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Xencor Inc (XNCR -3.01%)
Q1 2021 Earnings Call
May 5, 2021, 4:30 p.m. ET

Contents:

  • Prepared Remarks
  • Questions and Answers
  • Call Participants

Prepared Remarks:

Operator

Good day and thank you for standing by. Welcome to the q1 2021 Xencor conference call. At this time all participants are in listen only mode. After the speaker's presentation there will be a question and answer session. To ask the question during the session, you will need to press star one on your telephone. Please be advised that Today's conference is being recorded. If you require any further assistance, these press star zero. I would now like to hand the conference over to your speakers today. Mr. Charles miles, head of corporate communications and Investor Relations. Sir, please go ahead.

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Charles Liles -- Head of 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 releases [email protected]. Today on our call battle day yet, president and chief executive officer will provide a corporate overview and review recent partnership news. Alan Yang, chief medical officer will review clinical updates in john Cush, 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 increments that may make forward looking statements, including statements regarding the company's future financial and operating results due to market conditions, the plans and objectives of management, future operations, the company's partnering efforts, capital requirements, future product offerings, research and development program 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 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 the forward looking statements, including but not limited to those factors contained in the risk factor section, or most recently filed a report on form 10k and quarterly report on form 10 Q. With that, let me pass the call over to Bassil.

Bassil Dahiyat -- President and Chief Executive Officer

Thanks, Charles and good afternoon everyone. Sinclair's approach to creating antibody and cytokine therapeutics is based on our x pet protein engineering platform. It's built on our extensive protein engineering now how combined with our suite of x NAB SC 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 x MeV 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 x men by specific platform, the newest x map component to create antibodies that bind two or more different antigens simultaneously. And also to engineer cytokines with structures optimized for particular therapeutic uses.

Now are many partnerships really highlight its plug and play nature? Currently, we have 15 ongoing partnerships for economic technology, which have now resulted in two marketed products wuxian ultomiris for rare blood disorders, and more focuses on juvie 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 73. One, their anti SARS kobie. Two antibodies incorporates our extend FC technology based on an interim analysis of the phase three common ice trial, which demonstrated an 85% reduction in hospitalization or death and high risk adult outpatients with COVID-19 receiving fear seven 831 as monotherapy compared to placebo.

The primary importance of trial by the way. Now extended was integrated into vSphere 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 x Mab FC technologies outside our core focus of oncology and autoimmune diseases and demonstrates x NAB vast applicability to underserved areas like serious infectious disease. Now, if authorized beer 73 one would then become third antibody with our academic technology to reach the market. That's switching back to internal programs. We're currently running seven phase one studies evaluating x map five specific antibodies and cytokines. This way we're taking multiple simultaneously simultaneous shots on goal and clinic. And the proof of concept data we generate will guide which programs we independently advance which we partner in which we will terminate our Alan Yang, our chief medical officer review updates for our clinical portfolio now.

Allen Yang -- Chief Medical Officer

Thanks, Bassil. since our last update about two months ago, we dosed the first subject in the phase one study of x About five six for our wholly owned aisle to FC fusion engineer to selectively activate regulatory T cells or T regs for the treatment of autoimmune diseases. The goal of an IoT therapy for auto Monday's auto immune disease is to provide sustained, low intensity activation of T regs while avoiding the pro inflammatory systemic activation of effector T cells. And aisle two therapy that is selected for t regs with an expanded therapeutic window compared to historic oil two approaches would have broad potential across many different autoimmune diseases.

And preclinical studies indicate this may be the case for our program is engineered with reduced potency to improve tolerability improve improve duration of action for this normally toxic cytokine and using our x map hydrodynamic Hydra heterodyne America c domain and extend technology enhances its HalfLife x man 564 is now our second side of client in the clinic. Joining x map 306 our engineer io 15 for oncology that is partnered with Genentech. The single ascending dose study will characterize the safety tolerability and pharmacokinetics of XML 564 and healthy volunteers and 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 by specific antibody drug candidates. First for x map 717 are PD one ctla four dual checkpoint by specific antibody in mid 2021.

