Xencor Q1 2023 Earnings Call Transcript

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May 8, 2023

There are 12 speakers on the call.

Operator

Afternoon and thank you for standing by. Welcome to Xencor's First Quarter 2023 Conference Call. All participants are in a listen only mode. After the speakers' presentation, there will be a question and answer session. Please be advised that this call is going to be recorded at the company's request.

Operator

Now, I would like to turn the call over to your speakers today, Charles Lillies from the Head of Corporate Communications and Investor Relations. Go ahead, Charles.

Speaker 1

Thank you and good afternoon. Earlier today, we issued a press release which outlines the topics we plan to discuss today. It's available at www.sencor.com. Providing abbreviated comments on the call is Basil Dakhyak, President and Chief Executive Officer. Afterward, we will open up the call for your questions and we will be joined by Alan Yang, Chief Medical Officer John Des Jarlais, Chief Scientific Officer John Cush, Chief Financial Officer as well as Nancy Valente, Chief Development Officer.

Speaker 1

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 future market conditions, plans and objectives of management, future operations, the company's partnering efforts, capital requirements, future product offerings and research and development programs. These 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 section of our most recently filed Annual Report on Form 10 ks and Quarterly Report on Form 10 Q. With that, I'll pass the call over to Basil.

Speaker 2

Thanks, Charles, and good afternoon, everyone. At Sencore, we use our array of modular protein engineering tools to create a broad internal development portfolio of antibodies and engineered cytokines In oncology and autoimmune disease, we target novel biologies with our candidate designs, including CD28 co stem bispecifics, More tumor selective CD3 bispecifics and potency reduced cytokines. This broad portfolio lets us take multiple, simultaneous shots on goal in the clinic and use the proof of concept data from our early stage studies to guide which programs we advance, which we terminate and which we partner, So that we use our resources on programs with the greatest potential for success and make room in our portfolio for the next wavevexnab bispecifics in engineered cytokines. Continue to enroll patients in Phase 1 and 2 trials across our wholly owned portfolio for oncology and 1 autoimmune XmAb candidates. Last month at AACR, we presented on our preclinical portfolio of XmAb CD28 co stimulatory bispecific antibodies, which are focused on our which are the focus of our research now and are a very exciting new area in immuno oncology.

Speaker 2

XmAb CD28 bispecifics are designed to activate T cells Our poster highlighted our platform's rapid candidate generation and the broad opportunity for CD28 using data from 5 CD28 bispecific antibodies targeting variety of solid tumor targets like CEA, TROPE-two and STEAP-one. We've initiated preclinical development of a second internal CD28 program with a plan to file the IND next year. Recall that our lead clinical CD28 program XmAb808 targets B7 H3 and is in Phase 1. Our next data presentation will be later this quarter when we expect to present data from our regulatory T cell targeting cytokine XmAb564 at the U. S.

Speaker 2

Congress of Rheumatology in Milan. We plan to present updated biomarker data from the single ascending dose study that we initially presented in November 2020 And for my last comment, I'd like to welcome a new member of the leadership team at Xencor. Last month, we announced the appointment of Nancy Valente as our Chief Development Officer. She'll be responsible for all of Xencor's clinical activities and will join our CSO, John Desjolais and me in the scientific leadership of the company. We're delighted to welcome Nancy to our team and look forward to benefiting from her deep expertise in developing drugs like Gazyva, Poliviv, and Chlestin HEMLIBRA.

Speaker 2

She was in a unique position to see our development programs, technology and people up close for the last 8 months as a member of our Board of Directors from which she's resigned And chose to commit to work full time here. Welcome aboard, Nancy. Now with that, we'll open the call to your questions. Operator?

Operator

The first question comes from Mara Goldstein from Mizuho. Mara, your line is Hold on just one. Hi, thank you.

Speaker 3

This is support from Myra. Thank you for taking our question. I have a question on XmAb564. Congrats on getting the slot at Eula. Just curious, I know there will be additional biomarker data, but it I was wondering if you can guide in terms of what we should pay attention to.

Speaker 3

And then on XmAb 564, I'm just curious if competitors' datasets and development, including Nektar's, Red Pack and Amgen's compound, I'll give you a pause on this mechanism and why atopic dermatitis and psoriasis are selected as an indication for the MAD study. Thank you.

Speaker 2

Any other questions? That was about 4.

