Q4 2021 Xencor Inc Earnings Call

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Operator: After the speaker's presentation, there will be a question-and-answer session. Please advise that this call is being recorded at the company. Now, I would like to turn the call over to your speaker today, Charles Liles, Head of Corporate Communications and Investor Relations. Thank you. Please go ahead. Thank you, and good afternoon.

Good afternoon, ladies and gentlemen, and thank you first tightening by and welcome to Suncor fourth quarter and full year 2021 conference call. At this time all participants are in a listen only mode. After just speaker's presentation. There will be a question and answer session. Please advise that this call is being recorded.

At the company's request.

Now I would like to turn the call over to your speaker today, Charles Liles head of corporate Communications and Investor Relations. Thank you. Please go ahead.

Charles Liles: Earlier today, we issued a press release that outlines the topics we plan to discuss today. The press release is available at www.xencor.com. With me on the call are Basil Dahiyat, President and Chief Executive Officer, Alan Yang, Chief Medical Officer, John Deserlay, Chief Scientific Officer, and John Kuch, Chief Financial Officer. After their remarks, 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, Xencor management may make forward-looking statements, including statements regarding the company's future financial and operating results, future market conditions, and the plans and objectives of management.

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 Dot <unk> Dot Com with me on the call are Battle day, yet President and Chief Executive Officer, Allen Yang Chief Medical Officer.

John days or late Chief Scientific Officer, and John <unk>, Chief Financial Officer. After remarks, 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 <unk> 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.

Charles Liles: Future Operations, the company's partnering efforts, capital requirements, future products, 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 is subject to none of the risks and uncertainties and other factors that could cause actual results to differ materially from those anticipated by these forward-looking statements, including but not limited to those factors contained in the risk factor section of our most recently filed annual report on form 10k. With that, let me pass the call over to Bell.

<unk> 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 or unknown risks uncertainties and other factors that could cause actual results to differ material.

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 with that let me pass the call over to Basil.

Bassil Dahiyat: Thanks, Charles, and good afternoon, everyone. Today we released our earnings results, and now, in a bit of a change from past calls, we'll only make a few brief comments before spending the majority of today's call on questions. We've used our array of modular protein engineering tools to create our internal development portfolio in oncology and autoimmune disease, and we use the breadth of this portfolio to take multiple simultaneous shots on goal in the clinic. The proof-of-concept data we generate guides which programs we advance, which we terminate, or with which we partner.

Thanks, Charles and good afternoon, everyone.

Today, we released our earnings results now in a bit of a change from past calls will only make a few brief comments before spending the majority of today's call and questions.

We've used our array of modular protein engineering tool to create our internal development portfolio portfolio in oncology and autoimmune disease and we use the breadth of this portfolio to take multiple simultaneous shots on goal in the clinic.

The proof of concept data, we generate guides, which programs, we advance, which we terminate or which we partner we focused our efforts in 2021, making key portfolio advancement decision, specifically initiating phase II studies for of the Dalla map, our selected PD, one see Chile for bi specific antibody in prostate cancer and gynecologic tumors.

Bassil Dahiyat: We focus our efforts in 2021 on making key portfolio advancement decisions, specifically initiating Phase 2 studies for Vudalumab, our selected PD-1 CHLA-4 bispecific antibody, and prostate cancer and gynecologic tumors based on promising Phase 1 data. We entered into a collaboration with Janssen for the development of Promodimab, our CD20 by CD3 bispecific antibody, to add their expertise and resources to the program Determination of the Boba CodaMap, our CD-123 by CD-3 due to a challenging clinical profile in a changing treatment lens.

On promising phase one data.

We entered a collaboration with Janssen for the development of tableau to map, our CD 20 by CD three by specific antibody to add their expertise and resources to the program and enable novel novel combination trials in a highly competitive therapeutic area.

We terminated development of by Dakota map, our CD 123 by CD three due to a challenging clinical profile and a changing treatment landscape.

Bassil Dahiyat: Of course, we're continually applying our engineering tools to build drug candidates that tackle new or hard-to-address biologies. And several of our early-stage programs are advancing into clinical studies and reporting data this year, led by our reduced-potency cytokines in our 2-plus-1, CD3, and CD28 T-cell engagements. Our goal is a well-balanced portfolio of late and early stage programs in development that we can potentially advance to approval and ultimately the market, if the data supports that.

Of course, we continually applying our engineering tools to build drug candidate to tackle new work hard to address Biology's and several of our early stage programs are advancing into clinical studies and reporting data. This year led by our reduced potency cytokines and our two plus one C D. Three and CD 28 T cell engages.

Our goal is a well balanced portfolio of late and early stage programs in development that we can potentially advance to approval and ultimately the market if the data supports that.

Bassil Dahiyat: Supporting our development work is a growing partnership portfolio, including three marketed products producing royalties for us, such as Citrobamat, the Vir GSK antibody for treating COVID-19. We also have a broad clinical pipeline with our partners, such as the exciting new 2.1 CD3 T-cell Engager AMG 509 that we created for prostate cancer with our partner and gen, and they released early but very promising data for this month. Our own XMAD 819 shares the same 2.1 format and will start a clinical trial and renal. Now we'll turn to Alan Yang, our Chief Medical Officer, who will review a few recent highlights of our clinical programs and upcoming plans. Alan, Bassil.

The supporting our development work is the growing partnership portfolio, including three marketed products producing royalties for us such as petroleum that the Vir GSK antibody for treating COVID-19.

We also have a broad clinical pipeline with our partners such as the exciting new two plus one CD three T cell engagement AMG five O nine that we created for prostate cancer with our partner Amgen, which they released early but very promising data for this month.

1819 shares the same two plus one format and we'll start a clinical trial in renal cell carcinoma. This year.

Now, we'll turn to Allen Yang our Chief Medical Officer, who will review a few recent highlights of our clinical programs and upcoming plans.

Thanks Pavel.

Alan Yang: Today we'll review two of our wholly owned programs, VudalaMap and XMap564. First, we are wrapping up our phase one study with Budalumab. At CISTI, we reported data from maturing expansion cords, primarily metastatic, castrate-resistant prostates.

Today, we'll be at two of our wholly owned programs through Dallas and X amount of plastic for <unk>.

First we were wrapping up our phase one study with two downtown SSE, we reported data from maturing expansion cohorts, primarily metastatic castrate resistant prostate cancer renal cell carcinoma, and a basket of other potential indications, we observed a consistently tolerable profile predominantly image immune related adverse events, including rash.

Alan Yang: Reno Selkar Sonoma, and a basket of others We observed a consistently tolerable profile for dominantly immune-related adverse events, including rash, pruritus, and liver enzymes. But we have observed a low incidence of adverse events like colitis and pneumonitis that have been typical with historical combinations of PD-1 and CTLA-4 antibodies, which supports a hypothesis that Goudalemab is selected for binding double positive cells, and importantly..., this could make it easier to use for a patient.

Good writers and liver enzyme elevations, but we have to serve the low incidence of adverse events like colitis and pneumonitis that have been typical with historical combinations of PD, one and <unk> four antibodies, which supports our hypothesis ludella map is selective for binding double positive cells and importantly.

Just to be make it easier to use and patients for a more complete discussion of the results I would point you to our press release last fall and the poster available on our website.

