Allogene Therapeutics Inc (ALLO) Q4 2019 Earnings Call Transcript

Allogene Therapeutics Inc (ALLO 0.29%)
Q4 2019 Earnings Call
Feb 27, 2020, 8:30 a.m. ET

Contents:

• Prepared Remarks
• Questions and Answers
• Call Participants

Prepared Remarks:

Operator

Good morning, ladies and gentlemen. Thank you for standing by, and welcome to the Allogene Therapeutics fourth-quarter 2019 conference call. [Operator instructions] Please be aware that today's conference call is being recorded. I would now like to turn the call over to Christine Cassiano, chief communications officer.

Ms. Cassiano, please go ahead.

Christine Cassiano -- Chief Communications Officer

Thank you, operator, and good morning. Before market opened today, Allogene issued a press release that provides a corporate update and financial results for the fourth quarter and full year ended December 31, 2019. This press release is available on our website at www.allogene.com. We remind listeners that today's call is being webcast on our website and will be available for replay.

Joining me on the call today are Dr. David Chang, president and chief executive officer; Dr. Rafael Amado, executive vice president of research and development and chief medical officer; and Dr. Eric Schmidt, chief financial officer.

During today's call, we will be making certain forward-looking statements. These may include statements regarding the success and timing of our ongoing and planned clinical trials, regulatory filings, future research and development efforts, manufacturing capabilities and 2020 financial guidance, among other things. These forward-looking statements are based on current information, assumptions and expectations that are subject to change and involve a number of risks and uncertainties that may cause actual results to differ materially from those contained in the forward-looking statements. These and other risks are described in our periodic filings made with the Securities and Exchange Commission, including our Form 10-Q for the quarter ended September 30, 2019, as well as our upcoming Form 10-K for the year ended December 31, 2019.

You are cautioned not to place undue reliance on these forward-looking statements and the company disclaims any obligation to update such statements. I'll now turn the call over to Dr. David Chang.

David Chang -- President and Chief Executive Officer

Good morning and thank you for taking time to join us on our call today to discuss our fourth quarter and the year ahead. I am extremely pleased with what we have accomplished in 2019. We completed the hiring of senior management, built world-class capabilities across critical functions and initiated the build-out of our GMP cell-manufacturing facility in Newark, California, making steady progress toward bringing the facility online in 2021. Most importantly, we initiated two clinical programs: ALLO-501 in relapsed and refractory non-Hodgkin lymphoma and ALLO-715 in relapsed and refractory multiple myeloma.

Our research team is also working toward advancing additional programs in next-generation cell-engineering technologies, which we plan to introduce into clinical trials in the coming years. It is still early in 2020, but we are continuing the momentum we created last year and working at an accelerated pace. This year we anticipate reporting initial data for two key clinical programs: ALLO-501 in the second quarter of this year and ALLO-715 in the fourth quarter. We also look forward to expanding our clinical portfolio as we progress our next IND candidate, ALLO-316, which targets CD70.

All 200-plus employees at Allogene remain singularly focused on one goal: making AlloCAR T therapy and their life-saving potential a reality for patients. The team at Allogene intends to strengthen our leadership position in AlloCAR T therapy, and we recently laid out our three-part strategy to achieve this goal: number one, establish a platform that will be foundational to the success of AlloCAR T therapy; number two, validate the platform through the rapid clinical development of multiple product candidates; and number three, transform the future of AlloCAR T by advancing next-generation technologies to enhance the potency and selectivity of our cells. Let me walk you through our concept of platform validation and transformation. While there are similarities between allogeneic and autologous cell therapy, there are key immunological phenomena that need to be addressed to allow unrestricted use of allogeneic CAR T cells manufactured from one healthy donor for a large number of patients independent of HLA typing.

Specifically, one needs to control the risk of graft-versus-host disease and prevent early graft rejection. Once these issues that are key to the success of allogeneic cell therapy are addressed, the inherent benefits of AlloCAR T therapy can be realized, namely, the ability to deliver therapy faster and more conveniently to all appropriate patients as an off-the-shelf therapy at a reduced cost of manufacturing. Our novel platform approach to creating an allogeneic cell therapy is based on TALEN gene-editing, state-of-the-art cell manufacturing and the use of a novel lymphodepletion strategy. TALEN technology and our proprietary manufacturing processes allow us to efficiently edit out the T-cell receptor from AlloCAR T cells.

Early data from studies on our UCART19 candidate, as well as data being generated by others in the field, support the view that cells lacking T-cell receptors have limited ability to mount a graft-versus-host response. The second challenge, the ability to overcome early graft rejection, is critical to enabling AlloCAR T and requires a novel strategy that goes beyond the use of traditional chemotherapy-based lymphodepletion. We believe our lymphodepletion strategy, based upon the use of ALLO-647, our anti-CD52 antibody, as a selective and controllable lymphodepleting agent, differentiates us from others and is well suited to prevent early rejection of our AlloCAR T cells. We use ALLO-647 for the purpose of creating a selected and durable period of lymphodepletion to facilitate expansion and persistence of our AlloCAR T cells, which have been modified to be resistant to the effect of ALLO-647.

