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Xencor Inc (XNCR) Q4 2020 Earnings Call Transcript | The Motley Fool

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Xencor Inc (NASDAQ:XNCR)
Q4 2020 Earnings Call
Feb 23, 2021, 4:30 p.m. ET

Contents:

  • Prepared Remarks
  • Questions and Answers
  • Call Participants

Prepared Remarks:

Operator

Ladies and gentlemen, thank you for standing by, and welcome to the Fourth Quarter and Year-End Xencor Conference Call. [Operator instructions] After the speaker presentation, there will be a question-and-answer session. [Operator instructions] [Operator Instructions]

I would now like to hand the conference over to your speaker today, Charles Liles, Head of Corporate Communications and Investor Relations. Please go ahead, sir.

Charles LilesHead of Corporate Communications and Investor Relations

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 updates throughout our clinical portfolio; and John Kuch, Chief Financial Officer will review financial results. And then we’ll open up the call for your questions, and we’ll be joined by John Deserly, Chief Scientific Officer.

Before we begin, I would like to remind you that during the course of this conference call, 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 for future operations, the company’s partnering efforts, capital requirements, future product offerings, research and development programs and the impact of the COVID-19 pandemic on these topics.

These forward-looking statements are not historical facts, but are rather based on our current expectations and beliefs and are based on information currently available to us. The outcome of the events described in these 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 10-K and quarterly report on Form 10-Q.

First some housekeeping. We have renamed our programs that do not yet have confirmed non-proprietary names. In general, where there were five digits, we have shortened to just the final three digits. For example, XmAb20717 is now XmAb717.

With that, let me pass the call over to Bassil.

Bassil i. DahiyatPresident & Chief Executive Officer, Director

Thanks Charles and good afternoon everyone. Xencor’s approach to creating antibody and cytokine therapeutics is based on our XmAb protein engineering platform. It’s built on our extensive protein engineering knowledge 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 actions. 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’re focusing our R&D on the expansion and use of our XmAb bispecific platform to create antibodies that bind two or more different antigen simultaneously and also to engineer cytokines with structures optimized for a particular therapeutic use. We’re currently running six Phase I studies evaluating cytotoxic XmAb bispecific antibodies. This way, we are taking multiple simultaneous shots on goal in the clinic and the proof-of-concept data we generate will guide which programs we independently advance, which we partner, and which we will terminate.

Last quarter, we provided program updates for our plamotamab bispecific antibody program targeting CD20 and CD3, including plans for a potentially registrational Phase II trial we expect to start later this year. We presented interim Phase I data for XmAb717, our PD-1 x CTLA-4 bispecific antibody, which showed activity in multiple advanced solid tumors, including prostate cancer, and we announced that we are starting a multi-arm prostate cancer trial this year. We also presented updated data for vibecotamab, a CD123 x CD3 bispecific antibody in AML, where we identified a marker for patients more likely to respond to therapy, lower baseline leukemic disease burden.

Now, shifting to the preclinical front, we expect to begin the Phase I clinical trial early this year for XmAb564, our wholly owned IL-2 Fc fusion, engineered to selectively activate regulatory T cells for the treatment of autoimmune disease. It will be our second cytokine in the clinic and will join XmAb306, our engineered IL-15 for oncology, which is partnered with Genentech.

Following behind that, we expect to file an IND for XmAb819, our ENPP3 x CD3 bispecific for renal cell cancer later this year. And we are beginning development of our first CD28 bispecific, a B7-H3 targeting molecule for potentially broad solid tumor use, including in prostate cancer. Now, our broad XmAb platform also drives our partnering strategy, which provides revenue streams, but also the opportunity to expand our clinical development scale and combination therapy options.

For example, our Genentech partnership for XmAb306, which initiated dose escalation in combination with atezolizumab, Genentech’s anti PD-L1 antibody last quarter after starting monotherapy escalation last March. In our recently started CD28 prostate cancer discovery collaboration with Janssen against an undisclosed tumor target, also gives us access to their industry-leading prostate cancer portfolio for clinical combinations with our agents. Now, before we move on to our clinical portfolio today, I want to state that we did not experience significant COVID-19 disruptions to operations during the last quarter. We’ll continue to update you on impacts from COVID-19 if and when they emerge.

Now with that, I’ll let Allen Yang, our Chief Medical Officer, review updates to our clinical portfolio. Allen?

Allen YangSenior Vice President and Chief Medical Officer

Thanks, Bassil. Today, we’ll provide a few brief clinical updates, and we’ll be happy to address your questions in the Q&A session. Really dating to late 2019, we have been presenting early stage clinical data across many of our bispecific antibody programs, and the data have guided our decisions to advance several candidates into new studies scheduled to start in 2021. First, plamotamab is our CD20 x CD3 bispecific antibody that we are advancing for patients with B-cell malignancies. And preliminary safety and antitumor activity from the Phase I dose escalation study in patients with relapsed or refractory non-Hodgkin’s lymphoma were presented at ASH 2019.

Initial data indicated that plamotamab was generally well tolerated and demonstrated encouraging clinical activity as a monotherapy. Across this competitive class of molecule, we have observed similar efficacy and toxicity profiles, though some data sets have been smaller or more selective than others. We believe that the differentiation for CD20 in will bear out through which combination strategy elicits strong, durable efficacy and maximal tolerability for patients.

So this past November, we entered a clinical collaboration with MorphoSys and Incyte to investigate the chemotherapy-free triple combination of plamotamab with tafasitamab and lenalidomide in patients with relapsed or refractory diffuse large B-cell lymphoma. Plamotamab mechanism of action as a CD20 directed CD3 bispecific redirect T cells to tumors, and tafacitamab is a CD19-directed XmAb antibody that we engineered with our cytotoxic Fc domain and subsequently licensed to MorphoSys in 2010

These two antibodies combine powerful and distinct immune pathways and tafacitamab itself is easy to use, tolerable and can generate prolonged durable responses. It’s the first agent approved for second-line diffuse large B-cell lymphoma, and it has already received NCCN listing. MorphoSys and insight will provide tafacitamab for the studies, which we will sponsor and fund. We anticipate the first study will start this year. Other studies, additionally planned, include triple combination in relapsed or refractory follicular lymphoma and first-line diffuse large B-cell lymphoma.

