Good day and thank you for standing by. Welcome to the Q1 2021 Xencor Conference Call. At this time, all participants are in a listen-only mode. After the speakers' presentation, there will be a question-and-answer session. [Operator Instructions] Please be advised that today's conference is being recorded. [Operator Instructions] I would now like to hand the conference over to your speaker today, Mr. Charles Liles, Head of Corporate Communications and Investor Relations. Sir, please go ahead.

Thank you and good afternoon. Earlier today, we issued a press release, which outlines the topics we plan to discuss today. The press release is available at www.xencor.com. Today on our call, Bassil Dahiyat, President and Chief Executive Officer, will provide a corporate overview and will review recent partnership news. Allen Yang, Chief Medical Officer, will review clinical updates. And John Kuch, Chief Financial Officer, will review financial results. And then we'll open up the call for your questions. Before we begin, I would like to remind you that, during the course of this conference call, then Xencor management may make forward-looking statements, including statements regarding the Company's future financial and operating results, future market conditions, the plans and objectives of management, future operations, the Company's partnering efforts, capital requirements, future product offerings, research and development programs, and the impacts of the COVID-19 pandemic on these topics. The forward-looking statements are not historical facts, but rather, are based on our current expectations and beliefs, and are based on information currently available to us. The outcome of the events described in the forward-looking statements are subject to known and unknown risks, uncertainties, and other factors that could cause actual results to differ materially from the results anticipated by these forward-looking statements. Including, but not limited to, those factors contained in the risk factors section of our most recently filed annual report on form 10K and quarterly report on form 10Q. With that, let me pass the call over to Bassil.

Thanks, Charles and good afternoon, everyone. Xencor's approach to creating antibody and cytokine therapeutics is based on our extant protein engineering platform. It's built on our extensive protein engineering know-how combined with our suite of XmAb Fc domains. Which we use to build novel molecular structures, improve natural protein and antibody functions, and create new mechanisms of therapeutic action. The plug and play portability of our XmAb Fc domains and the speed of our protein engineering capabilities enable us to rapidly explore different targets and biologies so we can select the most promising programs to take forward. We've been focusing our work on the expansion and use of our XmAb bispecific platform, the newest XmAb component, to create antibodies that bind two or more different antigens simultaneously, and also to cytokines with structures optimized for particular therapeutic uses. Now, our many partnerships really highlight it's plug and play nature. Currently we have 15 ongoing partnerships for XmAb technology, which have now resulted in two marketed products. Alexion's Ultomiris for rare blood disorders and MorphoSys' Monjuvi is the first second-line treatment for patients with diffuse large B-cell lymphoma. Just this past March, our partner Vir Biotechnology, with its partner GSK, submitted an emergency use authorization application to the FDA for VIR-7831, they're anti-SARS-CoV2 antibodies that incorporates our Xtend Fc technology. Based on an interim analysis of the Phase 3 COMET-ICE trial, which demonstrated an 85% reduction in hospitalization or death in high-risk adult outpatients with COVID 19 receiving VIR-7831 as monotherapy, compared to placebo. The primary endpoint of the trial, by the way. Now Xtend was integrated into VIR-7831 for the purpose of reducing the dose administered and potentially enhancing its lung tissue bioavailability. Now, this partnership exemplifies our commitment to enabling the broad use of XmAb Fc technologies outside our core focus of oncology and auto-immune diseases and demonstrates XmAb's vast applicability to underserved areas like serious infectious disease. Now if authorized, VIR-7831 would then become the third antibody with our XmAb technology to reach the market. Now, switching back to internal programs, we're currently running seven Phase 1 studies evaluating XmAb bispecific antibodies and cytokines. This way, we're taking multiple simultaneous shots on gold clinic. And the proof of concept data we generate will guide which programs we independently advance, which we partner, and which we will terminate. I'll let Allen Yang, our Chief Medical Officer, review updates for our clinical portfolio. Allen?