The initial proof of concept for ALLO-647 comes from the UCART19 studies. These studies, which used both low- and high-dose fludarabine- and cyclophosphamide-based lymphodepletion, provided compelling evidence that chemotherapy-based lymphodepletion alone may not be sufficient. While the majority of patients who received an anti-CD52 antibody as part of their lymphodepletion regimen experienced clinical benefit, those who only received FluCy failed to demonstrate cell expansion and were not responsive to therapy. We believe ALLO-647 provides us with a unique opportunity to selectively control the depth and length of lymphodepletion, thereby allowing us to explore and determine the optimal window for AlloCAR T cell expansion and persistence in a variety of clinical settings.

In summary, we believe we have the only lymphodepletion platform capable of inducing durable lymphodepletion without impacting the viability of AlloCAR T cells. Our lymphodepleting agent, ALLO-647, is not associated with the broader cytopenic effects of chemotherapy because it is targeted only in cells that express CD52 and can be flexibly dosed. No other platform can do that. This leads us to the validation that we hope to obtain from our clinical trials.

We are on track to present initial data from ALLO-501 ALPHA trial in relapsed and refractory non-Hodgkin's lymphoma in the second quarter, and our ALLO-715 trial for relapsed and refractory multiple myeloma in the fourth quarter this year. These Phase 1 trials are designed to assess safety and establish an appropriate AlloCAR T cell dose. In addition, these trials are designed to test different dose and dosing schedules of ALLO-647 to optimize lymphodepletion in preparation for Phase 2 trials. We believe our ongoing trials could validate our lymphodepletion strategy and thereby leverage it across our broader pipeline.

Later in this call, Rafael will provide additional color on our progress in the Phase 1 ALPHA trial for ALLO-501. In addition, we have made progress to introduce our next-generation ALLO-501A construct into clinical testing. As you may recall, ALLO-501A, previously referred to as ALLO-501.1, was created to eliminate the rituximab recognition domain in ALLO-501, with the intent of using ALLO-501A broadly across different subtypes of non-Hodgkin's lymphoma and in a pivotal trial. We have submitted and gained clearance for a new IND and expect to initiate an abbreviated Phase 1 portion of ALLO-501A trial in the second quarter of this year.

The learnings from ongoing ALPHA study, including our work to optimize the dose of ALLO-647 and ALLO-501, will be leveraged to rapidly explore and confirm the safety and efficacy of ALLO-501A in a limited number of patients before we seek to advance the program to a potentially pivotal Phase 2. This now takes us to transformation. Our goal is to always remain at the forefront of innovation in the field of AlloCAR T therapies. This will require us to research and develop next-generation technologies derived from internal and external sources.

Our internal research team has developed a novel technology that mimics the effect of cytokine stimulation selectively within AlloCAR T cells. We call this technology TurboCAR. TurboCARs have the potential to improve the overall fitness of AlloCAR T cells, thereby enhancing their potency, expansion and persistence. Preclinical research has demonstrated that TurboCARs increase the antitumor efficacy in the in vivo models, and we are excited to move this approach to the next stage of preclinical development, starting with the advancement of a BCMA-directed TurboCAR.

More recently, we have entered into clinical collaboration with SpringWorks Therapeutics to evaluate ALLO-715 in combination with their investigational gamma secretase inhibitor, nirogacestat, in patients with relapsed and refractory multiple myeloma. Gamma secretase is an enzyme that cleaves BCMA from the surface of myeloma cells. In preclinical models, nirogacestat has been shown to prevent the cleavage and shedding of BCMA, leading to an increase in the cell surface density of BCMA and reduced levels of soluble BCMA. In addition, emerging clinical data suggests that gamma secretase, in addition, may augment the antitumor efficacy of BCMA-targeted autologous CAR T therapy.

We expect to initiate a combination trial of nirogacestat and ALLO-715 in the second half of this year. In the long term, our collaboration with Notch Therapeutics is off to a strong start. Our research teams are working together to develop a process for the production of AlloCAR T cells derived from induced pluripotent stem cells or iPSC-based study material. Success on this front could enable a more streamlined supply chain, greater cell product consistency and the potential to create more highly engineered therapies.

We are looking forward to keeping you updated on our progress in this emerging field. I will now turn the call over to Rafael, who will update you on our research and development activities.

Rafael Amado -- Executive Vice President of Research and Development and Chief Medical Officer

Thank you, David, and good morning to all of you on the call today. I'd like to start with a quick update on our lead program, ALLO-501, for relapsed/refractory non-Hodgkin's lymphoma. As David noted earlier, our Phase 1 trial for ALLO-501 is ongoing, and we're looking forward to sharing the initial data from the ALPHA trial at a medical meeting in the second quarter. While the focus of any Phase 1 dose-escalation trial is appropriately on safety, we're also using this trial as an opportunity to optimize our lymphodepletion strategy.