Next, XmAb717 and is our most advanced tumor microenvironment activator, and its mechanism is a dual selected targeting of T cells that express the checkpoints PD-1 and CTLA-4. in November, we presented updated interim data from an ongoing Phase I study at SITC last year. 717 was generally well tolerated in patients across multiple types of advanced solid tumors. And as of September — as of the September 2020 data cutoff, a complete response was observed in a patient with melanoma and partial responses were observed in multiple tumor types, including melanoma, renal cell carcinoma, non-small cell lung cancer, ovarian cats and castrate-resistant prostate cancer, or CRPC.

In the first half of this year, we plan to initiate a Phase Ib study of XmAb717 for patients with certain molecular subtypes of castrate-resistant prostate cancer, as a monotherapy or in combination with other agents, depending on the subtype, as these patients represent a high unmet medical need. This year, we also look forward to presenting more data from the Phase I expansion cohorts as data was rather early at SITC, but we have continued to mature in the prostate, renal cell and basket cohorts, for example.

Moving on, we have previously discussed initial dose escalation data from the ongoing Phase I study of Tideman, a CD3 bispecific antibody that targets the somatostatin receptor in patients with neuroendocrine tumors or, NETS. NETS are an indolent slow-growing tumor type and we are following these patients to evaluate progression-free survival and clinical utility of tideman in this patient population.

From the early data, we know that Tideman was generally well tolerated at the dose identified for the study expansion. And biomarker analysis are consistent with its proposed mechanism of action. So we’re in the final stages now of initiating a new clinical study in patients with merkel cell carcinoma and small cell lung cancer, which are somatostatin expressing tumor types known to be responsive to

Now our broad XmAb platform also drives our partnering strategy, which provides revenue streams, but also the opportunity to expand our clinical development scale and combination therapy options.

For example, our Genentech partnership for XmAb306, which initiated dose escalation in combination with atezolizumab, Genentech’s anti PD-L1 antibody last quarter after starting monotherapy escalation last March. In our recently started CD28 prostate cancer discovery collaboration with Janssen against an undisclosed tumor target, also gives us access to their industry-leading prostate cancer portfolio for clinical combinations with our agents. Now, before we move on to our clinical portfolio today, I want to state that we did not experience significant COVID-19 disruptions to operations during the last quarter. We’ll continue to update you on impacts from COVID-19 if and when they emerge.

Now with that, I’ll let Allen Yang, our Chief Medical Officer, review updates to our clinical portfolio. Allen? Thanks, Bassil. Today, we’ll provide a few brief clinical updates, and we’ll be happy to address your questions in the Q&A session. Really dating to late 2019, we have been presenting early stage clinical data across many of our bispecific antibody programs, and the data have guided our decisions to advance several candidates into new studies scheduled to start in 2021. First, plamotamab is our CD20 x CD3 bispecific antibody that we are advancing for patients with B-cell malignancies. And preliminary safety and antitumor activity from the Phase I dose escalation study in patients with relapsed or refractory non-Hodgkin’s lymphoma were presented at ASH 2019. Initial data indicated that plamotamab was generally well tolerated and demonstrated encouraging clinical activity as a monotherapy. Across this competitive class of molecule, we have observed similar efficacy and toxicity profiles, though some data sets have been smaller or more selective than others. We believe that the differentiation for CD20 in will bear out through which combination strategy elicits strong, durable efficacy and maximal tolerability for patients. So this past November, we entered a clinical collaboration with MorphoSys and Incyte to investigate the chemotherapy-free triple combination of plamotamab with tafasitamab and lenalidomide in patients with relapsed or refractory diffuse large B-cell lymphoma. Plamotamab mechanism of action as a CD20 directed CD3 bispecific redirect T cells to tumors, and tafacitamab is a CD19-directed XmAb antibody that we engineered with our cytotoxic Fc domain and subsequently licensed to MorphoSys in 2010 These two antibodies combine powerful and distinct immune pathways and tafacitamab itself is easy to use, tolerable and can generate prolonged durable responses. It’s the first agent approved for second-line diffuse large B-cell lymphoma, and it has already received NCCN listing. MorphoSys and insight will provide tafacitamab for the studies, which we will sponsor and fund. We anticipate the first study will start this year. Other studies, additionally planned, include triple combination in relapsed or refractory follicular lymphoma and first-line diffuse large B-cell lymphoma. Next, XmAb717 and is our most advanced tumor microenvironment activator, and its mechanism is a dual selected targeting of T cells that express the checkpoints PD-1 and CTLA-4. in November, we presented updated interim data from an ongoing Phase I study at SITC last year. 717 was generally well tolerated in patients across multiple types of advanced solid tumors. And as of September — as of the September 2020 data cutoff, a complete response was observed in a patient with melanoma and partial responses were observed in multiple tumor types, including melanoma, renal cell carcinoma, non-small cell lung cancer, ovarian cats and castrate-resistant prostate cancer, or CRPC. In the first half of this year, we plan to initiate a Phase Ib study of XmAb717 for patients with certain molecular subtypes of castrate-resistant prostate cancer, as a monotherapy or in combination with other agents, depending on the subtype, as these patients represent a high unmet medical need. This year, we also look forward to presenting more data from the Phase I expansion cohorts as data was rather early at SITC, but we have continued to mature in the prostate, renal cell and basket cohorts, for example. Moving on, we have previously discussed initial dose escalation data from the ongoing Phase I study of Tideman, a CD3 bispecific antibody that targets the somatostatin receptor in patients with neuroendocrine tumors or, NETS. NETS are an indolent slow-growing tumor type and we are following these patients to evaluate progression-free survival and clinical utility of tideman in this patient population. From the early data, we know that Tideman was generally well tolerated at the dose identified for the study expansion. And biomarker analysis are consistent with its proposed mechanism of action. So we’re in the final stages now of initiating a new clinical study in patients with merkel cell carcinoma and small cell lung cancer, which are somatostatin expressing tumor types known to be responsive to immunotherapy, and we would anticipate a much shorter time for tidutamab to potentially demonstrate clinical activity in this patient population, compared to neuroendocrine tumors. We expect to dose the first patient early in 2021. Finally, some brief updates on two other programs. A new study of XmAb698, which was formerly known as Amgen’s AMG 424 is being planned to start later this year, and we’ll update you on the indication closer to the study’s initiation. And for vibecotamab program in AML, we presented updated data at ASH in December of last year, where the efficacy and biomarker analysis indicated that responses appear to be associated with lower baseline disease burden. We continue the dose escalation study, and we are reviewing the data with our partner, Novartis, in planning additional studies. Bassil?

John J. KuchSenior Vice President & Chief Financial Officer

Thank you, Bassil. During 2020, our partnerships, collaborations and licensing arrangements continue to generate strong cash flow with $165 million upfront payments, milestone payments and royalties received, which helps offset the growing investment in our portfolio of clinical and early stage drug candidates.