Speaker 3

Thank you. That's all.

Speaker 2

Great. Let's get started. So the kind of biomarker data that we're going to present is really an elaboration in more detail On the phenotype of the T cells that the regulatory T cells in particular that were amplified in our single ascending dose study that we presented in November. So really characterizing how those look in more detail. I think we delivered the punch line in November remarkably durable with sustained Treg increases out to 21 days And we're excited by the opportunity to try to extend the dosing interval beyond what sort of the class has gotten to, which is every 2 weeks.

Speaker 2

So we're really quite enthusiastic still about the mechanism. I think the data from the competitor that you mentioned has to be put in the context of their Less than ideal selectivity for CD25. And John, do you have anything to add to that?

Speaker 4

No, I mean, just based on our in vitro comparisons, looking at various molecules and what's been available in various posters, We like our selectivity profile better. Ours is a little bit more surgically engineered to, you have preferential binding to CD25 plus Tregs and very carefully potency reduced to maximize the pharmacokinetic and Pharmacodynamic effects?

Speaker 2

So we're still quite enthusiastic about the potential of the mechanism of action. I think it's really about making sure you've engineered what you think is the right molecule to attack that MOA. Now you asked about our indication selection in our Phase 1b multiple ascending dose We also started treating patients in November of last year. We picked atopic dermatitis and psoriasis and there's 2 goals of that study. 1 is to rapidly Determine a good dose and schedule with multi dose and we wanted to pick indications that we could rapidly enroll and that we could also directly view clinical outcome quite easily.

Speaker 2

So these skin autoimmune diseases allow you to do that, look at actual clinical response, correlate that to Tregs And your safety profile. We think in particular for atopic dermatitis, there remains a strong opportunity for good agents that can have long dosing intervals and good safety.

Operator

Thank you. The next question comes from the line of Edward Tanalff from Piper Sandler. Your line is open.

Speaker 4

Great. Thank you. Can you hear me okay?

Operator

Yes.

Speaker 4

Hi, guys. Can you hear me okay? Yes, great. Hey, so I apologize if I missed this, but what if anything are you guys going to be showing at ASCO and when should we get the next Medallia Okay. Thanks.

Speaker 2

Yes. We're not presenting any new data at ASCO this year. As you Recall our tempo of presentation has usually fallen towards the late in year conferences. And we'll guide on that Specifics on that as we get a little further on into the year and closer to whatever data updates we're going to do. We're not guiding full year data.

Speaker 2

We're really doing a little closer like we did just now for XmAb 564.

Speaker 4

Okay, guys. Looking forward to you, Lior.

Speaker 2

Thanks. Take care, guys.

Operator

Thank you. The next question comes from the line of Brian Tang from JPMorgan. Go ahead, Brian.

Speaker 3

Hey, guys. Thanks for taking my question. Maybe just one question on 564, your IL-two Fc. So you previously mentioned that psoriasis is a great starting point for you to get some proof of concept. As we look forward to Some data early data in psoriasis in early next year.

Speaker 3

I'm just wondering how do you think about the market opportunity for this molecule Given that this may not be the ultimate market for you to move forward with 564, and any guidance Just from an analyst standpoint, how should we think about the TAM here for 564? Thank you.

Speaker 2

I'm sorry, how should we think about the what for 564? I missed that word.

Speaker 3

The total addressable market, for 564. Thank you.

Speaker 2

Got it. Got it. Tam, sorry. So, I think we made a point of adding atopic dermatitis into the Phase 1b mix and we will be dosing patients in cohorts there as we step up a little bit in dose Because we do think AD has still a significant unmet need both for just the breadth Of the number of severe patients as well as the need for longer acting agents, we know that there's a lot of excitement about lebrikizumab coming on with a monthly, which is better than dupilumab, which is every 2 weeks and is really bound by the target mediated clearance there. So we think there is we try to be thoughtful about adding things that can both have proof of concept as well as A meaningful potential for differentiation into our Phase 1b.

Speaker 2

But remember that this goes to your total of addressable market. There's a wide range of indications You could potentially reach with a broad autoimmune drug. We know that some of our competitors are developing also with colitis. There is development going on in other kinds of diseases like Type 1 diabetes, like in Just a wide range. So as for total addressable market, I think you could be sort of incredibly broad right now or you could wait to see how we Define it further as we pick additional indications as we come out of this Phase 1 later, say in 2024.