There are two things to consider. First, unlike the autologous Phase 1 trials that have the benefit of extensive academic and drug development research to inform lymphodepletion, the allogeneic field is starting from a much earlier point, and there is little precedence regarding the optimal cell dose and lymphodepletion regimen. The second consideration is how we can best harness one of the most differentiating tools in our platform, ALLO-647, our anti-CD52 antibody, to produce the best possible outcomes. We have recently completed enrollment on the three cell-dose-escalation cohorts in this three-plus-three trial and have moved to enrolling additional patients that allows us to better understand the impact of varying ALLO-647 doses or schedules.

Our sensational oncology team is collecting the data necessary to evaluate several potentially important parameters. This includes the depth and duration of lymphodepletion; patterns of host lymphocytes, including NK, B and T cell depletion; recovery; and AlloCAR T cell expansion and persistence. We believe our methodical, exhaustive scientific approach to understanding these biomarkers and their correlation with antitumor activity is essential to create the best possible outcome for patients. We are leveraging strong momentum in the execution of this trial, and we intend to fully explore and elucidate the optimal treatment regimen prior to advancing ALLO-501A, mentioned in David's remarks, into a Phase 2 trial.

The work being done in the ALPHA trial will inform our ALPHA2 trial, which will start the clinical transition from ALLO-501 to ALLO-501A. The ALLO-501 construct being studied in the ALPHA trial shares the same gene engineering as UCART19 and includes a rituximab-binding epitope as a safety off switch. The clinical candidate which Allogene acquired from Pfizer was designed to be used in acute lymphoblastic leukemia. Early on, Allogene elected to take a parallel path by beginning clinical trials on ALLO-501 in relapsed/refractory non-Hodgkin's lymphoma.

This allowed us to test our lymphodepletion strategy while engineering a modified next-generation product, which we now refer to as ALLO-501A. While we expect the initial data from our 501 ALPHA trial to facilitate identification of an optimal dosing of our lymphodepletion strategy, we recognized early on that the rituximab off switch would limit commercial potential in a clinical setting where rituximab is commonly used. For this reason, ALLO-501A is devoid of the rituximab off switch, which would allow us to serve a broader patient population, including those non-Hodgkin lymphoma patients with recent rituximab exposure. As David noted earlier, we're happy to report that we have made rapid progress with the preclinical development of ALLO-501A, and our IND has been cleared by the FDA.

We anticipate that the abbreviated Phase 1 portion of the ALPHA2 trial will commence in the second quarter of this year. We expect to enroll approximately 10 patients and will apply the optimized dosing of ALLO-647 elucidated in the ALPHA trial as we move toward a potential Phase 2 pivotal trial. In our second clinical program, we have created a robust anti-BCMA strategy, which includes ALLO-715 as a platform therapy for the treatment of relapsed/refractory multiple myeloma. UNIVERSAL, our Phase 1 trial with ALLO-715, continues to actively accrue and treat patients.

This trial will also explore optimal dosing of all components of the lymphodepletion regimen, including ALLO-647, fludarabine and cyclophosphamide. We will be assessing endpoints such as safety, tolerability, the depth and duration of lymphodepletion, cell expansion and antitumor activity as key determinants of success for ALLO-715. We are on track to report initial data from this trial in the fourth quarter of 2020. Our anti-BCMA program will also investigate ALLO-715 in combination with the SpringWorks investigational gamma secretase inhibitor, nirogacestat.

We will determine the best route to initiate a combination trial and expect to begin in the second half of this year. The third leg to our multiple myeloma strategy was unveiled earlier this year as part of the broader look at our pipeline. We have named ALLO-605 as our lead anti-BCMA TurboCAR candidate, which, in preclinical models, increases AlloCAR T cell activation and enhances their phenotypes on function. ALLO-605 is advancing in preclinical development, with an IND planned for 2021.

Lastly, we continue to progress our preclinical work and have officially nominated ALLO-316, our anti-CD70 program, as our next AlloCAR T clinical candidate. We're excited by the opportunity to bridge hematologic malignancies in solid tumors with ALLO-316. Our focus for this product will be on active myeloid leukemia, T-cell malignancies and renal cell carcinoma. We expect to submit an IND by the end of this year.

In closing, I'm very excited with the strong momentum of both our discovery and clinical allogeneic programs. Both are progressing as planned, and we look forward to providing initial clinical results later this year. I'd like to turn now the call over to Eric to review our financials.

Eric Schmidt -- Chief Financial Officer

Thank you, Rafael, and good morning. In addition to the brief financial overview I will provide on the call today, you can read additional detail on our fourth-quarter and year-end financial results in our press release issued earlier today and in our 10-K, which will be filed with the SEC. We continue to be in a strong financial position with cash, cash equivalents and investments totaling $588.9 million as of December 31, 2019. In the fourth quarter, our research and development expenses were $49.4 million, which includes $6.4 million of noncash stock-based compensation expense.