We ended the year with cash, cash equivalents and marketable securities totaling $604 million compared to ending 2019 with $601.3 million. Based on current operating plans, we expect to have cash to fund research and development programs and operations into 2024, and estimate we will end 2021 with between $425 million and $475 million in cash and cash equivalents.

Total revenues on a GAAP basis for the year ended December 31, 2020, were $122.7 million compared to $156.7 million for the same period in 2019. The revenues earned in 2020 include; royalties and milestones from morphosis related to approval of Mondavi and Alexion royalties and a sales based milestone related to Ultomiris sales and several licenses of XmAb technologies and drug candidates, compared 2019 revenue, which is earned primarily from our Genentech and Astellas collaborations.

Total research development expenses in 2020 were $169.8 million for the year compared to $118.6 million in 2019, an increase was primarily attributable to increased spending on Xencor’s bispecific antibody and cytokine candidate technologies. Specifically on additional studies for our plamotamab and XmAb717 programs and our IL-2 program, XmAb564.

General and administrative expenses were $29.7 million for the year compared to $24.3 million in 2019, and the increase was primarily attributable to increased staffing, professional expenses and spending on intellectual property. Non-cash stock-based compensation expense for the year was $31.6 million compared to $31.9 million in 2019.

Net loss for the year was $13.7 million or $0.24 on a fully diluted per share basis compared to net income of $26.9 million or $0.46 on a fully diluted share basis for 2019. The net loss reported for 2020 compared to net income report for 2019 is primarily due to higher collaboration and licensing revenue report for 2019 and higher research and development expenses and lower milestone revenue reported in 2020.

With that, we’d now like to open up the call for your questions. Operator?

Questions and Answers:

Operator

Thank you. [Operator Instructions] Our first question comes from Ted Tentoff with Piper Sandler. Please proceed with your question.

Ted TentoffPiper Sandler — Analyst

Great. Thank you very much, and really excited about all the progress and everything going on at the company. I just wanted to get a sense of what you might be showing at AACR this year. And I know it’s a little bit early to be calling out specific conferences with respect to clinical updates, do you think that the 717 update might be at ASCO? What do you think you’ll be showing in June? Thanks.

Bassil i. DahiyatPresident & Chief Executive Officer, Director

Hi, Ted. I’ll take that one. This is Bassil. So for ACR, I mean, we can’t disclose what we’re going to be presenting until, of course, the abstracts published. We always try to use various oncology conferences to highlight both our preclinical progress as we continue to expand our platforms as well as clinical programs.

We have guided for XmAb717, we’ll have data this year. We’ll get more specific and granular on timing as we get closer. And to be clear, the kind of information we’re going to present should be the mature data from the expansion cohorts that weren’t — that were really quite immature at SITC last November.

Those would be in particular the prostate cancer cohort, which was quite early as well as the renal cell carcinoma cohort and then rounding it out with the basket cohort of other indications that are — where there’s no PD-1 approved. So it will be that full data set, and we’ll be able to also guide much more specifically on our prostate cancer trial that will be starting this year as well as other trials.

Ted TentoffPiper Sandler — Analyst

Perfect. Great. Thanks, Bassil.

Bassil i. DahiyatPresident & Chief Executive Officer, Director

Thanks, Ted.

Operator

Thank you. Our next question comes from Mara Goldstein with Mizuho. You may proceed with your question.

Mara Goldstein`Mizuho — Analyst

Yes. Thanks. So just on the molecular subtypes in the CRPC study, can you maybe just kind of give us a little bit more granularity as to what that is? And just conceptually what that looks like in terms of patients on demographics and populations? And then I’m just curious about the private company transaction that was in the press release. And when you’ll be in a position to disclose some more details on that? And how that relates to just sort of strategy from a BD perspective?

Bassil i. DahiyatPresident & Chief Executive Officer, Director

Sure. Maybe I’ll take the second one first. That’s a fairly easy one, then I’ll touch on the molecular subtypes, me and Allen. But on the private company, when we can announce more granularity, it’s really up to them. They are currently in stealth mode and working very hard to move the company to the next steps.

From a BD perspective, we’ve had just a suite of different molecules we’ve characterized preclinically over the years that use different Fc technologies to try to gain an advantage. And these all happen to be an autoimmune disease. They were all molecules we made a number of years ago that were never part of our plans developed clinically that really makes sense for this particular company to start pursuing. And so we help them get going by licensing in these assets.

It’s again about non-core assets, things that aren’t core to our focus on oncology, on bispecific antibodies and on cytokines that we want to see moving. And we think taking equity in a company where we like the leadership team is a great way to see value from that. So again, it’s about from a BD strategy standpoint, how to use the depth of our technology and non-core assets and create value and hopefully, value for patients.

Now on the molecular subtypes, without the trial, hopefully, will be up and running in the coming months, we’ll be able to get into all the gory details. But until they’re certain, we want to be cautious, but I’ll say and maybe lead into Allen that we are going to be talking about the CRPC setting, and there’s just a variety of places where there’s either small molecules or chemo. So Allen, you want to comment on what we know about that field and defer the specifics of our trial until we’re certain.

Allen YangSenior Vice President and Chief Medical Officer

Yes, Bassil. I think, first of all, we’re very excited about the early 717 data in prostate cancer. And without giving details of the trial design that we’ve established, I can just talk about prostate cancer in general. So, after we saw clinical activity. When you look at prostate cancer in general, it’s really breaking down by molecular subtypes. And remember, this is a Phase 1b. So it can be given 717, will either be given as a monotherapy or as a combination therapy.

And so if you think about what’s approved for prostate cancer, in terms of checkpoint inhibitors, for MSI high, people are using checkpoint inhibitors already as a monotherapy. In other subgroups like homologous recombination, deficient prostate cancer PARP inhibitor or a PARP inhibitor is now approved.

And then there are other forms that are more aggressive that may be treated with chemotherapy more aggressively. And there, you might want to think of a combo with chemotherapy. So without saying much on the trial design, which we’ll disclose later in the year, that’s sort of how we’re thinking about it.

Mara Goldstein`Mizuho — Analyst

Okay. And if I could just actually ask one question for John, and it’s about Ultomiris and the sales-based royalty — rather sales based milestone payment. Should we think about additional payments for 2021?

John J. KuchSenior Vice President & Chief Financial Officer

We don’t guide on those. We do have $20 million in sales-based milestones remaining under the agreement. But your model is probably better than ours as far as predicting what the sales side to be honest with you Mara.

