. Are there any drawbacks to having long-term B cell aplasia? It looks like these B cells are -- the T cells are very, very persistent after 2 years.

That is correct. So one of the things that obviously you need -- we need to keep in mind is that the first thing that you have to do in a disease setting, like acute leukemia, is survive. We shouldn't kid ourselves all of these patients that are in a relapsed/refractory setting are going to die based on the current standard of care. So the first order of business is survival. And I think what we do see is there's a clear correlation between the persistence and the durability of effect. Now obviously, if you have long-term activity of the CAR T cells, you will also have an impact on your overall B cell compartment, and you certainly will have a B cell compartment that is going to be suppressed for that period of time. What we do know from the experience obviously in NHL patients who've been exposed to rituximab for years is that, that actually can be well-compensated in many of these patients by other parts of the immune system. Obviously, one of the things we have here is an improvement in terms of the performance also of the T cell compartment. So I think there's good proxies with regards to obviously the experience on rituximab. But indeed, we have an ability to compensate from an immune system perspective. But there's -- certainly, for as long as there are active CAR T cells in the patient, there will be a suppression of the B cell compartment.

All right.

Yes. I mean -- it's Martin here. I mean if I can add a tiny bit to that. I mean so for things like ALL, CLL, follicular and mantle, it's going to be very likely you're going to need long-term persistence. We need to keep these patients in remission. So I think that's -- long-term B cell aplasia is very likely the price you have to pay for continuing remission in these patients. Remember, the bone marrow resident plasma cells aren't killed or -- because they don't express CD19 CAR. So many patients are still able to make antibodies against pathogens they've encountered in the past. And then for -- there are relatively rare patients that run into recurrent respiratory infection. There is a mitigation, which is proved in immunoglobulin, which is a reasonable mitigation so you can get other people's antibodies. And this is very similar, as Christian said, to the problem with patients with long-term rituximab maintenance, for example, in cancer. So you're right. It is a clinical problem. It's a price we're paying. And for patients who have a clinical problem with it, there is a relatively simple mitigation set.

It makes sense for deep-seated diseases like ALL that's deep in the bone marrow that you would need very long-term monitoring of the T cells. And I think the data from blina kind of points in that direction as well. Congratulations on the positive update.

Thanks, Gil. Thanks for joining.

Our next question comes from Mara Goldstein with Mizuho.

Great. In the indolent Hodgkin's -- non-Hodgkin's lymphoma study, you had that one patient that relapsed just before the 6-month mark and then was rescued with radiotherapy. And I'm curious as to what you think is going on there to see that patient respond to radiotherapy. And then secondarily, if you could just talk a little bit about the update for later this year and what we can anticipate in that update. And if you also have any thoughts on timing around pivotal data in the FELIX study for next year, sort of early, late or mid-2022, that would be great.

It's Martin here. Maybe I should take the first part of your question...

Thanks, Mara. Maybe Martin, you can take the...

Yes.

Exactly.

And then I'll hand on to you, Christian, yes. Sorry. Okay. So I mean -- again, it's a very small study. So it's really difficult to make any conclusions. So in terms of the skin relapse, so this is actually very interesting. There are some sanctuary sites that the disease can relapse in. And that's ocular, subcutaneous and, in some cases, CNS. And it's interesting that CAR Ts are actually very good at -- if you have a patient, for example, with skin lymphoma and you give CAR T cells, it's actually quite a good treatment for that. But interestingly, when -- after the initial peak of CAR T expansion and then you sort of enter into kind of low-level persistence, you do sometimes see patients breaking through in those sort of sanctuary areas. So presumably, that's what happened in these patients. And actually, the nice thing about skin disease is you can give quite specialized radiotherapy that doesn't penetrate very deeply, like electron beam radiotherapy. So it's something that we do see these kind of sanctuary site relapses. And I guess it's -- since you can give very localized radiotherapy, it's not really surprising that a patient responded. But sort of more than that, with just this one patient, I can't really say anymore.

But what -- just out of curiosity, do you know if that patient experienced CD19 loss of expression? Or...

No, no. When we did this, it came back [indiscernible] CD19-positive.

Our next question...

And then the second part of the question -- sorry, we're -- we still have a second part of that question -- questions. And that was the update at the -- data update at the end of the year. So obviously, a key focus of the data update at the end of the year will be the additional cohorts that Martin was talking about. So obviously, longer-term follow-up on the cohort we just discussed on indolent lymphoma, but we're also expecting updates from the cohorts in the additional non-Hodgkin's subset as well as the first view of the data with primary -- on the patients with primary CNS lymphoma as well as an update on the Phase I experience with the AUTO1/22 in pediatric ALL as well. So that's sort of for the end of the year. And obviously, we'll keep on updating kind of the durability information on ALL from the ALLCAR population as well. As we're going into next year, the key update with regards to the FELIX study, we expect to be able to report on the primary end point in the middle of the year and then towards the end of next year, also update -- provide the durability information on the trial.