We plan to initiate a phase two 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 one B study, but we have transitioned into a phase two study. We continue to expect that we will present more data from the ongoing phase one studies expansion courts later this year as the data mature and to this study, we have add an additional cohort of patients with relapsed or refractory melanoma with a more tightly defined disease population. partly due to map our CD three by specific antibody that targets sspr. Two, we plan to initiate clinical study in patients with Merkel cell carcinoma and small cell lung cancer sstr to expressing tumor types known to be responsive to immunotherapy in mid 2021.

Due to a COVID-19 related staffing issue at the study site. Study start-up activities were delayed by a few months. shifting to promote a map under our strategic clinical collaboration with Morphosis we are investigating the chemotherapy free triple combination of promote a map our CD 20 by CD three by specific antibody with top us diplomat and lenalidomide in patients with certain lymphomas. We plan to initiate the first of these studies in patients with relapsed or refractory diffuse large B cell lymphoma, an aggressive type of non Hodgkins lymphoma in late 2021 or early 2022. Once we have finalized the recommended dose in our ongoing Phase One study and complete operational preparation for the multinational trial, we plan to present updated data from the phase one study later this year. Briefly for s map six nine as a cd 38 by CD three by specific antibody, which was formerly known as Amgen AMG four to four, we plan to support investigator initiated studies, and a new study is currently being planned to start later in 2021.

Last, we anticipate filing an ind for x Mab 819, our MVP three by city three by specific for renal cell cancer later this year, and initiating a phase one study in early 20 22x. Map 819 uses our multi valence two by one by specific format, which has two antigen binding domains for the tumor target, providing more selective binding for the high NPP three density expression on tumor cells, compared to the lower density on normal cells. The Binding activity of the x map t plus one format extends the range of targets amenable to CD three biospecifics for example, our partner engines AMG 509 program, carding c one and prostate cancer uses this format. In summary, we continue to advance our pipeline by graduating molecules into phase two, and are bringing new more novel agents into the clinic. Bassil?

Bassil Dahiyat -- President and Chief Executive Officer

Thanks, Allen. Now we're always looking to grow this pipeline with new programs, as we have with our itu t REG and MPP. Three programs and Alan just mentioned

Alarm along this front. Last month at the ACR annual meeting. We presented data from four preclinical stage programs including our third cytokine and aisle 12 fc fusion protein for oncology, two additional x mF two plus one CD three by specific antibodies. These ones target cloud and six, and GPC three, as well as our PDL, one by cd 28. By specific program, all four posters are available on our website. Now I'd like to take a moment to review this targeted cd 28 platform, which is a new class of T cell engagers designed to complement other mechanisms of T cell activation, such as checkpoint inhibition, or CD three engagement. cd 28 is a key immune costimulatory receptor on T cells that has been difficult in the past to safely and effectively engage therapeutically by targeting a cd 28 binding domain to a tumor by using a by specific 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 b 783. By cd 28 by specific antibody for potentially broad solid tumor use, including in prostate cancer will be seven HDS highly Express molecules advancing through preclinical development. Now, of course, the focus of our new collaboration with Janssen that we announced a few months ago is to discover a cd 28 by specific antibody against a prostate tumor target. 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 experts technologies, the clinical advancement of XM candidates as well as royalties from sales approved products. There were no COVID-19 impacts of partnering revenue that we were aware of during the first quarter, but we'll continue to monitor potential impacts of course. Last quarter, we disclose that we'd entered into a license agreement with a privately held company, which remained undisclosed at that time.

Now we can disclose that this company is zenoss biopharma, a new cross border company developing immune based therapies for patients in China and around the world. We grant them worldwide rights to develop three preclinical programs incorporating x map SC domains for development and autoimmune diseases. We received a 15% equity interest in the company and are eligible for royalties. We also entered a new academic collaboration last quarter with UCLA to extend the use of our zmapp technology. Pairing novel targets proposed by scientists to UCLA and Zen cores monitor suite of x map technology platforms.