Mara Goldstein`Mizuho — Analyst

Okay. Thank you.

Bassil i. DahiyatPresident & Chief Executive Officer, Director

Thanks, Mara.

Operator

Thank you. Our next question comes from Gregory Renza with RBC Capital Markets. You may proceed with your question.

Gregory RenzaRBC Capital Markets — Analyst

Thank you. Hey, Bassil and team thank you so much, and congrats on all the progress. Bassil, maybe just taking a step back and certainly a question that we’ve received is really what Xencor could look like in, say, three to five years? Certainly, a great deal going on a lot as you alluded to a lot of programs advancing a suite of them actually and understanding the management of risk and opportunity assessment. So I’m just curious, how the current profile of so much going on would sort of translate to opportunities going forward, as these programs advance and potentially derisk? Thank you.

John J. KuchSenior Vice President & Chief Financial Officer

Yes. So the strategy — that’s really a question sense to our strategy. Thanks for asking. The strategy is about trying to find different molecules we can make that have differing scientific and business risks to put it in the clinic that have a good hypothesis for how they could help patients. And then letting the data guide us. And as the data guides us, some programs we will out-license or terminate. For example, we out-licensed our XmAb7195 IGE reducing antibody. When it didn’t make sense for us to proceed anymore, we did that deal with Aimmune it’s now Nestle.

And so it’s about data driving the decisions. We now have data for plamotamab and XmAb717 that gives us clarity on the next step of development. And we hope to continue letting the data from those programs either drive them forward or result in maybe an out-licensing agreement a cessation. It all depends on the data and having a rich pipeline behind it. So we don’t feel tied to any one program at the early stages of development. However, as we start moving into mid-and-later stages, and we’re starting a potentially registrational trial with plamo, we’ll see how that goes. But as we start moving to those stages, we’ll commit more and more resources to the programs that pull us, make sure we apply stringent filters to the earlier programs.

And I think our profile will change, if all goes well in the clinic, to a company that is really focusing on getting mature assets through approval and ultimately to market by ourselves, if all goes well, always maintaining a rich early clinical base, but being pretty ruthless about culling that. So I think that the early clinical data, we hope — our program base will always remain. It will just start becoming only a piece of the puzzle as our later-stage programs or program even, emerge and really solidify.

Gregory RenzaRBC Capital Markets — Analyst

That’s great. Thank you so much for the color. I appreciate that.

Operator

Thank you. Our next question comes from Alethia Young with Cantor. You may proceed with your question.

Alethia YoungCantor — Analyst

Hey, guys. Thanks for taking my questions. Congrats for the progress. Just I wanted you to take a step back and kind of talk a little bit about the IL-15 program. I know there’s, some others in the space and kind of the promise of that potential target. And if you have any update with the Roche collaboration, that would be great.

And my second question is just as it relates to PD-1 CTLA-4 program, just kind of wanted to get a broad picture of how enrollment time lines are going in light of some of the COVID volatility that we’ve seen? Thanks.

Allen YangSenior Vice President and Chief Medical Officer

I’m sorry, which program was that you were asking about time lines?

Alethia YoungCantor — Analyst

CTLA-4, PD-1.

Allen YangSenior Vice President and Chief Medical Officer

Got you. Okay. So for the first one, I’ll comment on our collaboration with Roche. And maybe John, you can touch on the design philosophy we use that we hope differentiates us. But the collaboration with Roche is a 55-45 P&L split. We’re sharing clinical development costs and hopefully profits.

We share a decision-making in the clinic. And right now, they’re executing the Phase I escalation study. They did advance from just doing monotherapy escalation to escalation in combo with atezolizumab last quarter. We can’t disclose data until we’ve agreed on a publication plan with Genentech, which we’re working on, but we really can’t say when information would come out.

I think we can say that, as new studies emerge or as we engage in different new steps of the existing study, we will, of course, announce those as makes sense. But as for data publication plan will come, maybe, John, you want to talk about how we fit in the space?

John J. KuchSenior Vice President & Chief Financial Officer

Yeah. Yeah. So the — I mean, probably the most — the molecule that’s been out there the longest is the ALK-803 that’s an IL-15/Fc fusion. There’s also an earlier stage molecule, a PEGylated IL-15 from NKTR. And we also compare ourselves to the NKTR-214, which is a PEGylated IL-2 that basically acts like an IL-15, right, because it talks with the same receptors.

And the key distinction with XmAb306 is that we started with IL-15 fusion, using our heterodimers, made a nice stable molecule. And then, based on observations we had in terms of PK with that molecule as well as just understanding the way that these molecules work in terms of their mechanism of action, we kind of did the kind of a edacious thing of actually dramatically reducing the potency of the molecule.

So we took the wild-type IL-15 Fc fusion. Fc fusion made a few mutations, took the potency down a couple of orders of magnitude. The idea being that these things get cleared through the receptors when interact with them. And so what we found preclinically is that with that put the reduction, we actually got dramatically better half-life for the molecule of depot and because the molecule lasted longer, we actually got better pharmacodynamics. So we’ve got a higher peak of peripheral NK and T-cell expansion in cynomolgous monkeys, as well as a longer duration of that peak. And so we hope and we think everything pretty well set up for that — those kind of properties to translate well into humans.

Alethia YoungCantor — Analyst

Great.

Allen YangSenior Vice President and Chief Medical Officer

Do you want me to take — or Bassil, do you want to take the interruption.

Bassil i. DahiyatPresident & Chief Executive Officer, Director

Oh, I’m sorry. I completely forgot…

John J. KuchSenior Vice President & Chief Financial Officer

The question about enrollment and COVID on PD-1, CTLA — I apologize. Sorry, go ahead, Allen.

Allen YangSenior Vice President and Chief Medical Officer

Yes, no problem. So we said that in terms of the PD-1, CTLA-4 or 717, we haven’t noticed really any sort of decline or delays in our enrollment. First of all, I’d like to thank the teams, all the teams at Encore, they’ve been working really overdrive during the pandemic. And COVID has interrupted hospital supply chains and hospital systems, but the teams quickly adapted to things like remote and virtual monitoring. And so I think there’s two factors here.

Cancer is a large unmet need. If you have cancer, despite the pandemic, you need to be treated. We have an active molecule which is also very important. And so we’ve noticed that the studies are enrolling well and to our schedule. So we haven’t noticed any delays in that program. Thanks, Ali.

Alethia YoungCantor — Analyst

Great.

Operator

Thank you. Our next question comes from Jonathan Chang with SVB Leerink. You may proceed with your question.