Thanks, Bassil. Since our last update about two months ago, we dosed the first subject in the Phase 1 study of XmAb-564, our wholly-owned, IL-2 Fc fusion engineer to selectively activate regulatory T-cells or Tregs for the treatment of autoimmune diseases. The goal of an IL-2 therapy for auto immune disease is to provide sustained low-intensity activation of Tregs while avoiding the pro-inflammatory systemic activation of effector T-cells. An IL-2 therapy that is selected for Tregs with an expanded therapeutic window compared to historic IL-2 approaches would have broad potential across many different autoimmune diseases. And pre-clinical studies indicate this may be the case for our program. It is engineered with reduced potency to improve tolerability, improve duration of action for this normally toxic cytokine. And using our XmAb heterodimeric Fc domain and Xtend technology enhances its half-life. XmAb-564 is now our second cytokine in the clinic, joining XmAb-306, our engineer IL-15 for oncology that is partnered with Genentech. The single ascending dose study will characterize the safety, tolerability, and pharmacokinetics of XmAb-564 in healthy volunteers. And it will include an analysis of key immunomodulatory biomarkers. For the remainder of the year and into early 2022, we are planning to initiate several additional clinical studies to advance our wholly-owned bispecific antibody drug candidates. First, for XmAb-717, our PD-1 CTLA-4 dual-checkpoint bispecific antibody. In mid 2021, we plan to initiate a Phase 2 study for patients with certain molecular subtypes of castration-resistant prostate cancer as monotherapy, or in combination, depending on the subtype. As these patients represent a high unmet medical need. Previously, this was planned as a Phase 1B study, but we have transitioned it to a Phase 2 study. We continue to expect that we will present more data from the ongoing Phase 1 study's expansion cohorts later this…

Thanks, Allen. Now we're always looking to grow this pipeline with new programs, as we have with our IL-2 Treg and ENPP3 programs that Allen just mentioned. Along this front, last month at the AACR annual meeting, we presented data from four pre-clinical stage programs, including our third cytokine and IL-12 Fc fusion protein for oncology, two additional XmAb 2+1 CD3 bispecific antibodies. These ones target [indiscernible] and GPC3, as well as our PDL1 by CD28 bispecific program. All four posters are available on our website. Now I'd like to take a moment to review this targeted CD28 platform, which is a new class of T-cell engager designed to complement other mechanisms of T-cell activation, such as checkpoint inhibition or CD3 engagement. CD28 is a key immune co-stimulatory receptor on T-cells that has been difficult in the past to safely and effectively engage therapeutically. By targeting a CD28 binding domain to a tumor by using a bispecific antibody, we have to boost the activity of T cells in a tumor-specific way to enhance T-cell directed therapies. Our most advanced wholly-own, lead CD 28 candidate is a B7H3 by CD28 bispecific antibody for potentially broad solid tumor use, including in prostate cancer, where B7H3 is highly expressed. This molecule is advancing through clinical development now. Of course, the focus of our new collaboration with Janssen, that we announced a few months ago, is to discover a CD28 bispecific antibody against a prostate tumor target. A core part of our business is to complement our internal development portfolio with partners like Janssen and many other leading companies in the industry. These partnerships generate payments from the licensing of XmAb technologies, the clinical advancement of XmAb candidates, as well as royalties from sales-approved products. There were no COVID-19 impacts to partnering revenue that…