For the full-year 2019, research and development expenses were $144.5 million, which includes $10 million in expenses associated with the signing of our Notch collaboration. The total research and development expense for the year includes $19.4 million of noncash stock-based compensation expense. General and administrative expenses were $15.2 million for the fourth quarter of 2019, which includes $7.5 million of noncash stock-based compensation expense. For the full-year 2019, general and administrative expenses were $57.5 million, which includes $26.6 million of noncash stock-based compensation expense.

Our net loss for the fourth quarter of 2019 was $61 million or $0.58 per share, including noncash stock-based compensation expense of $13.9 million. For the full-year 2019, our net loss was $184.6 million or $1.83 per share, including noncash stock-based compensation expense of $46.1 million. Turning now to the financial guidance for 2020. We will continue to invest heavily in our clinical programs.

By the end of this year, our goal is to complete enrollment in the Phase 1 ALLO-501 trial, progress our Phase 1 ALLO-715 trial, and initiate Phase 1 trials for ALLO-501A and the ALLO-715 combination study with nirogacestat. And as noted in David's earlier comments, we also look to advance the build-out of our Newark manufacturing facility. As a result, we expect our full-year 2020 net losses to be between $260 million and $280 million. This includes an estimated noncash stock-based compensation expense of $70 million to $75 million and excludes any impact from potential business development activities.

With that, we will now open the call for your questions.

Questions & Answers:

Operator

[Operator instructions] Our first question comes from Marc Frahm with Cowen and Company.

Marc Frahm -- Cowen and Company -- Analyst

Hi. Thanks for taking my questions. So maybe thinking to this update we're going to get in the second quarter from the ALPHA trial, recognizing that ultimately, you do need to switch over to the 501A program, but will this data set be mature enough that, if it weren't for 501A, you would be able to make a decision to move forward into a Phase 2 and kind of have those next steps laid out? Or is it still going to be kind of a work in progress, that you need more maturity on some of these different preconditioning regimens and the different cohorts?

David Chang -- President and Chief Executive Officer

Yes. Marc, this is David. I'll take your question. The question that you're asking is a very important one, and certainly, there are many different aspects that goes into answering the question.

In terms of a couple things that -- how you should be thinking about it is, internally, lymphodepletion is something that we see as a generalizable concept, and that is one of the reasons that, in the ALPHA study, we are spending a considerable amount of effort to optimize the lymphodepletion. And as we know, as you know, we have been varying the ALLO-647, both dose and dosing schedule, to do that, and we'll certainly have a lot of data by the time that we present the findings in the second quarter. And with respect to the question of making the transition from ALLO-501 into ALLO-501A, one has to realize the chimeric antigen receptor portion of the construct remains identical. The only thing that has changed is taking out the rituxan switch, which in 501 was expressed as a separate protein.

So we consider this as a relatively minor change, and we believe that the learnings from the 501 study will be directly translatable as we move forward with the ALLO-501A. And that is the reason that we believe that this can be done as an abbreviated Phase 1 study, as we have said in our prepared statement.

Marc Frahm -- Cowen and Company -- Analyst

OK. When you say abbreviated Phase 1, can you give us some clarification as to what exactly does that mean? I mean, do you have to start from as low of a dose as you did in the ALPHA trial, but you can go up in single patients? Do you go one dose down? Can you just do the exact regimen that you selected from ALPHA and just reconfirm PK? What does abbreviated mean?

David Chang -- President and Chief Executive Officer

I think one thing that I have learned over the years that I've been involved in the CAR T trials is that anything that we do in preclinical setting, we like to confirm in the clinical studies. So when we talk about abbreviated approach, you're exactly to the point. I mean, dose escalation will be somewhat simplified, and the real intent is to confirm whatever we saw in 501 can be reproduced in the 501A study. So with that, certainly, there will be more color to it as we present the data, which I think has to -- you have to wait for that.

Marc Frahm -- Cowen and Company -- Analyst

OK. Thank you.

Operator

Our next question comes from Salveen Richter with Goldman Sachs.

Salveen Richter -- Goldman Sachs -- Analyst

Thanks. Good morning. So with regard to the NHL study, 501, where we're going to see data in the first half here, second quarter, are you primarily thinking of ACR and ASCO as the presentation settings for these data sets -- for this data set? And then secondly, as you look to taking other programs into the clinic, so the multiple myeloma program, the program with SpringWorks, amid others, how are you thinking about leveraging further steps in optimization, be it the preconditioning regimen, where you could play with timing of dosing, as well as duration of dosing and other aspects and any kind of non-preconditioning efforts here?

David Chang -- President and Chief Executive Officer

OK. Salveen, I'm going to take the first part of the question, and I will ask Rafael to answer the second question regarding how we are leveraging the learnings from the ALPHA study in our other programs. The question around exactly when the data are presented, we do get that question. We are very close to the second quarter, and at this point, I think it would be fair to say that the target for our presentation is either ASCO or EHA meeting.