Jonathan ChangSVB Leerink — Analyst

Hi, thanks for taking my questions. First question on B7-H3. How does your CD28 approach and program compared to other B7H3 approaches and programs and development?

Bassil i. DahiyatPresident & Chief Executive Officer, Director

Sure. I mean, I can answer this generally, I guess, the hope here is to use B7-H3, a marker that’s expressed on brain tumors and is particularly bright in places like prostate, as a way to overcome T-cells, maybe quiescence or resistance to activation from things like checkpoint therapies or CD3. So it’s not bringing a cytotoxic payload. It’s bringing a co-stimulatory payload. And hopefully, that doing so in a targeted way can assure tumor-specific effect and avoid side effects. I think the attractiveness of CD28 is really about its centrality in the immune system. And John, maybe you can comment on that.

John R. DesjarlaisSenior Vice President, Research & Chief Scientific Officer

Yes. So the way that T-cells are activated are — they get — they need multiple signals. So signal one, they get through the T-cell receptor, interaction with MHC or artificially through a CD3 bispecific classic T-cell engager molecule. In this case, we’re triggering signal two, right? The CD28 is Vtex for signal two, if you want to expand T cells in vitro, you couple signal one and signal two with CD3 and CD28 on Bs and expand T cells. So we’re just trying to make that happen in the tumor micro environment, specifically at the tumor cell T cell interface.

And since B7-H3 is brightly expressed in a lot of different tumors we’re trying to promote that interaction and that triggering a signal two right at that interface. Now in contrast to a lot of the other programs that are out there, the nice thing about a CD28 bispecific, at least this is our philosophy, is that — and we can show that signal two all by itself doesn’t actually accomplish anything. And so from a safety perspective, we believe that broadly targeting a broadly expressed tumor-associated like B7-H3 should be safe. And then we’re going to couple that with either PD-1 blockade or CD3 bispecific to promote the signal one that you’re getting through the T cell receptor.

Jonathan ChangSVB Leerink — Analyst

Got it. Thank you. And just final question, when could we see additional plamotamab or clinical data?

Bassil i. DahiyatPresident & Chief Executive Officer, Director

We expect to have more plamotamab data later this year. We’re wrapping up the dose regimen setting, that’s hopefully you’re complete, and we should have it at and we hope at a medical conference right after that.

Jonathan ChangSVB Leerink — Analyst

Got it. Thank you.

Operator

Our next question comes from David Nierengarten with Wedbush. You may proceed with your question.

David NierengartenWedbush — Analyst

Just a quick follow-up on the updated clinical data for plamotamab, but that’s the monotherapy data, presumably, right? And then a couple of questions on the combo studies with Incyte and MorphoSys. Do you plan on reporting or data that year, who is it under control of? And then what are you thinking of as a bar for success comparing amendedly across clinical studies to the other CD3, CD20 bispecifics that are in development? Thanks.

Bassil i. DahiyatPresident & Chief Executive Officer, Director

Yes. So the plamo update would be for monotherapy. And for the combination studies with Incyte and MorphoSys, we control the studies. And obviously, there’s a collaborative element to the data, but we remain committed to presenting data when it’s meaningful and interpretable. We don’t — this is not a partnership that is likely to hold that data back like a large company and some of our other partnerships that we’ve had.

The bar for success in relapsed/ refractory DLBCL, I think it’s great you have two highly active regimens coming together, the CD20, CD3 and the tafasitamab plus len. Maybe Allen, you can comment on how ORR and PFS play off of each other here.

Allen YangSenior Vice President and Chief Medical Officer

Yes. So let me back up and answer a couple of questions. So how we’re going to put the molecules together. We’re not going to disclose the study design. But I think the way you think about these is — there’s actually three agents here. They have slightly different mechanism of actions. The lenalidomide likely synergizes the CD19 and it probably will synergize the CD20 as well. And so that’s one way to think about it.

The other thing to think about is toxicity profiles, CRS, mainly for the bispecific T-cell engagers. And for the lenalidomide, it’s really cumulative neuropathy and maybe some myelosuppression. And so could you put it together in a way to sort of minimize the toxicity and increase the efficacy. And that’s something that we’re going to we have been actively thinking about.

And in terms of milestones, I think or sort of reference benchmark, it’s highly dependent on the disease population. Is the second line diffuse large B-cell lymphoma, is it third line or after two other therapies? And then is it monotherapy or single agent. I think the data for monotherapy you’re seeing good response rates, how durable they are is not clear. And that’s why I think everybody is after sort of their monotherapy data is moving quickly to combinations. And different companies after ASH have declared what their combinations are. And I sort of like our combination because I think it’s really novel and it’s chemo free.

David NierengartenWedbush — Analyst

Got it. Thank you.

Operator

Thank you. Our next question comes from Arlinda Lee with Canaccord. You may proceed with your question. Yes, your line is on mute, please unmute.

Arlinda LeeCanaccord — Analyst

Hi, guys. Congrats on the progress. I think I had some questions on some of your other IO — IO combinations, whether those are still — you still think that you’re going to have data on the on those and if you could provide an update on 104 and 841? Thanks.

Allen YangSenior Vice President and Chief Medical Officer

Yes. So you’re talking about our XmAb104 and XmAb841 program, the respectively, PD1 by ICOS bispecific for tumor microenvironment activation and the CTLA-4 x LAG-3 bispecific. Those are both in dose escalation. They started this escalation about a year after 717. So they’re a little bit behind.

We are expecting to announce data when dose escalation is complete. We have a package. We haven’t guided yet on that. I will point out that it was about two years from the start of the 717 trial to data and word about 18 or 19 months now from those trials starting. So without committing to a specific date, I think we’re starting to approach when we’ll be able to guide on new data from those or data period from those.

Arlinda LeeCanaccord — Analyst

Okay. Great. Thank you.

Operator

Thank you. Our next question comes from Tom Shrader with BTIG. You may proceed with your question.

Kaveri PohlmanBTIG — Analyst

Hi. This is Kaveri Pohlman for Tom. Thanks for taking our question. So my first question is for CTLA-4. There are other approaches in the clinic that include Fc enhanced molecules, can you share your thoughts on the role of active Fc domain for this drug? And with the data expected for Fc active molecules this year, do you plan to develop your own Fc enhanced antibody?

Bassil i. DahiyatPresident & Chief Executive Officer, Director

I’ll say that, we don’t have any plans for developing an Fc enhanced anti-CTLA-4 antibody. In fact, our molecule or PD-1 CTLA-4 as well as our other one, our CTLA-4 LAG-3, both have Fc receptor-binding silence. So there’s no effector function drive there. And they rely on the co-target, whether it’s PD-1 or LAG-3 to give us selectivity and also to drive further activity by hitting another checkpoint.