Alan Yang: For a more complete discussion of the results, I would point you to our press release last fall, and the posts are available on our website. However, within the analysis, we want to highlight our prostate cancer cohort. Prostate cancer is heterogeneous, and we enrolled mostly late-line patients. Eight patients had medullar lymph disease, that is, some kind of metastatic lesion in a visceral organ or lymph node that could be measured by resistance or response.

Though within the analysis, we wanted to highlight our prostate cancer cohort prostate cancer is a heterogeneous disease and we'd hold mostly late line patients eight patients had it does hold a disease that has some kind of metastatic lesions in a visceral, oregon or less note that could be measured by resist for response and four we were able.

Alan Yang: In four, we were able to evaluate response. And two of these four had durable, impressive six- and nine-month partial response. And it has encouraged us to advance with that one, Matt, in process to advance with that one, Matt, in process with that one, Matt, in process with that one, The first phase 2 study, which started last fall, is in patients with metastatic castrate-resistant prostate cancer, who are post-Andruin deprivation therapy and post-first line team, We are using standard genotyping profiling to find actual risk phenotypes, which would guide us to either a chemotherapy regimen or part inhibitor, and Vidalamab is built on top of that. Patients with no actual limitations will receive Vidalamab monotherapy.

To evaluate response and two of these four had durable impressive six to nine month partial responses and it has encouraged us to advance without map in prostate cancer.

The first phase two study, which started last fall is in patients with metastatic castrate resistant prostate cancer, who are post androgen deprivation therapy and post first line chemo, we are using standard Gino tightening profiling to find actionable risk phenotypes, which would guide us to either a chemotherapy regimen, our PARP inhibitor.

And with Allomap is dose on top of that patients with no actual mutations will receive with Allomap monotherapy.

Alan Yang: Later this year, we'll present early initial data from the study. We will only have a few months of on-treatment for a portion of patients, but it will allow us to get a first look at the safety of Dalamad in combination with other therapeutic agents that can have significant toxicities of their own. Historically, combination therapy with PD-1 and CTLA-4 dual blockade has been challenging, and we hope that Budalimab can improve on that.

Later this year will present early initial data from the study we will only have a few months of treat all treatment data for a portion of patients but allow us to get a first look at the safety of <unk> in combination with other therapeutic agents that can have significant toxicities of their own.

Historically combination therapy with PD, one see till a four dual blockade has been challenging and we hope that through dalla mab can improve on that.

Alan Yang: Of course, we will share whatever efficacy data we have collected at the time. Ultimately, we hope that this study defines combination strategies and subsets of patients with high unmet need that could define a simpler development path than previously available. We are also initiating a second phase two study, evaluating Budalimab monotherapy in a differently defined slice of prostate, that is a clinically defined, high-risk, metastatic, castrate-resistant phosphate where we saw two out of four partial responses in phase one. In addition, this study will examine select gynecological tumors as well.

Of course, we will share whatever efficacy data we have collected at the time ultimately we hope that this study defines combination strategies in subsets of patients with high unmet need that could define a simpler development path and previously available for prostate cancer.

We are also initiating a second phase II study evaluating <unk> monotherapy and <unk>.

Differently defined slice of prostate cancer that has a clinically defined high risk metastatic castrate resistant prostate cancer, where we saw two out of four partial responses in the phase. One. In addition, this study will examine oncological tumors as well we do not anticipate data from this second study in 2022.

Alan Yang: We do not anticipate data from this second study in 2020. Next, our wholly-owned cytokine XMAP564, a reduced-potency IL-2 that we are developing for autoimmune diseases. In contrast to cytokines being developed in oncology, it's engineered toward the IL-2 alpha receptor, CD25, which is overrepresented on regulatory T-cells compared to other T-cells, and we've also reduced the affinity for the Beta Gamma Result. The T-Rike hypothesis is just that the hypothesis that more regulatory T-cells can result in clinical benefit for autoimmune disease.

Next our wholly owned cytokine ex Maffei Asics for a reduced potency IL two that we are developing an autoimmune disease. In contrast, the cytokine is being developed in oncology, it's engineered towards the IL two alpha receptor CD 25.

Which is overrepresented on regulatory T cells compared to other T cells and we've also reduced the affinity for the beta gamma receptor while the T. Regs hypothesis is just that hypothesis that more regulatory T cells can result in clinical benefit for autoimmune disease. It was a perfect fit for our cytokine platform and represents an enormous opportunity.

John Kuch: It was a perfect fit for our cytokine platform and represents an enormous opportunity to enable new treatment modalities based on it. Currently, we're conducting a single ascending dose study in healthy volunteers, and this year, we'll present our first data from that trial, consisting of T cell and other biomarkers, safety, and pharmacokinetics. All critical information for terming our potential product post-boss. We also plan to initiate, in parallel, a multiple ascending dose study in select patient populations.

To enable new treatment modalities baseball T regs.

Currently we are conducting a single ascending dose study in healthy volunteers and this year, we will present, our first data from that trial, consisting of a T cell and other biomarkers safety and pharmacokinetic data all critical information for determining our potential product profile.

We also plan to initiate in parallel a multiple ascending dose study in select patient populations.

John Kuch: Now, as we wrap up, we wanted to briefly mention three other studies we are planning to initiate in 2020. First, the potentially registration and enabling phase 2 study evaluating promotimap in combination with tapacidimap and linolynamide in patients with remaps or refractory diffuse large B cell, Second, as Basil mentioned, the Phase I study of valuing XMAP 819 in patients with renal cell carcinoma in the first half of the Phase I study of valuing XMAP 819 in patients with renal cell and third, following the submission of an IND, the phase one study of the B7H3 by CD28 bispecific XMAP808 in patients with a day of solid tumors in the second half.

Now as we wrap up we wanted to briefly mention three other studies, we are planning to initiate in 2022.

First our potentially registration, enabling phase two study evaluating <unk> in combination with top of split them out and lenalidomide in patients with relapsed or refractory diffuse large b cell lymphoma.

Second as Bob mentioned, the Phase one study evaluating ex map 819 in patients with renal cell carcinoma in the first half of this year and.

And third following the submission of an IND. The phase one study of the <unk> III by CD 20 by specific ex map 808 in patients with advanced solid tumors in the second half of this year.

John Kuch: Now with that, I'd like to hand the call over to John Kush, our CFO, to review our financials. Thank you, Alan. Xencor's broad portfolio of partnerships, collaborations, and licenses will continue to generate strong cash flows in 2020.

Now with that I'd like to hand, the call over to John Kush, Our CFO to review our financial results John Thank.

Thank you Alan.

<unk> broad portfolio of partnerships collaborations and licenses continue to generate strong cash flows in 2021 during the year, we received over $200 million in upfront payments and milestone payments and royalties, which helps offset our growing investment pipeline is by civic and cytokine candidates.

John Kuch: During the year, we received over $200 million in upfront payments, milestone payments, and royalties, which helps offset our growing investment in our pipeline as bi-civic and cytokine candidates. A breakdown of 2021 proceeds was $80 million in royalties, including $52 million from our Vera partnership, $100 million upfront payment related to our second Janssen collaboration, and $20 million milestone payment. These proceeds strengthened our balance sheet, and we ended 2021 with cash, cash equivalents receivables, and marketable debt securities of $664.1 million compared to $610.2 million at the end of 2020.