What we've said is establish a framework with predefined terms, inter sponsored research agreements and potential license agreements to streamline and expedite any potential drug candidates that are selected for further development. UCLA agreement is our third collaboration focusing on novel target biology create a new generation of x lab by specific antibodies, joining those with an interest with a trait that and MD Anderson. Now with that I have a call over to john Cush, our chief financial officer who will review key highlights from our first quarter financials, john.

John Kuch -- Chief Financial Officer

Thank you Bassil. 10 cores broad protein engineering platform resulting partnerships and collaboration continue to generate revenue and provide value to support our growing portfolio of clinical and research stage by civic antibody and cytokines drug programs. cash cash equivalent for marker micro Investment Securities, totaled 577 point 1 million as of March 31 2021, compared to 604 million on December 31st 2020. The decrease reflects royalties milestone payments received related to licensing agreements net of cash used to fund operating activities for the first quarter. based on current operating plans expect to have cash on research and development programs and operations at the 2024. We currently estimate that we will end 2021 with between 425 475 million in cash and cash equivalents. total revenues for first quarter were 34 million compared to 32 point 4 million for the same period of 2020.

Revenues in the first quarter accrued revenue related to our gigantic collaboration milestone rather recognize Morphosis and the royalty revenue from electron Morphosis third revenues from the same period in 2020, which were primarily milestone revenue from Morphosis royalty revenue from websites and licensing revenue from our aimmune and affiliate collaborations. Research and Development expenditures for the first quarter were 41 point 4 million compared to 33 point 9 million for the same period in 2020. The increase is primarily due to increased spending on our x men 306 x men 564 and x men 819 programs. General administrative expenses for the first quarter were 8.2 million compared to 7.2 million and same period of 2020.

They increase primarily being related to an increase in staffing. Other income for the first quarter of 2021 was 13 point 2 million and included a gain of 12 point 9 million in equity received in connection with the licensing transaction, compared 2.7 million for the same period in 2020, which was which was primarily net interest income for the period. The net loss for the first quarter was 2.5 million or four cents on a fully diluted per share basis compared to a net loss of 8.1. 1 million, or 14 cents on a per share basis for the same period of 2020. The lower net loss reported for the first quarter of 2021 compared to net loss for the same period 2020 is primarily due to other income recognized from equity received in the first quarter 21 in excess to increase spending on research and development expenses for the period.

That cash share based compensation expense for the first quarter was 8.3 million compared to 6.59% period 2020. And total shares outstanding were 58 point 2 million as of March 31 2130, to 57 million as of March 31 2020. With that, we'd now like to open up the call for questions.

Questions and Answers:

Operator

Thank you, sir. As a reminder, to ask a question, you will need to press star one on your telephone. To draw your questions. You may press the pound key, please stand by while we compile the q&a roster.

And speakers, you have your first questions from dead 10 cents off of fiber center. therapies asked your question,

Ted Tenthoff -- Piper Sandler -- Analyst

Craig. Thanks so much guys. So much for caring whether or not we should anticipate an update for the Roche program for io 15 this year. And also going back to PD one ctla 4717 we'll be getting prostate cancer data but what other cohorts could we expect from that this year? Thanks so much.

Bassil Dahiyat -- President and Chief Executive Officer

Hey, thanks, Ted. So regarding our x men 306 iO 15 program. That's the oncology collaboration with Genentech, we we are discussing a publication climate genetec. 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 to dis escalation as a combination with the Tesla lism ab, their PDL, one molecule was 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 happened over the next over the next year.

With regard to Fm 717, or PD one ctla, four molecule, a Yeah, there are going to be additional cohorts that we disclose data for from from the expansion cohorts have the phase one study. So in addition to a much more mature data set from a prostate cancer cohort will 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 one approved indications. So we would expect all that in the second half of this year.