Okay. And Christian, just as it relates to ALLCAR, obviously, we have a little bit of data at this point from -- on the indolent NHL. But what is the, I suppose, threshold to continue -- to expect to continue? I mean clearly, the results so far are particularly enticing. And have you thought about how to expand that program?

So what we want to see is really how the product performs across these various non-Hodgkin's subindications and really, based on the profile we're seeing, actually picked the indication set that will push forward into the next stage of development. So we want to see kind of the performance across and the level of differentiation that we're picking up. And as Martin pointed out, one of the important elements, certainly also on the follicular side, is durability of effect and want to see continued maintenance of the remissions that we've been able to induce.

Our next question comes from Asthika Goonewardene with Truist Securities.

Congrats on the update and the positive data here. I guess most of mine have been already answered. But maybe on the broader topic of persistence, I want to ask Martin this. I know the CAT19 helps greatly with this. But I know you guys have done some [ long ] follow-up work in patients that you treated with the AUTO1. So I'm wondering how long are the CAR-positive TN and TSCM cells present in patients? And how much is that differentiated from, let's say, axi-cel? Guys, did you get my question? Are we still on?

I -- it's Martin. I missed the very last, compared to -- I just missed the very last sentence. Your just -- line went very fuzzy. So could you just repeat the last bit of your question?

Yes. Sorry, Martin. And I was wondering and how does that -- the long-term persistence of the CAR-positive TN and TSCMs, how does that comp with AUTO1? And how does that compare to axi-cel?

Yes. I mean it's a good question. I mean we're in a very fortunate situation with this product in that patients who have CAR T cells detected by PCR, we can still detect them by flow. So I mean some patients do lose their engraftment over time, but most patients still have CAR T cells by flow. Now I mean, axi-cel, right, Yescarta is a 28 zeta CAR, right? And there, I mean you've seen from Christian's slide with the marking that actually, that disappears very, very quickly. So there's not really a comparison, I don't think, between AUTO1 and axi-cel. You lose your CAR T cell marking with 28 zeta very, very quickly. I mean the one thing that we're able to see with AUTO1 that no -- nearly nobody else is able to is actually the flow in their long-term persistence cells. And there, you can pick up still stem cell, memory cell, T stem cell, memory cells. [ And as requested ], we published a paper in Nature Genetics where we studied the insertion site profile and the differentiation of AUTO1 T cells in peripheral blood up to a couple of years in our initial pediatric cohort. So I'll direct you to that for further reading.

Our next question comes from Ingrid Gafanhão with Kempen.

Sorry. I was on mute for a while there. Can you just remind us if the ZUMA-3 trial used any preemptive safety management or perhaps any other approach they might have used for risk mitigation? And I was wondering, do you think that this drop in CAR T persistence that they observed here can be related to this widespread use of steroids? Or do you think it's probably mostly related to the use of CD28 as [ a place monitoring only ]?

Right. So first off, with regards to the general profile that we've seen in terms of persistence for Tecartus and Yescarta, it's predominantly driven by the construct itself and the actual CD28 signaling, we believe, as the predominant driver of that behavior. With regards to the safety management, the safety management was evaluated in the Phase I part of the ZUMA-3 trial and published in Blood earlier this year. The authors did indicate a more aggressive intervention with steroids and tocilizumab to be used in Phase II. The Phase II publication, The Lancet in the supplemental section, would suggest that there may not have been a consistent use of premedication or early medication of the patients. It suggests that it is -- it was similar to what was used elsewhere. However, it was not really specified in any way, shape or form in that -- in the document. So I don't think we can comment on what was actually used. What we do know is the totality of steroid use and the totality of toci use as well as vasopressor use, which was actually disclosed in the actual publication but not the timing of which.

Our next question comes from Eric Joseph with JPMorgan. If your line is muted, could you please unmute the line? Would you want to just go ahead and move on to the next question?

Let's do that.

Our next question comes from Kelly Shi with Jefferies.

This is [ Dave ] on for Kelly Shi from Jefferies. Congrats on the progress. My question is just following on the earlier question. What will be the bar for starting the pivotal trial for each of these indications?

Well, thanks for joining. And we -- as we have indicated obviously, first of all, we want to understand the actual profile that we have in the various subindications. I think when you look at the bar, you can look actually and particularly with follicular, mantle cell, DLBCL on the approved products, which give you a very clear level of the bar that you have to hit. But we haven't actually specified beyond the specifics of where we actually need to hit for us to take the program forward. That is premature at this point.

And I'm not showing any further questions at this time.

All right. Then, well, thank you all for joining for this update from the EHA conference, and we're looking forward to keeping you updated on the additional progress and wish you all a great day. Thank you.

Ladies and gentlemen, this does conclude today's presentation. You may now disconnect, and have a wonderful day.