So yeah, we’ll be interested to look at other kinds of data that comes out from other programs and go from there. I think we’re excited by having a dual checkpoint approach that I think drives down different pathways than trying to use enhanced effector function for clustering or cytotoxicity. I mean, John, did I miss anything there?

John R. DesjarlaisSenior Vice President, Research & Chief Scientific Officer

Yeah. I would just emphasize that the Fc enhanced approaches are largely built-mostly built off of mouse data. Where a significant MOA for anti CTLA-4s is through TREC depletion since TRECs are bright for CTLA-4. The current consensus based on clinical biomarker data, for ipilimumab is that it is not actually depleted TRECs in humans. And so we prefer the approach on our molecule. And of course, you wouldn’t want to do this with a PD-1 binding arm anyway, of having silent factor function and no ability to promote depletion.

Kaveri PohlmanBTIG — Analyst

Got it. And just the last one. So the search for tumor-specific target is so extensive in the industry what does MD Anderson brings that novel? Do you think you need deeper biology to get targets? Also, does the deal help you to move the programs to Phase I trials?

Bassil i. DahiyatPresident & Chief Executive Officer, Director

I’ll answer on the deal structure. Maybe John can chime in on why he’s excited about working with the MD Anderson scientist. On the deal structure, for the Discovery partnership, they pay for all of their discovery costs and all of their preclinical costs. We have an exclusive option to take rights to the program, and we’ve agreed to contribute our technology, our XmAb technology and assist them if necessary, making molecules.

So we would imagine the typical kind of deal would be if they show exciting preclinical data, we would take it over for clinical development, though I think a natural collaborator for that clinical development that you probably want to consider would be the MD Anderson folks. Maybe John, on the why they’re so exciting-their data is so exciting.

John R. DesjarlaisSenior Vice President, Research & Chief Scientific Officer

Yeah. Well, I guess the best way to put it is, I’d love to have relationships like we have with MD Anderson set up with every major research university, because there’s a lot of different ideas out there. But we prioritized for MD Anderson, because it’s one of the top cancer institutes in the country and so-in the world. So that’s a really great place to start. We’re hoping to get new eye fresh ideas for them. They’ve got a lot of discovery efforts ongoing at MD Anderson, and that’s a very-like you said, it’s sort of teed up for a further clinical relationship downstream. And I’ll also point out, we are definitely eager to find novel targets. We’ve announced our collaboration with Atreca for exactly the same reason.

Kaveri PohlmanBTIG — Analyst

Great. Thank you and congrats on the progress.

Operator

Thank you. Our next question comes from Etzer Darout with Guggenheim. You may proceed with your question.

Etzer DaroutGuggenheim — Analyst

Great. Thanks for taking my questions and congrats on all the progress in 2020. I guess, the first one, maybe a sort of a 2+1 strategy question with the program moving forward. Interesting data so far in affinity tuning, but guess where do you see the technology position versus other emerging technologies like conditional activation, epitope masking, etc, aimed at enhancing tumor selectivity?

And then the question-second question, just wondered, if you could talk a little bit about what’s baked into the end of 2021 cash guidance? And can we assume that it’s predominantly maybe a step-up in R&D from the breadth from plamotamab on activities that are planned for 2021? If you could help with those. Thank you.

Bassil i. DahiyatPresident & Chief Executive Officer, Director

Yeah. Maybe, I’ll touch on the second question. Your question on what’s driving the-the spending in the 2021 cash guidance. It’s going to be increases in development programs, not just plamotamab, which -as you move to the next stage of trial absolutely, you’re correct, it’s going to drive increased spending. It’s also increase spending around XmAb717 as we go into prostate cancer with its own trial and probably start additional studies and other indications as well as additional spending in our XmAb306 collaboration with Genentech for IL-15 as that program progresses. I think those are the primary drivers of new R&D program spend, and R&D program spend is absolutely the big driver of the cost growth.

And on the 2+1, where does this technology position relative to these other approaches for sort of getting that more selective antibody activity. I would say using avidity and that kind of binding property to get to different target densities. It’s kind of a very well-proven phenomenon in antibody engineering. Going back to the days of the designs of Herceptin and Erbitux, and I think these novel approaches, while extremely exciting, and I think they have a lot of potential really have yet to bear out that the selectivity is going to be there, in the real — in real practice, in vivo, it’s going to play out.

So we’re very excited to watch those. We’re certainly up and minded. We think that an avidity approach not just has the advantages, though of selectivity, but there’s other ones. I mean, John, do you want to touch on the different tricks you can do with the 2+1 format that’s, by the way, very stable and very straightforward and easy to make.

John R. DesjarlaisSenior Vice President, Research & Chief Scientific Officer

Yeah. Not only that, I mean back to the original question, I would say that what I like about the avidity tuning approach is I feel like I can confidently translate from some in vitro assays in terms of binding selectivity as well as killing selectivity of bright versus dim reagent cell lines, I feel like they can confidently translate that information into — with putting it other various pieces of information together like IAC data from human tumors and feel like that’s going to translate well.

What I do think — I’ve always felt like with the other conditional activation approaches, they’re a little bit more faith-based. Hope — there’s certainly data out there that, yes, there are a lot more proteases, certain proteases in the tumor than the porphyry. But at the end of the day, you’re crossing your fingers, hoping that, that all plays out well in terms of toxicity and therapeutic index.

Etzer DaroutGuggenheim — Analyst

Got it. Well thank you. Thanks again and congrats on all the progress.

Operator

Thank you. Our next question comes from Dane Leone with Raymond James. You may proceed with your question.

Dane LeoneRaymond James — Analyst

Hi. Thanks guys and congratulations on the updates. So for me, I just wanted to go back. Can you clarify, is the IL-15 program, the 55-45 P&L split with Genentech, is that for the US only? Or is that global?

Bassil i. DahiyatPresident & Chief Executive Officer, Director

That’s global.

Dane LeoneRaymond James — Analyst

Okay. So that is global. Okay. Then on — can you remind us on the Ultomiris and Monjuvi royalties, is that — are you lagged in terms of how those get paid out?

Bassil i. DahiyatPresident & Chief Executive Officer, Director

John, do you want to take that one, John Kuch?

John J. KuchSenior Vice President & Chief Financial Officer

We record the royalties as they record sales. So for both of them we have to estimate, what the sales are to book our royalties. Alexion reports ahead of us. So it’s really easy to pick it up. For purposes of Monjuvi, we have to estimate what the sales are. In this case, we picked it up off the insight earnings release.