Breakdown of 2021 proceeds was $80 million in royalties, including $52 million from our their partnership 100 million dollar upfront payment related to our second Janssen collaboration and $20 million milestone payments. These proceeds strengthen our balance sheet and we ended 2021 with cash cash equivalents receivables and Mark will.

Securities of $664 1 million compared to 610.2 million at the end of 'twenty 'twenty.

Operator: We estimate that we'll end 2022 with between $500 and $550 million in cash, cash equivalents, receivables, and marketable debt securities. And based on current operating plans, we expect to have cash to fund research and development programs and operations through the end of 2025. I refer you to our press release this afternoon and our SEC filings for further information about our recent financial results. With that, we'd now like to open up the call to your questions.

We estimate that will end 2022 with between 500 and $550 million in cash cash equivalents receivables and marketable debt securities and based on current operating plans. We expect to have cash to fund research and development programs and operations through the end of 2025.

I refer you to our press release this afternoon, and our SEC filings for further information about our recent financial results.

Operator: Operator? As a reminder, to ask a question, you will need to press star 1 on your telephone. To withdraw your question, or if your question has been answered, press the pound or head. Your first question comes from the line of Jonathan Chang from SVB Learing.

With that we'd now like to open up the call for your questions operator.

As a reminder to ask a question you will need to press star one on your telephone the withdraw your question or if your question has been answered press the pound key.

Your first question comes from the line of Jonathan Chang from SBB Leerink. Your line is now open.

Jonathan Chang: Your line is now open. Hi, guys. Thanks for taking my questions and congratulations on a productive year. For the first question on Vodalamab, can you discuss reasons for confidence in the safety profile of the drug and its potential in combination treatment? Sure, I'll let Alan take that.

Hi, guys. Thanks for taking my questions and congrats on a productive year.

First question on the Dalla map.

He discussed is in store.

Our confidence in the safety profile of the drug and its potential in combination treatment.

Sure I'll, let Alan Alan take that I think it's basically just from what we've observed yeah. If you look at the data from the Phase one study that we presented at 60 and you look at the AE profile, you know traditionally with PD one Cta for combinations you would expect a lot of discontinuation is about a third of patients discontinue the <unk>.

Alan Yang: I think it's basically just from what we've observed. Yeah, if you look at the data from the phase one study that we presented at CITSE and you look at the AE profile, you know, traditionally with PD-1 CTLA-4 combinations, you'd expect a lot of discontinuations; about a third of patients discontinue the product. We did not have those problems, and it's primarily due to colitis and GI symptoms, and we don't have that problem.

We did not have those problems and it's probably hard to colitis and Gi symptoms and we don't have that problems. The the Gi toxicity rate was around 10%.

Alan Yang: The GI toxicity rate was around 10%. If you look at the AE profile, the most common immune-related adverse event in about a third of patients was rash, which is, you know, a milder AE. So we believe that even though we're targeting both PD-1 and CTLA-4, it's a highly tolerable profile compared to two drugs in the.

If you look at the AE profile, the most common immune related adverse events and about a third of patients was rash, which is you know a milder AE. So we believe that even though we're targeting both PD one ANSI till it for it's a it's a highly tolerable profile compared to two drugs independently.

John Kuch: And second question, on your cash guidance, can you provide some color around what assumptions are being made in terms of receiving potential milestone payments and royalties from partners? Yeah, well, I'll let John take that, but I think the word of the day here is that we're very conservative in future revenue flows when we do our planning. Thank you, Basil.

Understood.

And second question on your cash guidance I can provide some color around what assumptions are being made.

In terms of receiving potential milestone payments and royalties from partners.

Well I'll, let John take that but I think the word of the day here is that we're very conservative in future revenue flows when we do our planning.

John Kuch: Yes, Jonathan, as you know, we're very conservative as far as forecasting milestones, only near-term milestones that we have visibility on from our partners. With respect to royalties, we look to, again, the guidance that's provided by our partners. So, for example, GSK has provided some guidance as far as potential sales of Citroen MAP in 2022, which I believe are somewhere in line with 2021.

Thank you Bassil, yes, Jonathan is as you know, we're very conservative as far forecasting milestones only near term milestones that we have visibility from our partners.

With respect to royalties, we look to again the guidance is provided by our partners. So for example, a GSK has provided some guidance as far as potential sales is a trove of map.

In 2022, which I believe are somewhere in line with 2021 so we're going to forecast capital levels, maybe a little bit discounted.

John Kuch: So, we're going to forecast comparable levels, maybe a little bit discounted. So, generally, that's how we look at things, and we do not forecast any new revenues. So when we think about the year-on-cash position, we do include some potential revenue, but again, it's conservative, and it assumes certain spending levels based on starting certain clinical programs. Okay. And I'll just sneak in one last one.

So generally that's how we look at things and we do not forecast any new revenue. So when we think about the year end cash position. We do include some potential revenue, but again its conservative and it assumes certain spending levels based on starting a certain clinical programs.

Bassil Dahiyat: On XMAP-306, are you able to provide any additional color on the tumor types and combination strategies of interest? Thank you. No more than what we've said in the past, which is that we think there's a lot of potential in both NK cell-mediated therapies for combination as well as T cell-mediated therapies. Of course, Genentech is already running the T-centric combination in the dose escalation phase, and we're looking forward to them starting the expansion cohorts with T-centric soon.

Understood and.

I'll just sneak in one last one on X snap <unk> zero specs.

Are you able to provide any additional color on the tumor types in combination strategies up interest. Thank you.

No more than what we've said in the past, which is that we think there's a lot of potential in both NK cell.

Mediated therapies for combination as well as T cell mediated therapies of course, gentex already running the test centric combination in the dose escalation and we.

We're looking forward to them starting the expansion cohorts with to centric soon.

Bassil Dahiyat: I think NK cell-mediated therapies are very promising, and I mean the top of the list of NK cell-mediated therapies are all traditional antibodies that people have been using for a number of years. You know, the Rituxans, Interceptins, and Dartumimabs of the world are all things that are possible. What we have, we're making plans now; we'll be very specific when we kick off those trials, and we do hope to be able to announce all of that this year.

I think NK cell mediated therapies are very promising and I mean, the top of the list of NK cell Immunotherapies are all distributional antibodies that that people have been using for for now a number of years you know the the rituxan and herceptin and dark humor maps of the world are all things that are possible when we.

We're making plans now will be very specific when we kick off those trials, which we do hope to be able to announce all of that this year.

Got it thanks for taking my questions. Thank you.

Kaveri Pohlman: Thanks for taking my questions. Thank you. Your next question comes from the line of Kaveri Pohlman from VTIG. Your line is now open. Yeah, good afternoon.

Your next question comes from the line of Caveri Polman from BP agents. Your line is now open.

Kaveri Pohlman: Thank you for taking my questions and thanks for the update. My first question is related to 306, the cytokine program again, and its applicability in combination with NK cell therapies. So there was a recent publication in Blood that showed that exogenous IL-15 administration led to faster NK cell therapy rejection in AML patients compared to patients who received low-dose IL-2 with the cell therapy. Just wanted to get your thoughts there.

Yeah. Good afternoon. Thank you for taking my questions and thanks for the update.

First question is related to three of the cytokine program again, and the clock Likability in combination with NK cell therapies.

A publication in blood journal that showed that evolved enough IL 15 administrations lets you foster NK cell therapy rejection.

M outpatient.

Cancer patients will receive low dose IL two with the cell therapy.