Ted Tenthoff -- Piper Sandler -- Analyst

Awesome. Thank you so much, and excited to see IoT go into the clinic. Yes, we are two.

Operator

Your next question from mera Goldstein of Missoula security. Ma'am, your line is open.

mera Goldstein -- Missoula security -- Analyst

Can you hear me?

Bassil Dahiyat -- President and Chief Executive Officer

Yes.

mera Goldstein -- Missoula security -- Analyst

Awesome. Thank you. So I wanted to ask two things. The first is around the strategy of converting that phase one B in prostate cancer to phase two, 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 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, and a competitive advantage using, you know, that kind of technology as you are versus let's say, engineer cytokines, and other fusion proteins in the like.

Bassil Dahiyat -- President and Chief Executive Officer

Yep. So, I guess on the first question, that the shift of the FF 717 p one c two like for a study in prostate cancer that multi that basket study, why shift from phase one to phase two? My understanding and Alan you should pipe in here was that it was simply a better reflection of what the study actually was doing, given that we have to go forward. Yes, we selected for that study. Merely that you anything to add on? Yeah, no, it is a little bit of nomenclature. Remember a phase one B could be looking at comedy. So we've already sort of disclosed that this will explore 717 with sort of key combinations of either chemotherapy or targeted agents. And you know, whether you call it a phase one, B, or phase two with a safety run, and I think, OK, to the 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 two, in planning to go to eventual phase three. Yeah. Now, on your second question, Mark, the cytokine strategy we're taking for this really rapidly evolving and growing field of engineered cytokines. I'll maybe ask john de les, who's actually in the call here to answer questions, to chime in about, you know, how our design strategy has some commonalities for how we're looking at all the cytokines. And yet, you know, 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. January.

Allen Yang -- Chief Medical Officer

Yeah, sure about, Mr. We, when we first tackled aisle 15, you know, we went in, we fuse out 15 to an FC, to make a long acting cytokine. And we made a critical key discovery. That is, you know, natural cytokines are limited in their ability to stay around, you know, 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 lasts a lot longer in circulation. And because of the last longer, even though it's lower potency, you can actually mediate as pharmacology for a longer period of time.

Also, you know, the fringe benefit of that reduced kotse was much better tolerability, and much, much better control over toxicities as he does escalate, that we turned around and applied that same concept to the owl to program or T reg expander. found 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 aisle 12 program as well as we detailed on our ACR festers. So that's the unifying theme is it which seems to be pretty unique in the community is going with you no longer acting and lower potency molecules.

mera Goldstein -- Missoula security -- Analyst

Thank you.

Operator

And speakers, your next question from Peter Lawson, of Barclays, your line is open.

Peter Lawson -- Barclays -- Analyst

Red, thanks for taking the question. Thanks for the updates. I just thought I have to when do we see David around that and kind of how do you think about picking particular tumors and combination partners? Oh, well, our aisle two is targeting activation of regulatory T cells. So that's our program focused in autoimmune disease. Our IO protein is the one that is the collaboration was known tech, as is our play with the cytokine for activating T cells along that same pathway. So you want do you want to start with the alphas teen? Or do you want to talk about the 564 program? Or else?

I'm just curious, if you if you're thinking of moving that out, too, as well into oncology or?

Bassil Dahiyat -- President and Chief Executive Officer

No, no, we don't have any intention to do that. It's biology is really tuned, as john said, Well, I guess john is tuned for potency. But in addition for that I'll to molecule, we actually took the direction like you know, some of our some other companies that are looking at same approach of increasing the relative binding affinity to the inhibitory well to the receptors were probably expressed on regulatory T cells, the the alpha alpha receptor, so we really feel that's much more appropriate for autoimmune indications. We haven't yet guidance, 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, as we get a little further into this, that we just opened the study about a week ago. Then the research hitch three points for that. I think you've talked about that for just curious where that is and where you're thinking of positioning that construct.