Dane LeoneRaymond James — Analyst

Okay.

John J. KuchSenior Vice President & Chief Financial Officer

Did that answer your question?

Dane LeoneRaymond James — Analyst

Yeah. So basically, it’s real-time, so it’s not on lag basis.

John J. KuchSenior Vice President & Chief Financial Officer

Yes.

Dane LeoneRaymond James — Analyst

Okay.

John J. KuchSenior Vice President & Chief Financial Officer

Correct.

Dane LeoneRaymond James — Analyst

I think we’re all just trying to figure out kind of where the blended royalty rates are coming in as the sales ramp. Okay. In terms of this year, we’ve kind of bounced around on the subject a bit for what the updates are going to be. What’s the — going back to plamotamab for a minute on the monotherapy data, what’s going to be the focus of this update? I mean, I guess, what are you hoping to tease out within the monotherapy settings at this point from a more mature data set that’s going to be informative? And are you planning on taking this asset forward as a monotherapy from this study out? Or are you going to be more focused on the combination with Bon-Juvie?

Bassil i. DahiyatPresident & Chief Executive Officer, Director

Yes. So, the data update would be just to really wrap up the Phase I dose escalation and give a clear picture of regimen and what you can learn about tolerability and efficacy from these small escalation data sets. But it’s just really wrap it up and finish it, and we expect to be fully rolling with our combination study with tafacitamab lenalidomide, and we do think combinations are the focus of the strategy because that’s where you’re going to have the regimens that have the most efficacy, and that’s what’s going to win the day in lymphoma, ultimately.

We are going to continue monotherapy development and we plan to have multiple expansion cohorts in this Phase I, while we go into combo with tafa-len in DLBCL, we’ll also continue monotherapy DLBCL in expansion cohorts and accrue a number of patients, and that can track along in its own bucket and continue the development.

And if the data looks really promising and exciting, we can — you could potentially go from — go with that data and advance to later development or even just accrue a lot of patients and that data set could be, if the data looks amazing, registrational itself, we’ll also look at other indications like follicular lymphoma and others.

Dane LeoneRaymond James — Analyst

Okay. That makes sense. In the prostate cancer cohort for the CTLA for PD-1. What — how large of a group is that — I just can’t remember what the dose expansion group was? In general–?

Bassil i. DahiyatPresident & Chief Executive Officer, Director

This is a separate position — the 20 patients in the Phase I expansion cohort in prostate.

Dane LeoneRaymond James — Analyst

Yes. So, what was the disposition of those patients generally at baseline? Or what was like the — what were you generally accruing for prostate cancer? Yes. Like how — pre-treated.

Bassil i. DahiyatPresident & Chief Executive Officer, Director

Yes. And — yes, go ahead.

Allen YangSenior Vice President and Chief Medical Officer

Yes. So, we didn’t select for certain molecular subtypes in the expansion cohort. They were castrate-resistant prostate cancer. And so they had to exhaust standard of care. And so most of them had seen chemotherapy. So, this was really not a chemo naive group and so they were a difficult group to treat.

Dane LeoneRaymond James — Analyst

Okay. And so sorry, just to clarify your comments around the landscape in prostate, where do you think like the unmet need is with certain new therapies coming in, PSMA would be one of them, I guess.

Bassil i. DahiyatPresident & Chief Executive Officer, Director

Well, they’re not in yet, right? I would say that there’s a big unmet need in post chemo after failed salvage in castration-resistant prostate cancer is a big unmet need still.

Dane LeoneRaymond James — Analyst

Okay. So, you’re thinking about it broadly not more specifically to a subtype?

Bassil i. DahiyatPresident & Chief Executive Officer, Director

Not unless the data guides us.

Dane LeoneRaymond James — Analyst

Okay. Sorry, I was just kind of trying to understand what you’re talking about with the subtypes earlier, whether that was something you’re you already have in mind to focus on or whether that was just —

Bassil i. DahiyatPresident & Chief Executive Officer, Director

No, it’s multiple ones that we’re going to explore to see which signals. If any signals emerge across subtypes that there’s a particular one or other, that’s great, right? Right now, we’re agnostic.

Dane LeoneRaymond James — Analyst

Okay. So, basically, you have this mixed expansion cohort of 20 patients and then you’re going to interrogate that cohort for like base lead?

Bassil i. DahiyatPresident & Chief Executive Officer, Director

I’m sorry. No, that’s we were unclear. So, we have this expansion cohort of 20 patients that’s mixed. We’re going to report that data. Also, this year, we’re going to start a completely new trial just in prostate cancer patients with multiple parallel cohorts of different molecular subtypes. It’s a whole other set of patients.

Dane LeoneRaymond James — Analyst

Okay. All right. Awesome. Thank you for getting me — with that one. I’ll stop ask you guys. Thanks.

Bassil i. DahiyatPresident & Chief Executive Officer, Director

No worries Dane. Take care.

Operator

Thank youOur next question comes from Peter Lawson from Barclays. You may proceed with your question.

Peter LawsonBarclays — Analyst

Hey. Thanks for taking the questions. Just kind of a follow-up on Dane’s question just around kind of that molecular subtype you’re looking for, is that kind of like PD-1 levels or PSA levels? Or like BRCA schools, HRD scores you’re thinking through? And I guess it is across kind of sub-indications, whether it’s kind of like post chemo, etc?

Bassil i. DahiyatPresident & Chief Executive Officer, Director

Well, I think it’s going to — go ahead, Allen. I mean, I think, again, without having disclosed the details, which will be coming out sooner not, I suppose.

Allen YangSenior Vice President and Chief Medical Officer

Yeah. Maybe the best way to think about this, Peter, and sorry for the confusion, is we treated sort of an unselected cohort as an expansion, and that was all-comers that were castrate-resistant prostate cancer. And because of that, many of them got chemotherapy, because that’s a standard of care. The challenge is moving forward in prostate cancer is that people are molecularly subtyping the disease. And the question we have is like where could we be effective, where it could be — generate the most value for patients? And it could be across all arms.

So from a logistics standpoint, you would want to have a clinical trial that anybody with prostate cancer, who walk through that door that’s metastatic could qualify for the study, so castrate-resistant, prostate cancer. So they come through the door, and we would want to have an arm or a basket. Now some of the baskets, like recombinant deficiency, they would normally get a PARP inhibitor. So you want to include those patients somehow, and then some other patients like MSI-high would just be a monotherapy.