Alan Yang: Is it more like a different biology or just the dosing play? Well, I think the complexities that happen when you give a cell graft to a patient make it hard to understand even how the growth factors like IL-15 or IL-2 are working. I think you continually see these kinds of challenges with cell therapies, whether they're auto-transplants or allotransplants. The power of an exogenous cytokine therapy, when you're not basing your efficacy on a cell that you're infusing but rather on another drug, is that you can count on the intrinsic biology of the natural NK cells that are in there. And that's a whole different game.

To.

Get your thoughts there.

More like a different biology or adjusted those in place.

Well I think the complexities that happened when you give a cell graft to a patient it makes it hard to understand even how the growth factors like IL 15, or IL. Two we're working I think you continually see these kinds of challenges with cell therapies, whether they're auto transplants or allo transplants.

The power of a exogenous cytokine therapy, when you're not.

Basing your efficacy on a sell the ear infusing, but rather on another drug is that you can count on the intrinsic biology of the natural NK cells that are in there.

Alan Yang: So, I don't know that that paper really leads very much on the approaches that we're taking, which is combining 306 with other drugs, rather than the challenges and unknowns of the experimental software. And can you talk about your rationale for combining Widelimab with PARP inhibitors? Is there a biology there, or is it just data driven? It's empiric based on what's being treated. For example, patients with prostate cancer that have a homologous recombinant deficiency, the PARP inhibitor is sort of the standard of care. And so we want to demonstrate that we can add on to that and see if we can synergize with that therapy. But it's mainly empirically driven. That's all the combinations I can think of.

And it's a whole different game. So I don't I don't know that that paper really needs very much on the approaches that we're taking which is combining three O six with other drugs rather than the challenges and unknowns that experimental cell therapies.

Got it okay.

Can you talk about your rationale for combining with Allomap with PARP inhibitors is it is there.

Iology, there or its just data it's.

It's in Paris based on what's being treated so patients with prostate cancer that have homologous recombination deficient the PARP inhibitors. The standard of care and so we wanted to demonstrate that we can add on to that and see if we can synergize with that therapy, but it's mainly empirically driven.

As all of the competition.

Kaveri Pohlman: I mean, there is a concept out there that, you know, if you're repair deficient, you give a proper inhibitor, you might generate more Neoantigens, right, and have more of a T-cell. Got it, thank you. Here, next question comes from the line of Gregory Renza, from RBC Capital Markets. Your language Here, next question comes from the line of Gregory Renza, from RBC Capital Markets. Thank you for taking our questions and congrats on the progress. Maybe it's just the first question on the Dalmat.

I mean, there is a concept out there that if you.

Repair deficient you'd give him a PARP inhibitor that you might generate more neo antigens, that's fair right.

And have more of a T cell response to build on.

Got it thank you.

Okay.

Your next question comes from the line of Gregory <unk> from RBC capital markets. Your line is now open.

Gregory Renza: I was wondering, as we expect to see some initial data from the trial this year, how would you characterize the benchmark for each molecular subtype to be clinically, clinically competitive? And what will the goal, no goal, decision making process look like when you have some data from the trial? Yeah, but before I hand this to Alan and talk about benchmarks, I will say that the data we're going to have this year is going to be a pretty early slice.

Hi, this is <unk>.

One for Greg. Thank you for taking our questions and congrats on the quasi.

Maybe just first question on with Alan and I was wondering.

We expect to see some initial data from that trial. This year, how would you characterize you know the benchmark for each well that subtype to be clinical it could be an equally competitive and what will the go no go decision, making process look like do you have some data from the trial, but before I hand, it to Alan to talk about bench.

Bassil Dahiyat: It's going to be only partially enrolled, of course, and pretty early on, and follow up for all of those, or all of us, folks, I should say. So we're going to get a very clear read, I think, from a small number of patients on some of the safety of combinations therapy. As for the benchmark, I'll have to wait for the full trial data, which is not going to be this year. So I'll just... Preface it with that, we're not going to have a really good epic this year, but maybe you can go to the bench for our sale.

I will say that the data we're going to have this year is going to be a pretty early slice.

It's gonna be partially enrolled of course and pretty early on and follow up for all or most of those are all of us folks I should say.

So we're going to get a very clear read I think from a small number of patients or in some of the combination therapy safety.

As for the benchmarks that'll have to wait for the full trial data, which is not going to be this year.

Preface it with that and we're not going to have really good ethics can be this year, but maybe you can go to the benchmark. So yeah. I think if you look at the expectations in castrate resistant prostate cancer.

Alan Yang: Yeah, I think if you look at the expectations and castrate-resistant prostate cancer for checkpoint inhibitors in general, the benchmark is fairly low. So if you look at the keynote 199 study, the response rate in chemo-refractory patients, which will probably be most of the patients that we see, is probably about 5% or less, depending on what their expression of PD-1 was. And if you look at the checkmate, I forget the number of the checkmate study, I want to say 650 or something, which looked at nivalumab and ipilimumab in combination. Depending on the population you looked at, the response rate was probably approaching 10%, right?

For checkpoint inhibitors in general the benchmark is fairly low. So if you look at the keynote 199 study the response rate and chemo refractory patients, which will probably be most of the patients that we see is probably about 5% or less depending on whether what their expression of PD. One was and if you look at the checkmate I forget the number.

The Checkmate study I want to say 650, or something which looked at Nevada map and it ballooned map in combination.

Depending on the population you looked at the response rate was probably approaching 10% right. So the expectation of checkpoint inhibitors in prostate cancer is fairly low and so we think there is clearly synergy when you compare those two studies.

Alan Yang: So the expectation of checkpoint inhibitors in prostate cancer is fairly low. And so we think there's clearly synergy when you compare those two studies, but the expectation was low. Now when you look at our study, granted it's still a small number of patients, we're seeing a higher response rate, but the numbers are too small. We think we will add chemotherapy, as well as PARP inhibitors, as well as other treatments, or, excuse me, monotherapy in certain populations. But I think anything above that should be pretty exciting, although it depends on the population.

But the expectation was low now when you look at our study granted still a small number of patients we're seeing a higher response rate, but the numbers are too small and so.

We think we will add to chemotherapy as well as PARP inhibitors as well as.

You know other therapies or excuse me monotherapy in certain populations, but I think anything above that should be pretty exciting it depends on the population like the marker negative group with chemotherapy, we would expect a higher response rate, but chemotherapy is not that effective.

Bassil Dahiyat: Like the marker negative group with chemotherapy, we would expect a higher response rate, but chemotherapy's not that effective. Great, thank you. And then just one more question, if I may, on Pomodumab.

Bassil Dahiyat: I think Rose Genentech is investigating their CD2033 in combo with Polibi. What are your thoughts on that combination approach and, you know, potential impact on the positioning opportunity for Pomodumab? Yeah, I mean, Polivy is, of course, being combined with it also in combo with other other things. It's not just those two things.

Great. Thank you and then just one more if I may.

And I think Roche Genentech.

Getting their CD 20 cities Green combo with <unk>.

What are your thoughts on that combination approach and potential impact on the positioning and opportunity for a modem.

Yes.

Levi is of course being combined with it also in combo with.

Other other things, it's not just those two things and really as a targeted chemotherapeutic agent I think it shares some of the same.