Rafael Amado -- Executive Vice President of Research and Development and Chief Medical Officer

Salveen, this is Rafael, and I'm going to address your BCMA question. So there's no question that the learnings from 501 can inform the BCMA program, and in fact, some of the changes in lymphodepletion that are introduced in 501 are mimicked in the 715 program. You may recall that there are other changes in lymphodepletion that were introduced at the beginning, at the outset in that study, which are designed to ascertain the value of adding cyclophosphamide and fludarabine to rituximab to ING 647 by itself, but we will be testing higher doses of ING 647 in that study as well. And obviously, things such as pharmacokinetics, PK/PD interactions, cell recovery, expansion and other parameters, we expect that the learnings from 501 will translate into 715, and therefore, I think it will help us accelerate decision-making as we see the data.

Salveen Richter -- Goldman Sachs -- Analyst

Thank you.

Operator

Our next question comes from Biren Amin with Jefferies.

Biren Amin -- Jefferies -- Analyst

Yes. Hi, guys. Thanks for taking my questions. Maybe if I could start with 501/501A.

How do your yields change with 501A versus 501 given your transduction efficiency is likely going to increase since you're not requiring the switch?

David Chang -- President and Chief Executive Officer

Biren, I mean, you're going straight into the very technical questions. Yes, when we change -- when you make the changes to constructs, viral titer and other things do change. And that's where we have a very strong process development team, as well as manufacturing team, and all these issues have been all worked out. And I can more or less tell you that the yield that we are getting from the manufacturing is really exceeding our expectations.

So I don't really see this being a major issue.

Biren Amin -- Jefferies -- Analyst

OK. And then I guess when you present the 501 data in second quarter, I just want to ask whether there's a risk where you're going to see the cells undetectable. So one of your CD19 competitors presented early data that actually used an assay where the cells were undetectable. So what's the risk of seeing a similar issue arise in 501?

David Chang -- President and Chief Executive Officer

Well, I mean, you're going into the data portion of our presentation, which we are not quite ready to talk about it. But let me just tell you, in terms of cellular kinetics and vector CAR T number, this is a topic that we have -- at least I, personally, have been working on for a number of years. And we took some of the necessary steps to make sure that we can get reliable biomarker data in our studies. So let me just stop there without revealing too much about exactly what we will represent, but the vector CAR T number is one of the important components of the translational research.

Biren Amin -- Jefferies -- Analyst

OK. And then maybe if I could ask a question on BCMA. So for the GSI program, when do you -- I guess when do you expect to start the Phase 1? Will it be after the Q4 data from 715? And I guess how are you planning on dosing the GSI with the CAR? And I guess, you know, David, at ASH a few months ago, Fred Hutch also presented their GSI data, and they saw some really good responses but also observed neurotoxin, I think, in about six of 10 patients. So do you anticipate that the safety profile would change with the use of GSI?

David Chang -- President and Chief Executive Officer

Great question. I'm going to ask Rafael to answer that question. Rafael has been looking into this particular area very intensely, and I feel we are pretty well prepared to embark on the Phase 1 study. Rafael?

Rafael Amado -- Executive Vice President of Research and Development and Chief Medical Officer

Yes. Thanks, David. So we plan to start the study in the second half of the year. We have a great collaboration with SpringWorks.

We're pretty excited about our initial interactions with them. We think the molecule has got a really good PK/PD profile. It doesn't penetrate the blood-brain barrier, so these issues of neurotoxicity have not really been observed. They've treated over 100 patients, so the profile, safety-wise, is pretty well understood, which is very useful when you're doing a combination trial, and as you know, they've got a registration path, which obviously helps with regard to potential co-development.

So by the time we do this combination, we probably will know a lot about both lymphodepletion and dosing, and we think it will be the right time to start applying the combinations to try to understand whether increasing BCMA expression actually results in superiority of our product. But so far, the preclinical data is pretty strong, and we look forward to testing this combination, which hopefully will translate into better outcomes for patients.

Biren Amin -- Jefferies -- Analyst

OK, great. Thank you.

Operator

Our next question comes from Cory Kasimov with JP Morgan.

Matthew Holt -- J.P. Morgan -- Analyst

Hey, guys. This is Matthew on for Cory. So for my first question, just wondering if you can discuss what you expect to have in hand in terms of ALLO-647 based on lymphodepletion dose levels at the time of the abbreviated 501A trial initiation. Basically, I'm wondering whether you expect the lymphodepletion data to be mature enough to result in a more narrow range of dose levels for the abbreviated 501A study.

David Chang -- President and Chief Executive Officer

So Matt, this is David. Let me take that question. We have been saying that we will be leveraging the learnings from the 501 in other programs, including 501A, and also definitely in the 715 program. Lymphodepletion, because it's really dealing with the host lymphocyte counts before the cells are given, this is quite, in our view, a generalizable finding.