Operator

Our next question comes from the line of David Neergarten, Wabash Securities. Go ahead, David.

Speaker 5

Hey, thanks for taking my question. I just had a On the claudan6 CD3, just with the way the ovarian cancer market is evolving, kind of Where you would see it slot in potentially, I know it's early stages, but I was curious on that. Thanks.

Speaker 2

That's a tough one. I think it's a market influx, but still even with the agents that are coming on, Even the response rates are still not that dramatic and people relapse fairly quickly. We think with a distinct target That you would be aiming to be the first time the patients see anything hitting this target. I think you're going to start with the later line in the clinic, but try to move forward pretty aggressively. There's nothing that slammed the door certainly.

Speaker 2

And I think that a cytotoxic agent like this could have A lot of potential. And I know that there's competitive landscape with ADCs with other CD3s, but, I still think there's a wide a big unmet need.

Speaker 4

Yes. And I'll add with a completely different mechanism of action than some of those other molecules. I don't think there's Any emerging resistance against those therapies will really read too much on CD3.

Speaker 5

Could you Remind me at least, maybe not all of us on the phone, but is there a differential or A requirement or a likely requirement for testing of expression here or is it broadly expressed? I just can't remember off the top of my head.

Speaker 4

We think it's definitely going to be prudent to very closely monitor for pod and cystic expression.

Speaker 2

Okay, got it.

Speaker 4

There's definitely some heterogeneity.

Speaker 1

Okay. Thank you.

Operator

Thank you. The next question comes from the line of Dane Leone of Raymond James.

Speaker 1

Hi, thanks for taking the questions. Can you just give us an update on where you see the CECL-fourteen-fifteen program getting Thank you.

Speaker 2

Sorry, Dane, you were choppy. Where we can see the CTLA-four, did you say CTLA-four, PD-one?

Speaker 1

Yes, CTLA-four or PD-one bispecific

Speaker 2

specifically on data timing until we get a little closer to events. We've traditionally updated on that late in the year, but we're not saying anything definitive yet. We are enrolling well in our both of our Phase IIs, our combination chemo Phase II as well as our monotherapy Phase II. The first being in prostate only, the second in prostate as well as guide tumors. So, we'll We'll give guidance on data timing a little bit later.

Speaker 1

Okay. Thank you.

Operator

The next question comes from the line of Kaveri Pullman from BTIG. Kaveri, your line is open.

Speaker 6

Hi, good afternoon. Thanks for the updates and for taking my questions. So for IL-twelve, how do you think about this Given that there have been some disappointments in this space, can you tell us about your approach and how it could be different from others? And my second question is regarding mudalumab. If you could provide more color on your trial amendment for chemo combinations for CRPC.

Speaker 6

And you are enrolling 20 patients per cohort for different subtypes. Can you tell us what you would like to see from these cohorts to move forward? Thank

Speaker 2

you. So maybe for the IL-twelve question, John, if you want to address our differentiation there.

Speaker 4

Yes. Well, first of all, I mean, in terms of the disappointments, all we have is something about Assets being moved around. We actually don't have any of the data from that study yet. So it's really hard to interpret what that means. But our molecule is very different.

Speaker 4

It was specifically designed following off of what we learned From our IL-fifteen and IL-two programs, it was designed to have reduced potency to the tune of around 100 fold reduced potency. And what we've seen in our preclinical studies very similar to what we've seen in the human studies for the IL-fifteen and IL-two programs That potency reduction actually gives you a dramatic improvement in pharmacokinetics. It seems to also impact tolerability and we hope it will positively impact therapeutic index. We definitely saw evidence in the non human primates We have a much more gradual dose response of the pharmacodynamic activity with our IL-twelve than, for instance, compared to a wild type IL-twelve SC. So we think we'll have a lot more flexibility in Phase 1 to really zero in on the best The dose that gives you the highest therapeutic index.

Speaker 4

And I'll

Speaker 2

note there's a lot of noise around other programs that weren't actually engineered cytokines being injected systemically, Things that are very complex like oncolytic viruses and localized delivery programs, I just don't think those are relevant comparatives. I don't think those teach you anything. Now on to your boudalumab question number 2 about the more on the trial amendment to the chemo as well as what we think the bar for success is roughly. Alan, if you want to touch on that?