Alan Yang: And really, as a targeted chemotherapeutic agent, I think it shares some of the same challenges in treatment that traditional chemo has, and that's why we're going to a chemo-free approach in our combination studies. I think we're trying to get to where the field wants to go, and I don't know that that changes the landscape for us dramatically in our thinking. It's really another form of chemo. Yeah, I have to agree, Basil, that, you know, Polituzumab, you know, is an ADC, like chemotherapy. And, you know, the convenience for them is that they own that and can combine it.

Same challenges and treatments that that traditional chemo has and that's why we're going to a chemo free.

Broaching or a combination studies I think we're trying to get to where the field wants to go.

And I don't know that that changes the landscape for us dramatically at our thinking it's really another chemo.

Yeah, I have to <unk> that you know pull of twos of Nab.

And ADC like chemotherapy and the convenience for them is that they own that and if you combine them, but I'm actually more excited about some of our potential combination opportunities I think toughest sit a map lenalidomide and modem at scientifically makes more sense and there is a much better scientific rationale for synergy right.

Bassil Dahiyat: But I'm actually more excited about some of our potential combination opportunities. You know, I think Tafacitumab, lenalidomide, and Clamodimab scientifically make more sense, and there's a much better scientific rationale for synergy. Great, thank you very much.

Great. Thank you very much.

Mara Goldstein: Your next question comes from the line of Mara Goldstein from Mizuho. Great, thanks very much for taking the time to ask me that question. So if I can just ask another question about Vidalimab, and this really is coming off of some of the data that came out at ASCO-GU, particularly around the PROPEL study and looking at combinations with PARP inhibitors. Can you maybe just help us understand sort of the positioning of Vidalimab from a combination perspective at this point, looking at where the standard of care may be going? That's my first question. And then I did have a second question about Promodimab, which we can come back to. Sure, Alan, do you want to take that?

Your next question comes from the line of Mara Goldstein from Mizuho. Your line is now open.

Great. Thanks for much for taking the question. So if I can just ask another with Allomap question and that really is coming off of some of the data that came out at Pasco G, particularly around the propel study.

<unk> com.

Combinations with Piper.

Hi, Peter.

Could you maybe just help us understand sort of ticket positioning of the dollar map from a combination perspective at this point looking at where the standard of care may be going.

My first question and then I did have a second question on promoting that partaking come back here.

Sure Alan you want to you want to take that yeah. I just wanted to remind everybody that it's still early in our phase II I think clearly the the trended prostate cancers to sort of molecular would find prostate cancer and we have several buckets of aggressive molecularly defined.

Alan Yang: Yeah, I just want to remind everybody that it's still early in our phase two. Clearly, the trend in prostate cancer is to sort of molecularly define prostate cancer, and we have several buckets of aggressive, molecularly defined, you know, the homologous recombinant deficient, the MSI unstable group, as well as those that are biomarker negative. You know, and I think, you know, PARP inhibitors are going to be used. I think chemotherapy will still have a role as well, with dosetaxel and other agents.

The homologous recombination the MSI.

Stable group.

As well as those that are biomarker negative.

I think you know PARP inhibitors are going to be used I think chemotherapy will still have a role as well docetaxel and other agents and so the question is checkpoint inhibitors have limited activity can we add onto those therapies.

Alan Yang: And so, the question is, checkpoint inhibitors have limited activity; can we add on to those therapies? In fact, it's the first question that we hope to address, hopefully later this year, that we can slightly combine, you know, a PD-1 PTLA-4 targeting agent with other therapies. This has traditionally been very difficult.

The first question that we hope to address hopefully later this year that we can safely combine you know a PD one cta for targeting agent with other therapies. This has traditionally been very difficult. It's been tried in melanoma.

Alan Yang: It's been tried in melanoma, and I think the AE profiles were very discouraging. So, we're excited if we can put these together, and I think if we are successful, then that will sort of change the different sorts of subtypes of prostate cancer and how you treat them in earlier stages of disease, still within the castrate-resistant population. Okay, and then if I could just ask, on Promotimab... In looking at a combination trial with Linda Littemann and Peffa Sittemab, I'm just curious as to what your thoughts are around enrollment, just given the challenges that Yeah, I'd say we are very aware that enrollment in real estate factory DLBCL is very challenging because of the intense competition for many, many agents and, you know, the TA I don't; I don't think that's our primary worry.

I think the AE profiles, we're very discouraging. So we're excited if we can put these together and I think if we are successful then that will sort of change the different sort of subtypes of prostate cancer and how you treat them.

In earlier stages of disease still within the castrate resistant population.

Okay.

Okay.

Now if I could just ask him.

On promoting map.

Looking at a.

A combination trial with line of in mind I'm, just curious as to what your thoughts are around enrollment just given the I think there's some of the challenges.

That type of Fortinet has had in terms of picking up traction and again, if you can speak to that.

Bassil Dahiyat: I think it's just the competitive landscape among clinical trials, sort of fighting for that same patient. I think that the unique scientific approach, the chemo-free approach, and the mechanism of the domestic rationale are actually quite exciting for the physician community that we're talking to. That said, part of the reason why we think the Janssen partnership last fall or last winter for us was such an important move for Plamo is that they have the kind of resources that I think it's going to take to really put the pedal to the metal in a really challenging development competition environment.

Yeah, I'd say, we are very aware that enrollment in <unk> in relapse refractory D. L. B C. L. A is very challenging because of the intense competition for many many agents.

And and you know the task of having a bit of a slow pickup in their commercialization.

I don't I don't think that's our primary worry I think it's just the competitive landscape among clinical trials sort of fighting for that same patient I think that the the unique scientific approach the chemo free approach and the mechanistic rationale is actually quite exciting for the physician community that we're talking to.

That said part of the reason why we think the Janssen partnership last last fall or last winter for US was such a important move for plan, though is that they have the kind of resources that I think it's going to take to really put the pedal to the metal in a really challenging development competition environment.

Bassil Dahiyat: And I would just add, Basil, that our investigators are very excited about the scientific strategy of the combination. And then, currently, we're still enrolling our Phase I study in the expansion cohorts for diffuse Blart B cell lymphoma, and that cohort is enrolling rather well, and that's only in two regions, the United States and France, and we plan to go global with this study, so I'm confident that we can execute it. Alright, thank you, I appreciate it. Your next question comes from the line of Charles Zuse from Guggenheim. Jail Lancer Oop, Hey everyone, congrats on the progress and thanks for taking the questions.

And I would just add vessel, but our investigators are very excited about the scientific strategy of the combination and then currently we're still enrolling our phase one study in the expansion cohorts in diffuse large b cell lymphoma, and that cohort is enrolling rather well and that's only in two regions of the United States and France, and we plan to go global with this study so I'm confident that we can exit.

Q.

Alright, Thank you I appreciate it.

Right.

Your next question comes from the line of Charles <unk> from Guggenheim. Your line is now open.

Hey, everyone. Congrats on the progress and thanks for taking the questions. If I may ask my first question just one more on <unk> I guess, you know regarding your upcoming data or I guess in context of your trial, what sorts of prostate cancer sub populations do you think are potentially most.

Charles Zuse: If I may ask my first question, just one more on Voodalumab. I guess, you know, regarding your upcoming data, or I guess in the context of your trial, what sorts of prostate cancer subpopulations do you think are potentially most interesting? And also, how should we think about that in context of the broader landscape that continues to shift with things like ADT intensifications or new therapies like radioligands, you name it. How applicable will the data you generate in the coming days be to a potential patient population perhaps a few years down the road? Thanks.