So any learnings will be a fine stat. And to your question, as we have said in the prepared remarks, we have completed a dose escalation of ALLO-501 and we are actively recruiting patients into the ultimate lymphodepletion regimen cohort. So current projection is that we will definitely have some information, and that will be leveraged in how we move forward with ALLO-501 study.

Matthew Holt -- J.P. Morgan -- Analyst

Great. Thanks. And then I guess for the ALPHA trial, what should we keep in mind when comparing the initial data set to Phase 1 data sets from the CD19 autologous space?

David Chang -- President and Chief Executive Officer

Can you repeat the question? Sorry.

Matthew Holt -- J.P. Morgan -- Analyst

Just wondering, for the initial ALPHA data set, what should we keep in mind when comparing this to other initial Phase 1 data sets from the CD19 autologous CAR T space?

David Chang -- President and Chief Executive Officer

We are just being a little bit cautious about not talking too much about what will be presented at -- when we present the 501 data. I mean, the question that you are asking is a very important one. Certainly, we are trying to get the allogeneic cell therapy in terms of the safety and outcome to the point that is similar, if not better than, what has been reported with autologous. But you also have to realize that in a Phase 1 setting, we'll be dealing with a relatively small number of patients, as well as the fact that we are varying the lymphodepletion, so there's some different sets of information.

So just wait till we present the data.

Matthew Holt -- J.P. Morgan -- Analyst

Great. Thanks for taking my question.

Operator

Our next question comes from Tyler Van Buren with Piper Sandler.

Tyler Van Buren -- Piper Sandler -- Analyst

Hey, guys. Good morning. Congrats on the progress. With respect to the ALPHA data update next quarter, is it possible to just confirm the rough number of patients we should expect, and approximately what the split between DLBCL and follicular lymphoma is? And with respect to 647, I think you mentioned you're enrolling patients in the final lymphodepletion regimen.

So can you give us a sense of where 647 is in terms of the 39- to 90-mg range?

David Chang -- President and Chief Executive Officer

So we're going too much into the details of what is to be presented, so I'm going to, again, try to limit what I say, but let me just try to give some color to your question. In the prepared statement, we said that we completed the dose escalation. That alone should give a patient number of nine patients minimum, and certainly we are going beyond those nine patients in the dose escalation. So hopefully, that gives some color about what you may see.

And let me also emphasize that we get asked a lot about what's the duration data that you may present, but that is going to be very dependent on when the patient gets enrolled, and there are a lot of sort of dynamic nature of how the data is evolving, but when the presentation happens, we will be presenting all the available data at the time of the data cut.

Tyler Van Buren -- Piper Sandler -- Analyst

OK. That's helpful. And then for TurboCAR, can you say anything more about it with respect to what cytokine you guys may be using or maybe how it compares to some of the other approaches using the relatively well-known cytokines and why you guys chose to start with myeloma and if you plan to go into non-Hodgkin's?

David Chang -- President and Chief Executive Officer

Yes. For competitive reasons, we're not going to talk about which cytokine, but over the years, we have seen many different ways to enhance and provide extra so-called Signal 3 that is driven by the cytokines to the engineered T cells. And what we have seen, what I am seeing in the TurboCAR so far, is far better than anything else that I've seen before, so we are quite excited about this TurboCAR.

Tyler Van Buren -- Piper Sandler -- Analyst

That's very exciting. Thank you.

Operator

Our next question comes from Mark Breidenbach with Oppenheimer.

Mark Breidenbach -- Oppenheimer and Company -- Analyst

Hey, good morning guys, and thanks for taking the questions. David, I'm just wondering, is it realistic to expect that the lymphodepletion depth and duration requirements will likely be universal across different indications, ALL, NHL and multiple myeloma? Or do you think it's more probable that we'd see sort of different lymphodepletion requirements depending on the disease?

David Chang -- President and Chief Executive Officer

Great question. I wish I knew the answer. Over the years of doing clinical trials, and I am always surprised about the patient-to-patient or indication-by-indication differences, and that's exactly what we have to do in the Phase 1 study. So the way that you should be thinking about it is, as we understand the lymphodepletion and as we optimize the 647, we will have a very good framework to use that information and simplify the lymphodepletion exploration in other indications.

So that's how we are really leveraging the learnings from 501 in other programs, and I think that approach will be very effective in simplifying the lymphodepletion exploration in other indications.

Mark Breidenbach -- Oppenheimer and Company -- Analyst

OK. And just a quick follow-up. With regard to the ALPHA trial, I'm wondering if you're seeing a lot of screening failures due to recent rituximab exposure. And if so, would you expect enrollment in ALPHA2 to proceed at a faster rate than what you've been able to achieve in ALPHA?