Speaker 1

Yes, sure. So I'd just remind people on the 71704 study, the design. Remember, we had several groups in there. We had an aggressive variant group. We had a PARP naive homologous recombination deficient group, homologous recombination deficient PARP treated group, MSI high group and then a biomarker negative group.

Speaker 1

So it's really dependent on the group. Now several of the groups have chemotherapy. And so Depending on the chemotherapy regimen, you'd expect a response rate of about 40% to 50%. So for most regimens,

Operator

Our next question comes from the line of Charles Zhu of Guggenheim. Charles, your line is now open.

Speaker 7

Hi, this is Edward on for Charles. Just a question on 564 please. So how strong is the mechanistic link between sort of Inducing Treg levels as you've shown pretty clearly to actually having sort of a beneficial effect on the disease?

Speaker 2

There's 2 sets of data that read on that. 1 fairly recent coming from actually one of our competitors, the Respegg program that Lilly presented last Here showing clear and convincing activity at reducing psoriasis as well as atopic dermatitis signs and symptoms and in particular, a really profound durability post end of treatment. I'd say the other line of evidence comes from really the last decade and a half of work with low dose IL-two, wild type IL-two, which sort of mimics a CD25 selective molecule because of The high expression density and selectivity for Tregs are very low doses of ILU, modest selectivity. And there's efficacy that's been shown in Prior intractable autoimmune disease like ulcerative colitis, like Type 1 diabetes, like RA, like lupus, like I mean lots of other Indication. So those are the 2 threads of evidence.

Speaker 4

Yes. And I'll add, just going back to real basics, remember there's that disease ipex, where Patients have a defect in the FOXP3 gene, which is critical for producing Tregs and they have a whole array of various autoimmune type diseases from having that disease. So from a very basic perspective, Tregs are critical for preventing autoimmunity.

Speaker 7

Great. Thanks. And maybe just a follow-up if I can on The 104, the PD-one iClass, I think you mentioned in the press release that you are going forward with the colorectal MSS stable expansion. Just wondering, are you also Other potential expansion cohorts and kind of what pushed you to focus on that one at least for now? Thank you.

Speaker 2

Right now, we're focusing on the MSS colorectal cancer, really looking for a larger number of patients than we had in our expansion cohorts to see if we have the kind of activity that would suggest a relevant path forward in MSS CRC. What So we don't have other indications right now. We're focusing on the CRC. We'll disclose specifics at a later time, but We saw in our expansion cohorts things that suggested MSS might be viable for this agent in particular in combination with ipilimumab, which is how the study is designed in these additional sets of patients. And so we're eager to enroll it and gather the data and see.

Speaker 7

Great. Thank you very much.

Operator

Thank you. The next question comes from the line of Gregory Renza from RBC Capital Markets. Go ahead, Gregory.

Speaker 8

Hi. Can you hear me okay? Yes. Great. Hi, this is Ying Huang for Greg.

Speaker 8

Congrats on the progress and thanks for taking out questions. Maybe just on a high level, just with your current cash position, wondering how are you thinking about business development as we have seen M and A heating up in the space? And How would you balance the internal innovation and capital preservation in this cash cost macro environment? Thank you.

Speaker 2

Yes. We really do try to focus on having a high bar for putting molecules into the clinic, Because the clinic is where the spend really hits you, right? Our research is incredibly efficient on both cost and people basis. And that's what's been able to drive so many partnerships, so many license over the years. But right now, it's about being stringent about the molecules we put in the clinic and then getting even better, more aggressive and faster about making quick decisions from our early clinical data to either advance quickly or to stop the spend by partnering.

Speaker 2

I think you can see from our plimodimab deal a year ago that program is still progressing, but now that's really in Janssen's hands. So we try to balance That holding on to commercial rights for molecules of our own, so we can build the value of the company with the spend and we just want to be as fast and as nimble and as quick about The decisions we make, because it is, as you're right, a capital constrained environment. And partnerships have sustained us over many years, but partnerships acquire another party involved. So that's unpredictable. So I think it's we're being doubly stringent and strict about advancing programs and the design of our studies to be really efficient.

Operator

Thank you. The next question comes from the line of

Speaker 2

Maybe we'll go to the next question and see if we can circle back with him later.