Thank you, Bassil. Xencor's broad protein engineering platform and resulting partnerships and collaborations continue to generate revenue and provide value to support our core portfolio of clinical and research stage bispecific antibody and cytokine drug programs. Cash, cash equivalents, and marketable investment securities total $577.1 million as of March 31, 2021 compared to $604 million on December 31, 2020. The decrease reflects royalties and milestone payments received related to licensing agreements net of cash used to fund operating activities for the first quarter. Based on current operating plans, we expect to have cash to fund research and development programs and operations into 2024. And we currently estimate that we will end 2021 with between $425 million and $475 million in cash and cash equivalents. Total revenues for the first quarter were $34 million compared to $32.4 million for the same period of 2020. Revenues in the first quarter include revenue related to our Janssen collaboration, milestone revenue recognized from MorphoSys, and the royalty revenue from Alexion and MorphoSys. Compared to revenues from the same period in 2020, which were primarily milestone revenue from MorphoSys, royalty revenue from Alexion and licensing revenue from our Aimmune and Gilead collaborations. Research and development expenditures for the first quarter were $41.4 million compared to $33.9 million for the same period in 2020. The increase is primarily due to increased spending on our XmAb 306, XmAb 564, and XmAb 819 programs. General administrative expenses for the first quarter were $8.2 million compared to $7.2 million in the same period of 2020. The increase primarily being related to an increase in staffing. Other income for the first quarter of 2021 was $13.2 million and included a gain of $12.9 million in equity received in connection with the licensing transaction, compared to $0.7 million for the same period in 2020, which was primarily net interest income earned for the period. The net loss for the first quarter was $2.5 million or $0.04 on a fully diluted per share basis compared to a net loss of $8.1 million or $0.14 on a fully diluted per share basis for the same period in 2020. The lower net loss reported for the first quarter of 2021 compared to the net loss for the same period of 2020 is primarily due to other income recognized from equity received in the first quarter of '21 in excess of increased spending on research and development expenses for the period. Non-cash based compensation expense for the first quarter was $8.3 million compared to $6.5 million for the same period of 2020. And total shares outstanding were 58.2 million as of March 31, 2021, compared to 57 million as of March 31, 2020. With that, we would now like to open up the call for questions. Operator?

[Operator Instructions] You have your first questions from Ted Tenthoff of Piper Sandler.

I'm wondering whether or not we should anticipate an update for the Roche program for IL-15 this year. And also, just going back to PD-1 CTLA-4 717, we won't be getting prostate cancer data, but what other cohorts could we expect from that this year?

Thanks, Ted. So regarding our XmAb 306 IL-15 program, that's the oncology collaboration with Genentech. We are discussing a publication plan with Genentech. We don't have specific guidance for timing of data this year. I will point out that the dose escalation in a broad range of solid tumor patients continues monotherapy, which was started last March, as well as the, we're continuing the [indiscernible] as a combination with atezolizumab, their PD-L1 molecule, which started in Q4. So those are ongoing. We'll come up with guidance. Once we have agreement with Genentech on the publication plan, as well as, of course, keeping people abreast of any additional study starts that happen over the next year. With regard to XmAb 717 or PD-1 CTLA-4 molecule. Yes, there are going to be additional cohorts that we disclosed data for from the expansion cohorts of the Phase 1 study. So in addition to a much more mature data set from our prostate cancer cohort, we'll have a more mature data set. It was only partially enrolled for our renal cell carcinoma cohort, as well as more mature data from our basket cohort of multiple tumors that are not in PD-1 approved indications. So we would expect all of that in the second half of this year.

Your next question from Mara Goldstein of Mizuho Securities.

So I wanted to ask two things. The first is around the strategy of converting that Phase 1B in prostate cancer to Phase 2 and what you will achieve by that. And then, the second is around the cytokine strategy. I mean, clearly we're seeing the beginnings of a lot of early work with novel engineered cytokines and the like, and so, I'm just curious as to sort of what you're thinking from a competitive perspective and a competitive advantage using the XmAb technology as you are versus, let's say, engineered cytokines and other fusion proteins and the like.

Yes. So I guess on the first question that the shift of XmAb 717 PD-1 CTLA-4 study in prostate cancer that multi, that basket study, why shift from a Phase 1B to Phase 2? My understanding, and Allen, you should pipe in here, was that it was simply a better reflection of what the study actually was doing, given that we have the forward dose we selected for that study, merely that. Anything to add, Allen?

Yes, no, it is a little bit of nomenclature. Remember, a Phase 1B could be looking at combination. So we had already sort of disclosed that this will explore 717 with sort of key combinations of either chemotherapy or targeted agents. And whether you call that a Phase 1B or a Phase 2 with a safety run? And I think a Phase 2 is a better accurate description. We sort of know our dose. We know the combinations we want to try, and we're really looking for a signal in certain sort of molecular subgroups or clinical subgroups of prostate cancer. So it's more reflective of Phase 1 and planning to go to an eventual Phase 3.