Rafael Amado -- Executive Vice President of Research and Development and Chief Medical Officer

Yes. Mark, this is Rafael. I'll answer the question. I think that is a very perceptive observation in relation -- about rituximab exposure, but in spite of that, accrual has been very brisk, and we've been very fortunate to work with great investigators that have been very committed, and we're accruing, actually, as planned.

And we are exactly where we want to be with that study. Now with 501A, clearly, it'll be an easier study to accrue for the reasons that you mentioned, and we anticipate that it would go faster, but investigators are able to find patients for 501, and I think it's fantastic because it's allowing us to actually elucidate all these parameters that hopefully will allow us to move with 501A quicker. So you're right on your observation, but it's actually not really limiting our ability to enroll in 501.

Mark Breidenbach -- Oppenheimer and Company -- Analyst

OK. Terrific. Thanks for taking the questions.

Operator

Our next question comes from John Newman with Canaccord.

John Newman -- Canaccord Genuity -- Analyst

Hi, guys. Good morning. Thanks for taking my question. Just had a general question, David.

I know you don't want to get in too much of the details about the 501 study, but is there a chance that we might see some redosing data when we get a look at the data in the second quarter?

David Chang -- President and Chief Executive Officer

Great question. Redosing is one of the changes that we introduced into the protocol, and certainly, you will see some data. Exactly how many patients, I'm not going to say, but you will definitely see some redosing data.

John Newman -- Canaccord Genuity -- Analyst

OK. Great. And then just one follow-up question, and this is a little bit broader. I'm sure you remember very well back when Kite and Novartis both had their CD19 CAR T products in development in the autologous setting.

And there was a big debate about whether longer persistence with Novartis' product with the 4-1BB CAR was going to result in better efficacy versus the costim that Kite was using, which was CD28, and it ultimately turned out that the efficacy was almost the same. I know that we're dealing with a very different product here, because this is allogeneic, but can you maybe talk a little bit about how we should be thinking about persistence and detection of these cells? Is there a certain threshold that we should be thinking about? Because I know that this is different, and we have to worry about host-versus-graft here, but just curious as to how you're thinking about that.

David Chang -- President and Chief Executive Officer

Yes. John, the question that you are asking, that is a very complicated question to answer. I'm going to sort of answer it in a different way, which is really coming from the existing experience in non-Hodgkin's lymphoma. In non-Hodgkin's lymphoma, if you have a response at Month 3, the likelihood that that response will be maintained in a longer follow-up is very high, which means that whatever the initial killing of the tumor cells, that really has a great impact on the durability of the response.

And that's more or less how we are thinking about the cell persistence in this setting. And if you look at some of the autologous CAR T data, especially with the CD28 close tumor to domain containing constructs, you're talking about cell expansion and persistence probably two to three months, sometimes a little bit longer. And if we look at our own UCART19 data, that level of cell persistence is something that was able to be achieved in the UCART19 study, and certainly, when we present the data, we'll detail more findings on cell persistence that we see in the 501 study.

John Newman -- Canaccord Genuity -- Analyst

Great. Thank you.

Operator

Our next question comes from Ren Benjamin of the JMP Securities.

Ren Benjamin -- JMP Securities -- Analyst

Hi, good morning. Thanks for taking the questions, and congrats on the progress. I guess this is just a broader-picture question regarding your iPSC programs and how you're seeing the allogeneic space evolve. Is this something that evolves where there's space for both healthy donor cells and iPSCs? Do you think that iPSCs ultimately take over? How do you see this kind of shaping out moving forward?

Rafael Amado -- Executive Vice President of Research and Development and Chief Medical Officer

Hi, Ren, this is Rafael. I'll give it a try, but what you are asking is still unanswered. I think obviously the iPSC field is extremely exciting. For one, it allows us -- or it will allow the field to have a homogeneous product that is well characterized and inexhaustible, in theory, which would transform the field.

I think the characteristics of the T cells that emerged after iPSC differentiation, that still is being worked out. Will they be similar in terms of function, persistence, etc., as [Inaudible] T cells? Can they be engineered and still maintain the T cell differentiation capacity? Will they have the same molecule cytokines, receptors and ligands to penetrate and traffic through a tumor? I think all of these things will need to be evaluated, but we're starting to see what happens in the NK space differentiation for iPSC, and we see that promise, and we're pretty excited about it. And as you know, we're working pretty hard with Notch, which -- that collaboration is off to a really good start. And so in terms of how it will compare to autologous healthy donors, I think we will have to see how the future evolves.

At the moment, our focus in terms of the clinical trials is using allogeneic donors, and we are, I think, leading in recruiting and ascertaining what are the best parameters for dosing, lymphodepleting, issues such as the ones that have been asked, persistence, etc. And we plan to bring that forward to the clinic, but it will be an intrinsic process. We're working in parallel, and we expect that this technology will evolve and maybe become the future, or it may coexist with normal donor gene therapy as well. So I think it's a matter of sort of watching this space, and it's great.

At least, I feel it's fantastic that there are so many opportunities and that the technologies are advancing to make it easier, more available to patients, which would be the case in the iPSC setting.