Operator

Yes. Wonderful. The next line to be brought up on stage is going to be Jonathan Kang

Speaker 1

This is Matt Cowper on for Jonathan. Thanks for taking my question. I suppose just to piggyback on that last Question on cash, noticed that your R and D burn was a little higher this quarter. I was just wondering if that's something we could expect Going forward as you sort of launch these early stage programs. And then second question is just, I was wondering if you could provide any mechanistic rationale for The development of XmAb306 in multiple myeloma.

Speaker 1

Thanks.

Speaker 2

Maybe John, do you want to talk about the mechanistic rationale 3 6 in myeloma.

Operator

Yes.

Speaker 4

I mean, there's actually 2 components that it's extraordinarily good as we disclosed what about a year ago At expanding natural killer cells. And so, the combination with daratumumab, Turns out that daratumumab actually takes out some of the NK cells as it's working. And so that was sort of a natural idea on Genentech's Part 2, try to explore the combination with XmAb306 to expand the NK cells further to sort of mitigate that sort of fragile side effect. Hopefully, it will go beyond that and even further potentially daratumumab. And then the other combination with the CD3 engager, savastimab, that's also just motivated by some of our preclinical work.

Speaker 4

So recall natural killer cells are generally more sensitive to IL-fifteen because they express higher amounts of IL-two receptor beta. But it turns out we also were able to see preclinically that when you activate T cells such as with a T cell engager, You also upregulate IL-two receptor beta. And so it's really a natural question. We admire the fact that Genentech wants to floor 306 with multiple different kinds of modalities to see where it has the most utility.

Speaker 2

And maybe on the cost question, I wouldn't read too much into the quarterly fluctuations of the reported R and D spend. I mean, John, I think can you guide on our cash use this year? Cash is pretty consistent. To address your question,

Speaker 4

it can be lumpy, the early stage

Speaker 2

R and D, I mean, there's preclinical studies, But it's not going to be consistently increased quarter to

Speaker 4

the extent that it was over the previous year.

Speaker 1

Got it. Thanks for taking my question guys.

Operator

Thank you. Our next question comes from the line of Boris Peaker from TD Cohen. Go ahead, Boris.

Speaker 9

Great. Thanks for taking my question. This is Nick on for Boris. I just have a quick one on Ultomiris. So you guys mentioned in the press release that AstraZeneca announced the Phase 3 study initiation.

Speaker 9

So I was wondering if you guys are potential milestone payments from this Phase 3 like whether it comes to the end or whatnot? And then also will you potentially receive royalties from this additional indication if it is approved? Thanks.

Speaker 2

We received royalties on any indication from any country that there's valid patent claims worldwide regardless of the mode of administration, IV On the Phase 3? No, there's no more clinical milestones left. There's only a sales milestone left, which, we could get this year, we'll see.

Speaker 10

Okay, great.

Speaker 9

Thank you very much.

Operator

Thank you. The next question comes from the line of Michael King from EF Hutton. Go ahead, Michael.

Speaker 11

Hey guys, thanks for taking the question. Most of my asset specific questions have been answered. I just wonder if John might give us his thoughts on CD28 versus CD3 bispecifics, especially as applies to solid tumors and whether the odds of success in Solid tumors are going to be greater fluid in one or the other? Is there no real biology to predict what might succeed and what might not?

Speaker 4

Yes. You asked me my favorite question. In fact, I almost anticipated that this morning thinking about it. The easy the glib answer is We don't really know yet because there haven't been enough CD3s versus CD28s and there certainly hasn't been any sort of head to head studies against the same tumor associated antigen. There's nice validation of CD3s in solid tumors, A couple of different programs and there's really nice validation, recent validation for CD28 in solid tumors.

Speaker 4

But really to answer your question, the way I think of it, how differences might emerge. So a CD3 engager is basically going to it's going to take any T cell that it can find either in the periphery or the vicinity of the tumor. We don't know if those T cells are tumor reactive. They could just be bystander T cells and it's going to utilize those and it Yes, it takes advantage of having all those T cells around. CD28 really has to build off of an existing signal 1.

Speaker 4

And so if you're doing a combination, it would say a checkpoint inhibitor with a CD28, the single one actually comes through the T cell receptor recognizing neoantigen peptide MHC complexes on the tumor cell. And so I'm guessing and it's just pure speculation That CD28 would have potential for longer durability of response just because you're actually building up a memory T cell

Speaker 11

Okay. Thanks for taking the question, John.

Operator

Thank you. Our next question comes from the line of Peter Lawson from Barclays. Go ahead, Peter.