Allen Yang -- Chief Medical Officer

Yeah, I'll touch on the timeline. And then if john wants to jump in on on, you know how we're positioning it. So that molecule we hope to have in the clinic in 2022. It's an active preclinical development now with all the requisite manufacturing scale of activity and its activities just getting started. JOHN, yeah, in terms of thinking about applying that in your reasoning we've selected the 73 of the target is, is very broadly, they're very brightly expressed across a whole range of solid tumors. And we wanted a molecule that we could, you know, what we could use to target to, you know, tumors get, you know, tumor specific cd 48 costimulation, which is your signal to, and then you can use that to build on whatever signal one is being provided, right.

And that signal one can be provided, either by just natural T cell, you know, activity gets neoantigens, in which case, you'd probably want to be exploring that, you know, our b 73, cd 28 and a p one combination study, or signal one could come from any one of our T cell engagers, or classic CD three by civics, you know, in our solid tumor pipeline, the first of which will be an estp, three by CD three. And I guess beyond that, I would also say, the 73 is is a particularly interesting target and prostate cancer is very bright there. And we of course, we want to explore that in prostate cancer as well.

Peter Lawson -- Barclays -- Analyst

Thanks for taking the questions.

Allen Yang -- Chief Medical Officer

Thanks, Peter.

Operator

Speakers, your next question from Elysia. Y'all have kentaur. Ma'am, your line is open.

Leon Foley -- kentaur -- Analyst

Hey, guys,thanks for taking the call. This is Leon Foley here. We just have a follow up on aisled. To program since you just recently started the trial, can you just talk a little bit about you know, how your molecule is differentiated from others in the space and what advantages that you expect to see in a clinical setting?

Bassil Dahiyat -- President and Chief Executive Officer

Right, so the the design follows the the rule of our cytokine engineering john sort of laid out which was it's taking the natural oil to molecule and making mutations in it to dramatically dial down its potency, I think we're we're north of 100 fold less potent than wild cup out to fuse to an FC domain. Now, the things that make this particularly well suited for, for for our communities is our protein engineers biased the binding to actually have a significantly higher proposed ratio of binding to the cd 25 or l two or l two alpha receptor, then to the aisle to beta gamma receptors that receptors is is heavily expressed on regulatory T cells to buy for toys T rex so how do our designs differ from the sort of what's the positioning we hope that are dramatically lower potency as well as our FC domain, which contains our extend technology gives us an enhanced therapeutic window, we won't know until we see and that we can get you know, excellent t reg amplification?

Allen Yang -- Chief Medical Officer

In a dunno I missing anything on? Oh, and and maybe john, if you want to comment on the monomeric l to nature, and how that's distinctive in the industry? Yeah, no, that's a good point. So you know, we we divide ours using our sc heterodimers, which enables this, we designed ours to only have a single aisle to for the FC debate. Whereas competitors, like like Amgen, or other efforts have, by villanelle to we think having the monovalent aisle to actually helps reduce internalization through receptor binding. That's sort of a kind of a classic paradigm in terms of, you know, biologics and internalization. So, you know, bottom line is, again, we applied our potency reduction monomeric aisle to, we would hope that we have, you know, highly competitive, or even best in class, you know, pharmacokinetics and pharmacodynamics.

Leon Foley -- kentaur -- Analyst

Okay, great. Thanks. And, and, and I have another question on your rl 12 program. I know it's pre clinical, but just curious how you're thinking about somebody designing a molecule that can potentially addressed the narrow therapeutic window here.

Allen Yang -- Chief Medical Officer

I mean, john, you want to take that? I guess? Yeah, sure. Yeah. I'll take that.