Sting and and also how should we think about that in context of the broader landscape that continues to shift with things like ADT intensification or new therapies like radio ligand you name it how applicable well will the data you generate in the coming days.

Mike might be to a potential patient population, perhaps a few years down the road. Thanks.

Bassil Dahiyat: Yeah, I think the big picture answer on that is we're going to find out how well we work with things like chemo and the park inhibitors that are certainly going to have an important role in the future landscape. And we're going to do that in a way that's correlated to the molecular subtype, which is determined from the standard genotyping that's happening now in MCRPC post-chemo. So we think we'll be well positioned to make decisions, but this trial is about making decisions and understanding which way we can go scientifically, and as that landscape changes, we're fully anticipating adjusting to it.

I think the big picture answer on that is we're going to find out how well we work with things like chemo and PARP inhibitors that are certainly going to have an important role in the future landscape and we're going to do that in a way that's correlated to the molecular subtype.

Determined from the standard Genotyping, that's happening now in M. C. R. P. C post chemo. So so we think we'll be well positioned to make decisions, but this trial is about making decisions and understanding which way. We can go scientifically and as that landscape changes, we're fully anticipating adjusting to it yeah.

Bassil Dahiyat: Yeah, I think exactly. So I think the best parts you're talking about are the cosmic study by Exelixis. Depending on whether you believe the sort of site review or the central review, the response rate was less than 20%. For the radio isotope from Novartis, you're talking about the response rate, if you look back at the most recent study, was approaching 30%, I believe. And so those are high bars.

I think exactly so I think the best parts Youre talking about with the cosmic study by <unk>.

Depending on whether you believe the sort of site review of the Central review. The response rate was less than 20% for the radioisotope from Novartis Youre talking about the response rate if you look back in.

In the most recent study was approaching 30% I believe and so those are high bars now if you talk about what subsets were interested in our studies I don't think we've publicly disclose what the molecular phenotyping is but we are doing two different studies and we are looking at aggressive phenotype. So the aggressive phenotype either.

Alan Yang: Now if you talk about what subsets were interested in our studies, I don't think we've publicly disclosed what the molecular phenotyping is, but we're doing two different studies, and we are looking at the aggressive phenotype, whether the aggressive phenotype is molecularly defined or clinically defined. And we believe that from our phase one data, the early exciting data is that we had two patients with very aggressive disease that had good responses. And so we think that that could be a population for us as well.

<unk> defined or clinically defined and we believe that from our phase one data that early exciting data that we had two patients with very aggressive disease that had good responses and so we think that that could be a population for us as well, but again I think our data is still early we want to cast a wider net and that's why we're doing this phase two and then we can focus in.

Alan Yang: But again, I think our data is still early. We want to cast a wider net. And that's why we're doing phase two. And then we can focus in based on the data we see later on. Got it. That makes sense. Thanks for that detail and color.

Based on the data we see later on.

Got it that makes sense, thanks for that detail and color and if I may ask one more shifting gears, a little bit onto X mab five six for the.

Charles Zuse: And if I may ask one more, shifting gears a little bit onto XMAB564, the IL-2, what's your thinking around near-term clinical development of this particular asset? And how should we think about the potential patient populations that may benefit most from your Treg target approach? Yeah, I think early clinical development is, of course, first to establish the pharmacodynamic profile, and the tolerability profile of the agent. That single ascending dose, and also the multiple ascending dose will help with that.

The IL two I guess, what's your thinking around near term clinical development of this particular asset and how should we think about the potential patient populations that may benefit most from your T. Reg targeted approach. Thanks.

Yeah, I think the early clinical development is of course first establish the Pharmacodynamic profile Tolerability profile of the agent that single ascending dose and also the multiple ascending dose will help with that but the data that we're going to have this year should really give us a quick early read on are we being selective or we have to find T. Regs in that selective way to a <unk>.

Charles Zuse: But the SAD data that we're going to have this year should really give us a quick early read on whether we are being selective? Are we amplifying Tregs in that selective way to a magnitude that's at least benchmarked against competition, but that's also promising? And critically, the durability of that effect, because this is an autoimmune disease, and frequency of dosing can be a hugely important thing. And, of course

Magnus <unk>.

At least benchmarked against competition, but that is also promising and critically is durability of that effect. Because this is autoimmune disease and frequency of dosing can be a hugely important thing and of course, good tolerability. So would that S. A D data going into the M. A D. We're looking for two things we're looking for one.

Bassil Dahiyat: So with that SAD data going into the MAD, we're looking for two things. We're looking for one, a clear way to look at if you're causing disease modifying activity, because this whole hypothesis that enhancing Treg number and function is going to treat cancer is still just a hypothesis. Some exciting early glimmers of data from some programs, and of course, the old computing programs that we've seen, but also the old Lodos IL-2 data support that.

A clear way to look at if you are causing disease modifying activity.

Because this whole hypothesis that enhancing T. Reg number and function is going to treat diseases still just a hypothesis. Some exciting early glimmers of data from some programs and of course the old <unk>.

Competing programs that we've seen but also the old low dose IL two data supports that so we want to have with our molecule and indications, where we can clearly see or not see disease activity because of well well benchmark 10 points, we want to look at that in our <unk> study and that is for selecting indications, we think that it's going to be big exploration, but we want to go at.

Alan Yang: So we want to have, with our molecule, indications where we can clearly see or not see disease activity because of well-benchmarked endpoints. We want to look at that in our MAD study. And then as for selecting indications, we think that it's going to be a big exploration, but we want to go after ones that have both clear development paths, albeit competitive ones potentially, large indications, as well as we're identifying some small indications that we can maybe go after with a niche approach.

After ones that have both clear development path, albeit competitive was potentially large indications as well as we're identifying are some small indications that we can maybe go with a niche approach. So that's a very strategic type question without a lot of science and it did.

Alan Yang: So that's a very strategic type question without a lot of science in it. Did you have a more scientific aspect to what you were getting at? I can let Alan and John weigh in. Yeah, I would have... Oh yeah, I was just elaborating, and just scientifically or medically, I guess, what are perhaps some of the indications that Treg expansion might work better or worse for inflammatory diseases? Yeah, I mean, there's a number of autoimmune diseases, you know, there's the literature of life with publications showing the balance of key reg versus effector T cells and various autoimmune diseases, including diseases like lupus, but also a number of more, you know, niche indications like basil.

Did you have a more scientific aspect to what you were getting at I can let our John weigh in.

Yeah.

Oh, Yeah, no I was just elaborating and just just scientifically you're mathematically I guess what are perhaps some of the indications that T Reg expansion might work better or better or worse for inflammatory diseases.

I mean, theres, a theres a number of autoimmune diseases. There's the literature is rife with publications showing imbalance of T Reg versus effector T cells, and various autoimmune diseases, including diseases like lupus.

But also a number of more.

Which indications as Basil mentioned so.

Bassil Dahiyat: [inaudible] But ultimately, I mean, Tregs are a pretty important way of achieving homeostatic immune balance. It could be incredibly widely employed if it's actually effective. Yeah, and from an operational standpoint, I would just sort of reiterate, you know, we know that it's a competitive space, and I think that's why we're doing our SAD and our MAD in parallel. And some of the thinking that went into the disease selection for MAD was not only about a good model system where we can figure out the multiple sending doses and our schedule, but also one that we could execute quickly on and sort of have Got it, great. And I guess just one more on this one.