Yes. Now on your second question, Mara, for the cytokine, the strategy we're taking for this really rapidly evolving and growing field of engineered cytokines, I'll maybe ask John to interlay. Who's actually on the call here to answer questions, to chime in about how our design strategy has some commonalities for how we're looking at all the cytokines and yet how we're tweaking it for the individual ones. We agree, it's a really exciting area, which is why we're committing a lot of additional efforts and resources there. John, you want to get in here?

Yes, sure. Mara, when we first tackled IL-15, we went in, we fused IL-15 to an FC to make a long acting cytokine. And we made a critical key discovery that natural cytokines are limited in their ability to stay around very long in circulation. And so, the solution we came up with was to decrease the potency fairly dramatically. And in doing so, we found out that we actually make a much better drug. It lasts a lot longer in circulation and because it can last longer, even though it's lower potency, can actually mediate its form [indiscernible] for a longer period of time. Also, the fringe benefit of that reduced potency was much better tolerability and much better control over toxicities as you dose escalate. Now we turned it around and applied that same concept to the IL-2 program, our Treg expander, followed exactly the same result that we got dramatic improvements in pharmacokinetics and pharmacology when we reduce the potency. So far, that seems to be playing out really nicely with the asphalt program as well, as we detailed on our ACR tester. So that's the unifying theme, which seems to be pretty unique in the community, is going with longer acting, lower potency molecules.

Your next question from Peter Lawson of Barclays.

And just on IL-2, when did we see data around that? And how do you think about picking particular tumors and combination partners?

Well, our IL-2 is targeting activation of regulatory T-cells. So that's our program focused in autoimmune disease. Our IL-15 is the one that is the collaboration with Genentech, is our play with the cytokine for activating T-cells along that same pathway. So do you want us to talk about the IL-15 or do you want to talk about the 564 program?

I'm just curious if you're thinking of moving that IL-2 as well into oncology or…

No, no, we don't have any intention to do that. Its biology is really tuned, as John said, well, it's tuned for potency. But in addition for that IL-2 molecule, we actually took the direction, like some other companies that are looking at the same approach of increasing the relative binding affinity to the inhibitory, well, to the receptor that's more prevalent expressed on regulatory T-cells, the IL-2 alpha receptor. So we really feel that's much more appropriate for autoimmune indications. We haven't yet guided specifically on when we expect to have data from the single ascending dose. Essentially, it's a biomarker and safety study. The initial work in the clinic with that molecule could be later this year, but we'll guide specifically as we get a little further into the study. We just opened the study about a week ago.

And then the B7-H3 construct. I think you talked about that before, just curious where that is and where you're thinking of positioning that construct.

Yes. I'll touch on the timeline, and then if John wants to jump in on how we're positioning it. That molecule, we hope to have in the clinic in 2022, it's in active pre-clinical development now, with all the requisite manufacturing scale of activities just getting started. John?

Yes. In terms of thinking about applying that, the reason we selected B7-H3 as a target is it's very broadly -- they're very brightly expressed across a range of solid tumors. And we wanted a molecule that we could use to target tumors, get tumor-specific CD28 co-stimulation, which is your signal 2, and then you could use that to build on whatever signal 1 is being provided. And that signal 1 could be provided either by just natural T-cell reactivity against neoantigens, in which case you'd probably want to be exploring that -- our B7-H3 x CD28 and a P-1 combination study or signal 1 could come from any one of our T-cell engagers. They're classic CD3 bispecifics in our silent tumor pipeline, the first of which will be an ENTP3 x CD3. And I guess beyond that, I would also say B7-H3 is a particularly interesting target in prostate cancer. It's very bright there and we, of course, would want to explore that in prostate cancer, as well.

Your next question is from Alethia Young of Cantor.

This is Li for Alethia. We just have a follow-up on the IL-2 program. Since you just recently started a trial, can you just talk a little bit about how your molecule is differentiated from others in the space, and what advantages that you expect to see in the clinical setting?