Bassil Dahiyat -- President and Chief Executive Officer

Yeah. Again, we we found and you know, you can see, you know, a pretty nice story about this on our ACR poster. We found again, that the potency reduction gave us much better control. So when we when we put the owl to, I'm sorry, the outfall reduced version into monkeys and compared it to a wildstyle 12 Sep fusion. We found that as we dose escalated in human primates, that we saw much more gradual onset of, you know, a key pharmacodynamic marker which is ip 10 which is downstream of interferon gamma, right. That's what aisle 12 famously does.

So as we dose escalated our potency reduced version, it was a much smoother ramp up on that pharmacodynamic marker. And, you know, by comparison in the wild have all 12 St. And what that tells me is we're going to have a much easier ride when we does escalate, and we've got much better control over what's actually going to go on and the humans when we use this reduced potency molecule. So that's, that's what we have so far. That's what the preclinical data suggests, but obviously, we're gonna have to see what happens in the clinic.

Leon Foley -- kentaur -- Analyst

Okay, great. Thank you.

Operator

And speakers. Our next question from edzard are out of Guggenheim. Sir, your line is open.

edzard -- Guggenheim -- Analyst

Great, thanks. Thanks for the question. So really for the ex Mab, 564, I guess, you know, if you sort of see the appropriate therapeutic window, do you have any thoughts on how, you know sort of maybe the low hanging fruit indications, if you will, or maybe sort of maybe interesting indications that you could pursue? Initially, obviously, assuming success? And then I have a second question.

Bassil Dahiyat -- President and Chief Executive Officer

Yeah, we're not guiding on specific indications we're selecting yet that we're hard at work. putting ourselves in 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 will start after the sad. We think there's a lot of opportunity for these novel mechanisms of action, like t reg inhibition in in some of the smaller autoimmune indications. And so we're certainly looking there. But you know, the, I think, when you look at what are the competitive landscape in some of the larger indications where they're still open room, we think a lot of our competitors have already already hit those. So more to come on that we are working hard on that. Now, do you have a follow up question?

edzard -- Guggenheim -- Analyst

Got it? Yep. Just a second question, I guess, on sort of the initiation of the promoter math practice, in that setting, I guess, you know, based on the intro remarks is the data from the ongoing phase one, if you will, sort of the main hurdles to sort of getting that started in terms of sort of the timeline, you know, variability that you described.

Allen Yang -- Chief Medical Officer

I think it's pretty coincident with the operational pieces as well. And I think that, you know, we hope they'll all come together, we are dosing it to two week now, with a cue once a cue weekly run in period, you know, much likely seen from from other programs. So, squaring that away is ongoing, and we hope to have that data present late this year, like we've guided and hopefully start off the pace to.

edzard -- Guggenheim -- Analyst

Great, thank you, and congrats on over progress.

Allen Yang -- Chief Medical Officer

Thank you.

Operator

Speakers, our next question from Tom Schrader of btig. Sir, your line is open.

Tom Schrader -- btig -- Analyst

Thank you. Good afternoon. Thanks for the update and taking the questions just 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 just 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 IRT therapy with proleukin. So you just need to control that from coming on too strong, whether it's the T regs or amplifying your T effectors.

Allen Yang -- Chief Medical Officer

So the classic of Babel and other things. Another way of saying it is we you know, we, we optimize the activity of our owl to 40 reg, but there's no such thing as perfect flow activity.

So at some point, if you doze high enough, you're going to start, you know, 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 many, many faces. Do you think you're 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? Where do you think a good biomarker signal would be enough to go into more challenging applications?

Bassil Dahiyat -- President and Chief Executive Officer

Yeah, it's a great question, because that's something that with many programs, we mull over, I think we've run the history. Moreover, 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 you trust the biomarkers? I think that 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 in a competitive standpoint, even if you showed disease modifying activity there, I don't know how well it would translate. So I don't know if Zen core 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 kind of definitive for a go signal. There.

Tom Schrader -- btig -- Analyst

Great. Thank you very useful.

Operator

Speakers. Our next question from seeking shell of Varian Berg, please ask your question.