But ultimately I mean, it's T. Regs are pretty important you know way of achieving homeostatic immune balance and.

It could be incredibly widely applauded employed.

If it's actually effective from an operational standpoint, I would just sort of reiterate.

We know that it's a competitive space and I think that's why we are doing our S. A D and our MAA in parallel and some of the thinking that went into the disease selection for MA was not only about a good model system, where we can figure out the multiple ascending dose in our schedules, but also one that we could execute quickly on and sort of having.

Advantage in proof of concept as well.

Got it great and I guess, just one more on this one how are you thinking about this asset as it fits into your portfolio and you know are you thinking about it in house development out licensing or maybe some sort of a partnership.

Bassil Dahiyat: How are you thinking about this asset as it fits into your portfolio? And are you thinking about in-house development, out-licensing, or maybe some sort of partnership? Thanks. Right now, this is an asset that we think has extremely high scientific promise, and like all the other assets we put into the clinic, we hope that we can do the full development path and market it ourselves one day. And deviations from that hope for path are always driven by data, and they could end up anywhere.

Right now this is an asset that we think has extremely high scientific promise and like all the other assets, we put into the clinic. We hope that we can do the full development path and marketed ourselves one day and deviations from that hope for path are always driven by data and it could end up anywhere, but our goal knows is not to partner our goals to make drugs.

Got it thanks for taking all the questions.

Bassil Dahiyat: But our goal, no, is not to partner; our goal is to make drugs. Got it. Thanks for taking all the questions. Your next question comes from the line of Arlinda Lee from Kennecord. Your line is now open. Hi guys.

Your next question comes from the line of Arlinda Lee from Canaccord. Your line is now open.

Arlinda Lee: Thanks for taking my questions and congrats on the progress. I was thinking about your Amgen data from earlier this month, and I guess I had a couple of follow-ups. Can you remind me what happened with – I think Amgen also had a – Who has the rights to your CD38? Is that moving forward?

Hi, guys. Thanks for taking my questions and congrats on the progress.

I was thinking about here.

The Amgen data earlier.

Earlier. This from early this month and I guess I had a couple of follow up.

Can you remind me what happened with I.

I think Amgen also had.

Oh right to your CD 38 that returned is that moving forward and then maybe secondarily can you talk about how many other targets they can be going after and then and how that progress.

Arlinda Lee: And then maybe secondary, can you talk about how many other targets they can be going after and how that progress is moving along? And then thirdly, can you talk about other methods of transitioning your doctorate to CD38 in the future? 2-to-1 formatted things that you might have in the works.

Moving along and then thirdly can you talk about other.

<unk> won formatted.

Things that you might have in network. Thank you.

Bassil Dahiyat: Thank you. So I'll take that first set on the Amgen collaboration part quickly. They don't have any more targets they can choose from in the collaboration.

Sure I'll take that first set on the Amgen collaboration part quickly.

They don't have any more targets they can choose out of the collaboration that the timeframe choose targets.

Bassil Dahiyat: The time frame to choose targets ended a couple years ago. The CD38 program that was returned to us is now in an investigator-sponsored trial that we're collaborating with in hematologic malignancies, and that one's moving along, but they have no other target rights, and there aren't going to be any more programs from that collaboration. They have, at this point, just the steep one, the AMG 509 program. Now for the other two plus ones, maybe I'll let John start talking about that. Yeah, I mean, I think we've even had posters on multiple of our other 2-plus-1s that we've created. So Cloudin 6 CD3, that's a 2-plus-1.

A couple of years ago.

The security program that was returned to US is now in an investigator sponsored trial that we're collaborating with in hematologic malignancies, and where will that was moving along.

But they have no other target Reits and there aren't going to be any more programs in that collaboration.

I have at this point just the steep one AMG 509 program.

Now for the other two plus ones that maybe I'll, let let John start talking about that.

Yeah, I mean, I think we've publicly we've even had posters on multiple of our other two plus ones that we've created so.

Cloud and six CD three that's a two plus one of course, we have our 819 program. The E. P. P. Three by CD three.

John Deserlay: Of course, we have our 819 program, the EMPP3 by CD3, and, um... We're working to generate a whole pipeline, but there's a few of them that have been disclosed and you kind of get the sense of where we're going [inaudible] and get recall we also have a drink of collaboration we're working closely with them to see what comes out of that terms of new targets. Yeah, so I think for us we see that that initial bit of validation from the AMG509 program for this two plus one format in particular its ability to really attach strongly to Tumorantigen and a Ford CD3 activation in a way that is tolerable in at least in this instance in solid tumors really gives us a lot of confidence to really double down on solid Tumor targets for CD3s and using the selectivity we can potentially achieve here as the backbone.

Ed.

I think she is with me.

Copa can three CD three that we publicly disclose so we work of course, our lender working to generate a whole pipeline, but there's there's a few of them the habit disclose and you kind of get the sense of where we're going with that and recall. We also have our streak of collaboration we're working closely with them to see.

What comes out of that in terms of new targets, yes. So I think for US we see that that initial bid a validation from the 85 to nine program for this two plus one format in particular, its ability to really attach strongly to tumor target tumor antigen and and afford CD.

Three activation in a way that is tolerable in at least in this instance in solid tumors really gives us a lot of confidence to really double down on solid tumor targets for CD threes and using the selectivity, we can potentially achieve her as the backbone. So we're excited to start 819 in the clinic imminently in renal cell carcinoma.

John Deserlay: So we're excited to start at 819 in the clinic, imminently in renal cell carcinoma. Great, thank you. Your next question comes from the line of Peter Lawson from Barclays. Your line. A, thanks so much for taking the questions. Just, I guess, another question on UdanaMap. For this second half readout, I appreciate all the detail around safety and early in the response.

Great. Thank.

Thank you.

Your next question comes from the line of Beta Lawson from Barclays. Your line is now open.

Thanks, so much for taking the questions just I guess another question.

We've done on that.

For the second half readout I appreciate all the detail around it.

Kind of safety and early in the response cycle.

Peter Lawson: As we think about responses, should we be thinking about PSA 50 reductions, or is it... Do you think we can potentially see shrinkage of tumors and then kind of how difficult are these patients to treat? Is it kind of like a bone disease that we should be thinking about? You want me to take that? I think it depends on the molecular subtype, Peter. You know, I think for some patients, depending on the molecular subtype, they'll have more... Bony lesions or occult metastases. Some of the more aggressive phenotypes will have lymph node metastases or even visceral liver or lung metastases, and I've seen brain metastases.

As we think about responses should we be thinking about PSA 50 reductions or is it.

Do you think we can potentially see.

Shrinkage.

And then kind of how how difficult. These patients to treat is it kind of like there are any disease that we should be thinking about.

You want me to take that I think it depends on the molecular subtype, Peter I think for some patients depending on molecular subtype they'll have more.

Tony lesions or occult metastases and you would want to look at PSA some of the more aggressive phenotype. So we'll have lymph node metastases or even visceral liver lung metastases and I've seen brain metastases and so those you would try to look for traditional tumor shrinkage, but I think it depends on the subgroup again the way that.