Right. The design follows the rule of our cytokine engineering that John sort of laid out, which was, it's taking the natural IL-2 molecule and making mutations in it, to dramatically dial down its potency. I think we're north of a hundredfold less potent than wild type IL-2 fused to an Fc domain. Now, the things that make this particularly well-suited for autoimmune disease is, our protein engineers biased the binding to actually have a significantly higher ratio of binding to the CD25 or IL-2 alpha receptor than to the IL-2 beta gamma receptors. That receptors is heavily expressed on regulatory T-cells to bias it towards T-regs. So how do our designs differ from the -- sort of what's the positioning? We hope that our dramatically lower potency as well as our Fc domain, which contains our Xtend technology, gives us an enhanced therapeutic window. We won't know until we see. And that we can get excellent T-reg amplification. John, am I'm missing anything on -- and maybe John, if you want to comment on the monomeric IL-2 nature and how that's distinctive in the industry.

Yes, no, that's a good point. We designed ours using our Fc heterodimers, which enables this. We designed ours to only have a single IL-2 for the Fc domain whereas competitors like Amgen, or other efforts, have a bivalent Il-2. We think having the monovalent IL-2 actually helps reduce internalization through receptor binding. That's kind of a classic paradigm in terms of biologics and internalization. The bottom line is, again, we applied our potency reduction, monomeric IL-2. We would hope that we have highly competitive, or even best-in-class pharmacokinetics and pharmacodynamics.

I have another question on your IL-12 program. I know it's preclinical, but just curious how you're thinking about designing a molecule that can potentially address the narrow therapeutic window here.

John. You want to take that, I guess?

Yes, sure. I'll take that. You can see a pretty nice story about this on our ACR poster. We found, again, that the potency reduction gave us much better control. When we put the IL-12 potency-reduced version into monkeys and compared it to a wild type IL-12 Fc fusion -- we found that as we dose escalated in nonhuman primates, that we saw much more gradual onset of a key pharmacodynamic marker, which is IP-10, which is downstream of interferon-gamma. That's what IL-12 famously does. And so as we dose escalated our potency-reduced version, it was a much smoother ramp-up on that pharmacodynamic marker -- by comparison of a wild-type IL-12 Fc. And what that tells me is we're going to have a much easier ride when we dose escalate, because we've got much better control over what's actually going to go on in the humans, when we use this reduce potency molecule. So that's what we have so far. That's what the preclinical data suggests, but obviously we're going to have to see what happens at the clinic.

Our next question from Etzer Darout of Guggenheim.

So really for the XmAb 564 I guess, if you see the appropriate therapeutic window, do you have any thoughts on how, maybe the low-hanging fruit indications, if you will, or maybe interesting indications that you could pursue initially, obviously assuming success? And then I have a second question.

Yes. We're not guiding on specific indications we're selecting yet, though we're hard at work putting ourselves in a position to hopefully start them as soon as we come out of dose escalation. Of course, there's a multiple-ascending dose escalation component to the study that'll start after the SAD. We think there's a lot of opportunity for these novel mechanisms of action, like T-reg inhibition, in some of the smaller auto-immune indications. And so we're certainly looking there, but I think when you look at the competitive landscape in some of the larger indications where there's still open room, we think a lot of our competitors have already hit those. So more to come on that. We are working hard on that. Now, did you have a follow up question?

Got it. Yes. Just a second question, on the initiation of the plamotamab, tafasitamab study. And I guess based on the interim remarks, is the data from the ongoing Phase 1, if you will, sort of the main hurdle to sort of getting that started in terms of the time line variability that you described?

I think it's pretty coincident with the operational pieces as well. And I think that -- we hope they'll all come together. We are dosing at Q2 week now with a Q-weekly run-in period, much like we have seen from other programs. So squaring that away is ongoing, and we hope to have that data present late this year, like we guided. And hopefully start off the Phase 2.

Our next question from Tom Shrader of BTIG.

For 564, what is the theoretical safety concern from too many T-regs?

I don't know if it's from too many T-regs, I think it's a combination of being non-selective and having lots of T-cells period amplified is the problem. And that can cause your usual capillary leak syndrome, cytokine syndrome, the toxicities that are seen with IL-2 therapy, with proleukin. So you just need to control that from coming on too strong, whether it's the T-regs you're amplifying or T-effectors.