Varian Berg -- Wedbush Securities -- Analyst

Hi, good afternoon. Thanks for taking my questions. I have a few. The first one on several, one, seven, or you said that you're going to move through the combination trial in a prostate cancer? What kind of combinations? Are you thinking to potentially move to, to treat the perfect prospect groups there as the first one?

Bassil Dahiyat -- President and Chief Executive Officer

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

Allen Yang -- Chief Medical Officer

Right. Yeah, you know, I think it's fairly obvious. You know, there's some targeted agents that have been approved for, for prostate cancer like PARP inhibitors. And then the chemo therapies still use in a certain aggressive types as well. So you know, those subtypes, you'd have to combo with with checkpoint inhibitor, and so obviously, we're going to explore those.

Varian Berg -- Wedbush Securities -- Analyst

Got it? Okay. And, and then for the just curious about a cd 20 a biology here? What's the, I guess? broadly? What's the difference between city 28 by specific versus city three by specific from, I guess, safety and efficacy standpoint?

Is it more?

Bassil Dahiyat -- President and Chief Executive Officer

Yeah, that's a long question. JOHN, let me briefly go ahead. Yeah, there's Yeah, that's, that's a great question. You know, so this, the CD three is kind of a bigger hammer, right. So C three is signal one on the T cells. And it's, it's not it's not specific to any any particular T cell population, right, the point of a CD three is to grab any T cell in the city and more of a live it against the tumor. So of course, that's, that's going to be a little bit, you know, more challenging in terms of, you know, safety profile, you know, either in terms of CRS, but also in terms of just, you know, on target off tumor toxicity with the C 2080.

It's, it's a pretty intriguing concept, because it's providing the signal to, which can amplify a signal one, and then it can build off of a signal one that's coming elsewhere. Right. And, you know, like I was saying, what, with one of the earlier responses, this signal, one can come from an endogenous T cell reacting with a tumor cell, and now you're adding in that signal to with the T 28. And amplifying that natural endogenous t. So as a tumor response, or signal, one could come from a CD three by civic and you can combine the two. And so we're obviously contemplating both approaches.

Varian Berg -- Wedbush Securities -- Analyst

Got it. Thank you. Final quick one on 6698 cseries City survey molecule, I guess where do you see this molecule ago in in the future?

Allen Yang -- Chief Medical Officer

So right, right now we're following the lead of some investigators who were enthusiastic about a cd 38 cd three, you know, we'll note that Amgen decided to jump out of development. And really, this was a molecule we enabled with our technology but hadn't actually made for them. They just took our various building blocks and put them together for CD three c 38, and FC admin. And in myeloma, they felt that the AV profile wasn't consistent with a go forward to go forward with it. We'll say that without disclosing until we've got the trial up and running. There are other hematologic malignancies that express cd 38, where the tolerability profile might seem quite reasonable in that context, so more to come on now.

Varian Berg -- Wedbush Securities -- Analyst

Great, thanks very much. Congrats on the progress.

Operator

And speakers our last question from our Linda v. of Canaccord. genuity. Ma'am, your line is open.

Linda v. -- Canaccord. genuity -- Analyst

Hi, everybody. Yeah, this is that then call Looking for Linda, thanks for taking my questions. Loved mebane answered, I just wanted to ask if you on 717 and promote to map you know, a few PD one and ctla, four programs of data that have been presented at this point. And I'm just wondering regarding 717, how's the safety looking? versus niebo versus any of the combination regimens? And what do you guys ultimately hope to show? In the data?

Bassil Dahiyat -- President and Chief Executive Officer

I guess I'll ask the first is, first, what do you hope to show the data we hope to share that in, we can find an indication or we can, you know, make a difference for patients, whether that's an relapsed 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 mo ways, and the tolerability profile, the combination of ctla four and PD, one can move the needle that hasn't been moved before. And I think prostate cancer is a great potential example there. You know, regarding the safety profile we've observed so far, I'll let Alan cat take that question.