Ren Benjamin -- JMP Securities -- Analyst

And just as a follow-up, regarding donor cells and healthy donors, I know there's a lot of work going into the lymphodepletion regimens and things along those lines. Is there still a lot of work being done in terms of the ideal donor cells and types of donors that you want? Or do you feel that that's largely pretty much anchored down and everything else is -- you're focusing on later-stage parameters to change?

David Chang -- President and Chief Executive Officer

Ren, let me take that question. Based on the sort of successes that we are having with the manufacturing, I think we feel that donor selection became a little bit less of an issue. But that is an interesting topic that we are continuing to investigate, and certainly, as we do more manufacturing runs, we'll have more data point to really understand whether there is such an individual as a super donor. But ultimately, all these learnings will be applied to how we improve, continuously improve, the manufacturing process.

We cannot build a program based on super donors out there; that knowledge will translate into our manufacturing improvement. That's how we see it.

Ren Benjamin -- JMP Securities -- Analyst

Got it. And just one final one from me. Just going back to the redosing question, can you just talk us through what are the, I guess, alternative redosing protocols that you're evaluating?

Rafael Amado -- Executive Vice President of Research and Development and Chief Medical Officer

So I'll take that question. So the amendment that we announced at the last call does allow for redosing, in addition to dosing patients that have received autologous CARs in the past. We will see, probably, a few patients, as we're enrolling some patients that are being redosed. These are patients that have benefited or eventually developed stable disease.

There are some parameters in the protocol that allow for redosing, and of course, the patient has to convert to express CD19, and we have to rule out that there are antibodies against the donor, but if they meet the conditions, they are eligible for redosing, which is fairly simple in the allogeneic setting. If they are very close to the lymphodepletion, it could be given using the same lymphodepletion. If it's longer than a period of time where the cells have recovered, then they need to be conditioned again. So we will see some of those patients, and it will be, I think, very informative to see how patients behave after second dose, and also, likewise, how do they behave after having progressed on prior AlloCAR therapy, which are two of the changes that we made in the amendment.

We look forward to seeing what happens with those patients, but our main objective remains to understand the optimal lymphodepletion and to utilize to the maximum benefit the flexibility of our ALLO-647 antibody, which we think is -- it gives us a lot of flexibility. It's their stem cells, it allows for recovery of granules types and platelets relatively quickly and remains in maintained lymphodepletion to allow for engraftment. So that is really our singular focus now, is what is the optimal lymphodepletion regimen.

Ren Benjamin -- JMP Securities -- Analyst

Great. Thank you, and congrats on the progress.

Operator

Our next question comes from Sami Corwin with William Blair.

Sami Corwin -- William Blair and Company -- Analyst

Hi, David. Sami on for Raj. Thanks for taking my questions, and congrats on the progress. Just a couple of quick ones from me.

I was curious -- I know it's still early, but are you guys thinking that the TurboCAR ALLO-605 program will eventually replace ALLO-715? Or are you kind of thinking those two programs will advance in parallel? And then in regards to the redosing, are you redosing at the same dose or are you giving patients a higher dose upon the redosing? And then I have a quick housekeeping follow-up.

David Chang -- President and Chief Executive Officer

Yes. Sami, this is David Chang, and I will take the question around 605 and 715. Great question, but at this point, it's too early in terms of how we can answer it because we will really have to examine different approaches and how different approaches leads to a different patient outcome. And ultimately, based on that, we will make a decision on whether we go with one or more than one.

A multiple myeloma indication provides a lot of different opportunities, and I certainly believe that this is a field that can accommodate not just the first generation but the next generation in simultaneous ways. So that's one of the reasons that we are really ramping up our approach toward the BCMA in multiple myeloma.

Sami Corwin -- William Blair and Company -- Analyst

Great.

Operator

Thank you. This concludes the question-and-answer session. I would like to turn the conference call back over to management for any additional comments.

David Chang -- President and Chief Executive Officer

Well, thank you for joining us on this call today and your continued support of Allogene in what we know will be an exciting year for allogeneic cell therapy. Operator, you may now disconnect.

Operator

[Operator signoff]

Duration: 56 minutes

Call participants:

Christine Cassiano -- Chief Communications Officer

David Chang -- President and Chief Executive Officer

Rafael Amado -- Executive Vice President of Research and Development and Chief Medical Officer

Eric Schmidt -- Chief Financial Officer

Marc Frahm -- Cowen and Company -- Analyst

Salveen Richter -- Goldman Sachs -- Analyst

Biren Amin -- Jefferies -- Analyst

Matthew Holt -- J.P. Morgan -- Analyst

Tyler Van Buren -- Piper Sandler -- Analyst

Mark Breidenbach -- Oppenheimer and Company -- Analyst

John Newman -- Canaccord Genuity -- Analyst

Ren Benjamin -- JMP Securities -- Analyst

Sami Corwin -- William Blair and Company -- Analyst

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