And then, some of the other ones that have biomarkers may have more aggressive disease, you may need a chemotherapy. And eventually, you would want to include everybody that comes through the door and just have an understanding of the activity of 717 in each little basket molecularly. So, we’re not really narrowing the indications at this point. We’re sort of studying all the indications with the appropriate combination if needed based on the molecular subtype. Sorry, if that wasn’t clear before.

Peter LawsonBarclays — Analyst

No, that’s perfect. Thank you so much. Good to hear. And just a question around, I guess, the equity investment in an emerging kind of stealth company. Is that kind of a new thing that you’re thinking through? And then just the ideas about potentially selling royalties, I don’t know if you can, it just seems to be an increasing trend in the space.

Bassil i. DahiyatPresident & Chief Executive Officer, Director

Yeah. So on the equity piece, we get in these private companies or even new public companies, we don’t think of them as investments. We think of them as getting stock in lieu of cash upfront payments for licensing of our technology or licensing a preclinical asset, for example, in these cases. So it’s really when an entity wants to conserve its cash. And when we think the company has promised and could grow in value in part-based or maybe wholly based on the technology we’re licensing, we like the equity piece in lieu of upfront payments.

So it’s really just changing one element of a deal we would have. And we have royalties on all of those and milestones built into those deals also, and it just broadens the pool of people that we can get our technology into the hands up. Now on the selling of royalties, we’re always assessing the options of how to maximize value in the different assets we have, whether they’re financial assets like royalties, our own programs, we’re not — those are the kinds of things that that so many different considerations, we really can’t say anything specific.

Peter LawsonBarclays — Analyst

Okay. Perfect. Thanks. Thanks for taking the questions.

Bassil i. DahiyatPresident & Chief Executive Officer, Director

Thank you.

Operator

Thank you. Our next question comes from Zhiqiang Shu with Berenberg. You may proceed with your question.

Zhiqiang ShuBerenberg — Analyst

Thank you. Good afternoon, everyone. Thanks for taking my questions. My first question is on plamotamab. The first-line DLBCL combination study. I know MorphoSys and Incyte is running their own frontline study. I guess I just want to hear your thoughts there, why you want to run your own frontline study? And why do you think potentially that can beat R-CHOP in the frontline DLBCL?

And then second question is on the 564 program IL-2. I guess I want to hear your thoughts on why do you think your molecule potentially is better than any other IL-2 — IS-IL-2 for autoimmune diseases out there? And I guess, for this year, do you see a venue for you to present some of the biomarker data or even some of the activity data this year? Thank you.

Bassil i. DahiyatPresident & Chief Executive Officer, Director

So on the frontline DLBCL, we think that how these CD20, CD3 agents, combined with other agents, is really completely unknown now. And the opportunity to create a chemotherapy-free regimen as opposed to using R-CHOP, with that opportunity, we think, is very compelling, because of the drive and the interest in removing chemo from lymphoma therapy, toxicity concerns, long-term toxicity concerns. So we think just that strategic driver of having a chemo-free regimen that potentially has very high activity is worth that shot to compete with the chemo containing R-CHOP regimen.

Why is it better than R-CHOP? I think aside from being chemo free, we will — we’re going to be very interested in seeing the synergies we have with an immune stimulant like lenalidomide, right? And with what happens with tafacitamab hitting CD19 versus the CD20. Now, on — yes, and Allen, do you want to add anything? Or is that sufficient? Should I go to the IL-2.

Allen YangSenior Vice President and Chief Medical Officer

No. I guess the only thing I could add is, I mean, if you look at the data from the tafacitamab-lenalidomide combination, the response rate in relapsed/refractory was approaching what [Indecipherable] observed in his original R-CHOP study in the front line. So there is this possibility that adding instead of CD20 instead of — a CD20 bispecific instead of a CD20 antibody could sort of potentiate that. And again, it’s very early, but we are excited. And it’s something that we’re very keen on doing — sorry, Bassil. Back to you.

Bassil i. DahiyatPresident & Chief Executive Officer, Director

No, no, it’s great. And then IL-2, we believe that the lower the potency you can design into your cytokine, in this case, IL-2, the better tolerability you’ll see and the longer duration of action, and in particular, when you fuse to a long-acting FC, extend the pharmacodynamic effect. That’s hypothesis we’ve seen proven pre-clinically with both our IL-15 and IL-2, and we believe that does create a potential for a best-in-class therapeutic profile on both the tolerability side as well as the duration of action of boosting your target cells.

That’s the hypothesis. Again, preclinically, it’s the exact same strategy with our IL-15 XmAb306, we hope it plays out here as well. On data this year, we can guide on that, and we plan to — what our initial data timing is going to be as we start the trial, we’ll give further updates.

Zhiqiang ShuBerenberg — Analyst

Great. Just to clarify, both for IL-2 and IL-15 program, the FC domain remains being inactivated. Is that correct?

Bassil i. DahiyatPresident & Chief Executive Officer, Director

It has — it’s got no FC gamma receptor binding, that’s been completely ablated, and it has long half-life from our extend technology.

Zhiqiang ShuBerenberg — Analyst

Got it. Okay. Thank you very much.

Bassil i. DahiyatPresident & Chief Executive Officer, Director

Thank you.

Operator

Thank you. And I’m not showing any further questions at this time. I would now like to turn the call back over to Bassil Dahiyat for any further remarks.

Bassil i. DahiyatPresident & Chief Executive Officer, Director

Thanks so much, and thank you, everybody, for joining us today. Have a wonderful evening, and we look forward to updating you more over the course of the year. Bye-bye.

Operator

[Operator Closing Remarks]

Duration: 54 minutes

Call participants:

Charles LilesHead of Corporate Communications and Investor Relations

Bassil i. DahiyatPresident & Chief Executive Officer, Director

Allen YangSenior Vice President and Chief Medical Officer

John J. KuchSenior Vice President & Chief Financial Officer

John R. DesjarlaisSenior Vice President, Research & Chief Scientific Officer

Ted TentoffPiper Sandler — Analyst

Mara Goldstein`Mizuho — Analyst

Gregory RenzaRBC Capital Markets — Analyst

Alethia YoungCantor — Analyst

Jonathan ChangSVB Leerink — Analyst

David NierengartenWedbush — Analyst

Arlinda LeeCanaccord — Analyst

Kaveri PohlmanBTIG — Analyst

Etzer DaroutGuggenheim — Analyst

Dane LeoneRaymond James — Analyst

Peter LawsonBarclays — Analyst

Zhiqiang ShuBerenberg — Analyst

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