Another way of saying it is, we optimize selectivity of our IL-2 for T-regs, but there's no such thing as perfect selectivity. So at some point, if you dose high enough, you're going to start tickling effector cells and other cell populations.

And to just dig in a little bit to the last question. I mean this molecule could in fact play in many, many places. Do you think your likely first trial would be something like psoriasis where you get a clinical readout very quickly and then you'd be confident to try many other things? Or do you think a good biomarker signal would be enough to go into more challenging applications?

Yes, it's a great question because that's something that, with many programs, we mull over, and I think people around the industry mull over. Do you want to get some kind of disease modification signal, even if it's an indication that is not necessarily a great development path because of competitive density, or do you trust the biomarkers? I think that the thesis around T-regs' role in modifying disease activity is one risk that most companies seem to be willing to take as long as you can get the good biomarker movement. I mean, you know what you're trying to do, how that plays into disease. I wonder if, even if you proved it in something like psoriasis, which is probably a tough hill to climb from a development and a competitive standpoint, even if you showed disease-modifying activities, I don't know how well it would translate. So I don't know if Xencor really favors that approach as opposed to, like many of our competitors, looking at the T-reg counts and the other T-cells as the biomarker, that's really definitive for a go signal.

Our next question from Zhiqiang Shu of Berenberg.

The first one, on 717, you said that you're going to move to the combination trial in prostate cancer. What kind of combinations are you thinking to potentially move to, to treat different set, groups there? That's the first one.

We're not saying explicitly. I think -- and Allen, jump in if I'm missing anything -- but depending on the subtype and what's known about how they respond or don't respond to treatment, they will include both chemo combinations as well as some targeted therapies that make sense for certain molecular subtypes. I don't know if we can say more than that, Allen, right?

Yes. I think it's fairly obvious. There's some targeted agents that have been approved for prostate cancer like PARP inhibitors. And then the chemotherapy is still used in a certain aggressive type as well. So those subtypes you would have to combo with a checkpoint inhibitor, and so obviously we're going to explore those.

Got it. And then I'm just curious about the CD28 biology here. What's the -- I guess broadly, what's the difference between CD28 bispecific versus CD3 bispecific from, I guess, safety and efficacy standpoint. Is it more…

That's a long question. John, why don't you try -- I mean, I guess you could do it briefly. Go ahead.

Yes, that's a great question. You know, so this, the CD3 is kind of a bigger hammer, right. So CD3 is signal 1 on the T cells. And it's not specific to any particular T cell population, right. The point of a CD3 is to grab any T cell in the vicinity and mobilize it against the tumor. And so of course that's going to be a little bit more challenging in terms of safety profile either in terms of CRS, but also in terms of just on-target off-tumor toxicity. With the CD28, it's a pretty intriguing concept because it's providing the signal 2 which can amplify a signal 1 and then it can build off of a signal 1 that's coming elsewhere, right. And like I was saying with one of the earlier responses, this signal 1 could come from an endogenous T-cell reacting with a tumor cell, and now you're adding in that signal 2 with the CD 28 and amplifying that natural endogenous T-cell antitumor response or Signal 1 could come from a CD3 bispecific, and you could combine the 2. And so we're obviously contemplating both approaches.

Got it. Final quick one on 698 CD38-CD3 molecule. I guess where do you see this molecule go in the future development?

So right now, we're following the lead of some investigators who were enthusiastic about a CD38-CD3. We'll note that Amgen decided to jump out of development. And really this was a molecule we had enabled with our technology but hadn't actually made for them. They just took our various building blocks and put them together for CD38-CD3 and FC domain. And in myeloma they felt that the AE profile wasn't consistent to go forward with it. We'll say that, without disclosing until we've got the trial up running, there are other hematologic malignancies that express CD38 where the tolerability profile might seem quite reasonable in that context. So more to come on that.

And speakers, our last question is from Arlinda Lee of Canaccord Genuity.

This is Ben calling in for Arlinda. A lot of them have been answered. I just wanted to ask a few on 717 and plamotamab. A few PD-1 CTLA-4 programs have data that have been presented at this point. And I'm just wondering regarding 717, how is the safety looking versus nivo versus an IPI combination regimens? And what you guys ultimately hope to show in the data?