John Kuch -- Chief Financial Officer

Yeah, thanks. So you know, it's fair to say that the needle is the combination is probably more effective than PD one blockade alone. But clearly, you get a lot of toxicity, only about a third of patients who may not study past a few courses. So, you know, the most common toxicities kaleidos. This is the most common toxicity, the most common toxicity that leads to interruption or discontinuation. And so, we haven't seen that high frequency colitis. You know, we believe that the indications as basil alluded to is where PD one plus ctla, four, it's been shown to be synergistic. And perhaps, you know, you haven't seen that much improvement activity prostate cancer is a classic example of that.

Linda v. -- Canaccord. genuity -- Analyst

Okay, great. That's very helpful. I'm switching gears to supplement a map. And I understand that Morphosis might be driving a little bit of a bus here. It's a competitive space. And I'm just wondering, how do you think from an Automat? In a competitive positioning? And maybe Can you comment on what you think the development strategy will be expect? Maybe data in 2022? At some point?

Bassil Dahiyat -- President and Chief Executive Officer

Yes, I'll take that one. So the position of procurement, you're right, it's a very competitive area, cd 20, CD threes in an already competitive indication in lymphoma. And we think that, you know, 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 and as the best scientific rationale we can think of, and to see if we can go for the best approach. Sorry, the best combination approach that and this is a key point is chemotherapy free, a direction the field desperately wants to move in and lymphoma, just like has happened in, in leukemia, you know, based on the success like you know, CLL Brut nib and, and vanetta clacks, a use of antibodies. So the planto tafel Lem combination is tapa setTimeout.

And 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 plateau to a cd 20. CD three is effector cells, innate effector cells driven by the FC technology that we put into tests and Mab and cd 19 binding. So different target also than a cd 20 cd three. 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 is going for a chemotherapy free regimen that could be super active, and that that's how we hope to distinguish ourselves.

Linda v. -- Canaccord. genuity -- Analyst

Okay, great. So that would be a simpler regimen than existing regimens right now. Well, hopefully I get 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 outside before you before you go on to another one events. So,you know, maybe I can add some color?

John Kuch -- Chief Financial Officer

Yeah, maybe I'll add some color. So, you know, the strategies have been sort of declared by our competitors, right. And so there's two chemo regimens that are often used for the second line, it's either, you know, gem ox, or bendamustine, Re tuckson. And, you know, 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 gem ox, you know, as I was alluded to our strategy is, is sort of a little bit different tap acidum app, at least an address on inelegant will pay populations have been already approved for that second line indication. Right? And so now we're adding our CD 20 to their cd 19. And then of course lenalidomide potentiates, the cd 19. It could potentially potentially as the cd 20 as well. So, you know, that is the sort of differentiating approach. So we think our approach is vastly different from the others.

Allen Yang -- Chief Medical Officer

Okay, great. Sorry. No worries.

Bassil Dahiyat -- President and Chief Executive Officer

Sorry to interrupt you. So data readout, do you think might be 22 2022? Or maybe later? We're not guiding on that yet. We want to get Prowl started that will give specifics.

Linda v. -- Canaccord. genuity -- Analyst

Okay. Thanks again for taking my questions. Appreciate it. Thank you.

Bassil Dahiyat -- President and Chief Executive Officer

Alright, well, I guess if 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.

Operator

[Operator Closing Remarks].

Duration: 46 minutes

Call participants:

Charles Liles -- Head of Investor Relations

Bassil Dahiyat -- President and Chief Executive Officer

Allen Yang -- Chief Medical Officer

John Kuch -- Chief Financial Officer

Ted Tenthoff -- Piper Sandler -- Analyst

mera Goldstein -- Missoula security -- Analyst

Peter Lawson -- Barclays -- Analyst

Leon Foley -- kentaur -- Analyst

edzard -- Guggenheim -- Analyst

Tom Schrader -- btig -- Analyst

Varian Berg -- Wedbush Securities -- Analyst

Linda v. -- Canaccord. genuity -- Analyst

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