Speaker 8

Hi. This is Shay on for Peter. Thanks for taking our question. So just quickly first about buddolumab. So for the second study and the gynecologic tumors and high risk prostate, could you maybe speak to a little bit whether you're thinking of just pursuing monotherapy or is And for 808, the B7 H3 bispecific, could you maybe speak to where you see the highest

Speaker 2

I think with vedalumab, we expressly ran the Phase 2 monotherapy because we think there could be potential monotherapy in Those guide indications and in that slice of CRPC, I think Alan can address some of the data we got in expansion cohorts about why we believe that.

Speaker 1

Yes. I was just going to add that, so remember this is a 71705 study. So it's our second shot on prostate as a monotherapy. We define the high risk prostate group clinically as opposed with molecular markers and then we're looking at guide signals at an early marker in the expansion. The one thing is that we're looking at cervical endometrial as well as ovarian cancer, which is an unmet need and checkpoint inhibitors have shown activity And there hasn't been a lot of activity.

Speaker 1

I will also add one of the neat things about the 5 studies that it studies a better dose than schedule. So we're doing a flat Dose and every 3 weeks schedule as opposed to every 2 weeks. And then the other question was around B7 H3.

Speaker 4

Yes. I'll take that out. Yes. So, it's a great question about B73 for XmAb 8 a week, which solid tumor indications that we're most excited about. Prostate for sure is right at the top.

Speaker 4

There's certainly nice validation targeting B7 H3 in prostate cancer. And of course, we've got nice validation of CD28 biocipics actually working on prostate cancer. Other histologies that we would certainly think about would Small cell lung cancer based on some proof of concept data there targeting B7 H3. But B7 H3 is expressed across a lot of different solid tumors and we're going to want to take a look at a lot of.

Operator

Great. Thanks so much. Thank you. The next question comes from the line of Zhejiang Chu from Berenberg, go ahead.

Speaker 10

Great. Thanks very much for taking the question. I also want to ask A question around on your CD28 portfolio. Obviously, you present some preclinical data at AACR. I wonder Your criteria in terms of selecting the other targets for your future molecules and also how you decide to move 1 or more targets into the clinic.

Speaker 2

So the criteria is really based on Where we think CD28 could have the biggest impact, we think that's in tumors that have been cold for immune checkpoint therapy. We think the example given by the PSMA CD28 data presented by Regeneron last year suggests that this CD28 pathway could Turn on to response tumors that would be cold. They did that in prostate cancer, albeit in a very small number of patients. So there's a huge unmet need and a lot of patients that would be ecstatic if you could Turn on tumors that are nominally pretty cold, like small cell lung cancer, like colorectal cancer, like Ovarian. Ovarian cancer, like I mean, there's the list is longer than the list of tumors that actually respond well to immune checkpoint therapy.

Speaker 2

Even the ones with some labeled checkpoint inhibitors are pretty weak, right, like gastroesophageal and gastric, HCC, etcetera. So we're focusing on targets where there's a that's a big, big delta possible, right? It looks cold to checkpoints And where you could really maybe change the landscape, but also where you could clearly see a signal early in clinical development if you start seeing response. So I think that's important because we don't want to be lost in a sort of a swamp of trying to deduce whether It's the checkpoint or it's the combination agent, our CD28 driving the activity, like you might be if you were enrolling patients in melanoma or RCC, which are Pretty warm

Speaker 10

tumors. Got it. And just quick follow-up on the technology side of things. It appears all your CD28 and CD3 bispecifics you are going you are using 2 plus 1 format. So I guess is it Is 2 plus 1 your preferred format to go to other targets as well for CD3 and CD28?

Speaker 4

Yes, I would say, is the 2 plus 1 is a tool. It's just one of the tools in our toolkit. Yes. Every target is different, right? There's all kinds of considerations like density, how different is the expression on tumor cells versus normal cells.

Speaker 4

We like the 2 plus 1 for the CD3s because it gives us a little bit more, we believe room for it to design in the therapeutic index But, 1 plus ones are also on the table for the CD28.

Speaker 10

Great. Thanks very much.

Operator

Thank you for your questions. I would now like to turn it over to Basil Badiha for closing remarks.

Speaker 2

Thanks very much and thanks everybody for joining us this afternoon. We look forward to giving you further updates later in the year. Goodbye.

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