I guess I'll answer the first -- answer first , what do you hope to show in the data? We hope to show that in that we can find an indication or we can make a difference for patients, whether that's in a relapse-refractory setting, like some of the areas we're looking at, or even more exciting we think is in areas where there aren't checkpoints approved, where the combination of MOAs and the tolerability profile, the combination of CTLA-4 and PD-1 can move the needle that hasn't been moved before. And I think prostate cancer is a great potential example there. Regarding the safety profile we observed so far, I'll let Allen take that question.

Yes. Bassil, thanks. So it's fair to say that nivo-IPI combination is probably more effective than PD-1 blockade alone, but clearly you get a lot of toxicity. Only about 1/3 of patients remain on study past a few courses. So the most common toxicity is colitis. This is the most common toxicity, or the most common toxicity that leads to interruption or discontinuation. And so we haven't seen that high frequency of colitis. We believe that the indications, as Bassil alluded to, is where PD-1 plus CTLA-4 has been shown to be synergistic. And perhaps you haven't seen that much of an improvement activity, and prostate cancer is a classic example of that.

Okay, great. That's very helpful. Switching gears to plamotamab, and I understand that MorphoSys might be driving a little bit of a bus here. It's a competitive space. And I'm just wondering how do you think of plamotamab in a competitive positioning? And maybe can you comment on what you think the development strategy will be? Do you expect maybe data in 2022 at some point?

Yes. So I'll take that one. So the position [indiscernible], you're right, it's a very competitive area, CD20 CD3s, in an already competitive indication in lymphoma. And we think that the approach we're taking is recognizing that, that competition is going to be hard and that we need to go with something that is really combining the two most active regimens we can that has the best scientific rationale we can think of and to see if we can go for the best approach -- sorry, the best combination approach to that, and the key point is chemotherapy-free, a direction the field desperately wants to move in, in lymphoma, just like it has happened in leukemia based on the success in CLL, ibrutinib and venetoclax used with antibodies. So the [plamotafalen] combination is tafasitamab-lenalidomide is the most active and a very durable combination therapy in second-line and later aggressive lymphoma. It's a well-tolerated regimen, and it uses orthogonal mechanisms of action to plamo to CD20, CD3. It's effector cells and aid effector cells driven by the Fc technology that we put into tafacitamab and CD19 binding. So a different target also than a CD20/CD3. So it really seems like a really totally perpendicular mechanisms of action that hopefully can complement each other. And so we wanted to combine with the most active agent that was really tolerable. So that's our strategy. It's going for a chemotherapy-free regimen that could be super active. And that's how we hope to distinguish ourselves.

Okay, great. So that would be a simpler regimen than existing regiments right now?

Well, hopefully, again more tolerable and without the chemotherapy type of toxicities, which can often include long-term toxicities and secondary malignancy risks and there's a whole host of others. Okay. Go ahead. Go ahead, Allen. Sorry. Before you go onto another one, Ben.

Maybe I can add some color. So the strategies have been sort of declared by our competitors, right? So there's two chemo regimens that are often used for the second line. It's either GemOx or bendamustine Rituxan. And the strategies that our competitors are using are either to compete against that directly as a single agent or add on to that regimen like GemOx. As Bassil alluded to, our strategy is sort of a little bit different. Tafasitamab, at least in the transplant-ineligible population who have been already approved for that second-line indication, right, and so now we're adding our CD20 to their CD19. And then, of course, lenalidomide potentiates the CD19. It could potentially potentiate the CD20 as well. And so that is the sort of differentiating approach. So we think our approach is vastly different from the others. Sorry, back to you Ben.

No worries. I'm sorry to interrupt you. And so the data readout, do you think, might be in 2022 or maybe later?

We're not guiding on that yet. We want to get the trial started, then we'll give specifics. All right. Well, I guess that's the last question. We'd like to thank everybody very much for joining us today. Hope you have a wonderful rest of the afternoon and we look forward to catching up again and getting further updates on our progress throughout the year. Thank you.

This concludes today's conference call. Thank you all for participating. You may now disconnect.