Alan Yang: So those you would try to look for traditional tumor shrinkage. But I think it depends on the subgroup. Again, the way that the study was designed, there are different molecular subtypes. And you can imagine some of the subtypes, like PMSI, and microsatellite unstable, will be very difficult to enroll, so we may not have a lot of data. We do have a bucket for those that don't qualify for any

The study was designed theres different molecular subtypes and you can imagine some of the subtypes like <unk>.

Si micros.

Microsatellite stable will be very difficult to enroll so you may not have a lot of data we do have a bucket for those that don't qualify for any of those groups and that group will probably be early data, but it'll be a mix of different genetic phenotype.

Alan Yang: And that group will probably be early data, but it'll be a mix of different genetic phenotypes. But that group is also in combination with chemotherapy, so we'll see how that looks. Thank you. How many patients do you think we could see? I don't know if you mentioned that before.

But that group is also in combination with chemotherapy. So we'll see how that looks.

Okay. Thank you how many patients do you think we could see it if you mentioned that.

Alan Yang: We're guiding to probably on the order of a dozen or two at that point. Perfect, thank you. And then maybe a question for John, just around, you've touched upon guidance being conservative. Any kind of near-term milestones that we should be thinking about in the 2022 numbers? Nothing, nothing like that. The only one I can think of would be a possible sales milestone from Alexion, sales ramped up. We do have a 20 million dollar sales milestone which we expect possibly 22 if not 22 or 23. The rest of them are all development. Obviously, we're excited if Amgen advances its program, but we don't have any Timed Minus, so they're next up. Gotcha, but none We shouldn't be thinking about any of that in the garden.

We're guiding to probably on the order of a dozen or two at that point.

Perfect. Thank you.

Maybe a question for John just around you've touched upon.

Guidance is being conservative any kind of near term milestones that we should be thinking about.

In the 2022 number.

Nothing nothing that.

Oh other than possibly the only one I can think of would be possible sales milestone from Alexia.

Sales ramps up we do have a $20 million sales milestone, which we expect possibly 'twenty two if not 'twenty two 'twenty three the rest of them are all development. Obviously you know we're excited if amgen advances program, but we don't have any.

Timeline as to their next steps.

But none of those are in the guidance, we shouldnt be thinking about any of that in the guidance.

John Kuch: I was just... I was just... I was just... Are any of those in your kind of cash year-end guidance? Yeah, the election would be.

I'm, sorry, what was it.

Are any of those in the yoga.

Cash year end guidance.

Yeah, the election would be.

John Kuch: Like I said, the Amtn, we have to just... We don't have any more information than what they've disclosed publicly. Thank you. And then just finally on the B7H3, what tumor types are you hoping to enroll in that study? So we're not disclosing that yet, but I will say that, and it'll probably be a mix, I will say that we're obviously keenly interested strategically in prostate cancer. Our Budalimab program, our collaboration with Janssen, which gives us access to a number of their clinical stage and commercial stage prostate cancer agents.

The election would be like I said, the the Amgen we have to just wait.

We don't have any more information on what they've disclosed publicly.

Thank you and then just finally on the B seven H three what tumor types are you hoping to enroll in that study.

So we're not disclosing that yet, but I will say that and it would probably be a mix I will say that we're obviously keenly interested strategically in prostate cancer or <unk> program, our collaboration with Janssen, which access gives us access to a number of their clinical stage and commercial stage prostate cancer agents.

Bassil Dahiyat: But I think what we also wanna do is be thoughtful about the different mechanisms we can potentially benefit from here, both checkpoint inhibition as well as CD3 bispecifics. And so we're gonna be guided by sort of the availability and quality of combo agents as much as by the theory on which tumor type. Okay, thanks so much for all the details. Your next question comes from the line of David Dai from SMBC. Your line is now open. Yeah, hi.

But I think what we also want to do is we want to be thoughtful about the different mechanisms. We can potentially benefit here, both checkpoint inhibition as well as CD three bi specifics and so we're gonna be guided by sort of the availability of quality of combo agents as much as by the theory on which tumor types.

Great. Okay. Thanks, so much for all the details.

Your next question comes from the line of babies Die from SM BC. Your line is now open.

David Dai: Thanks for taking my questions. So I have a question about Vidaliumab. So, Phase II data is expected in the second half of this year. So besides the genetic subsites, can you also share with us any biomarker strategies that you're exploring to further identify predictive biomarkers that would support the benefits of Vidaliumab combinations in MCR-PC? And then could you also just comment on the cadence of data release? Would you expect to report the data at a medical meeting, or would it be a press release? Thanks. I'll answer the second one first.

Hi, Thanks, guys for taking my questions. So I have a question for <unk>. So.

The phase two data is expected in second half this year. So besides the generic subsidized can you also share with us any harm.

Our market strategy, you say, you're exploring to further to further identify predictive biomarkers, we're supportive benefits on with Allomap foundations and see RPC and then could you also just comment on the cadence of beta release would you would you expect to report the data at <unk>.

Medical meeting or would it be a press release.

Bassil Dahiyat: Our goal is at a medical meeting, but of course, it's still well before the abstract submission deadline, so we consider that an aspirational goal. We're hopeful optimists can get there, but we'll see about the other one about predictive biomarkers. I mean, you can get into the science of it.

I'll answer the second one our goal is at a medical meeting but of course, it's still well before abstract submission timelines. So we consider that an aspirational goal, where we're hopeful that we can get there, but we'll we'll see on the other one about predictive biomarkers.

Bassil Dahiyat: We're going to be looking at a lot of immune oncology-type biomarkers. But I am not certain that we are really gunning for predictability here. We're going to use the existing bucketing of the clinical gene types, and even the clinical definition of high risk biomarkers is, inaudible, I think something to strive for but not count on in your development program for immuno-oncology. All right, thank you so much. Your next question comes from the line of Etzer Darout from BMO Capital Markets. Your line of... Great. Thanks for taking the question and congrats on the progress here. The first one is really more a point of clarification for me.

I mean, you can get into the science of it we're going to be looking at a lot of immune oncology type Biomarkers I am not certain that we are really gunning for predictability here, we're going to use the existing buckets of the clinical gene types and even the clinical definition of high risk Biomarkers are.

I think something to strive for but not count on in your development program in immuno.

Oncology.

Alright, thank you so much.

Your next question comes from the line of Advair morale from BMO capital markets. Your line is now open.

Great.

Thanks for taking the question and congrats on the progress here first one is really more a point of clarification for me the promotive map combos with <unk> and Lenalidomide would that be with the sub Q or the IV formulation as you sort of open up these sites here and then.

Etzer Darout: The PlomodaMap combos with Monjuvia and lenalidomide, would that be with the sub-Q or the IV formulation as you sort of open up these sites here? And then a second unrelated question, back to sort of guidance, just wondered whether or not you expect any meaningful step up in R&D spend associated with PlomodaMap combo with Monjuvia specifically or just kind of a regular way as you kind of advance these multiple programs into the clinic? Thank you. So maybe, Alan, you want to take these? Yeah, I'll take the first one.

Alan Yang: So it will be IV, not the sub-Q form. Got it. On the spending, how do you take that one, John?

Second unrelated question back to sort of guidance just was wondering whether or not you expect any meaningful step up in R&D spend associated with promoted that combo with <unk>, specifically or just kind of regular way as you've kind of advance these multiple programs.

And to the clinic. Thank you.

So maybe Alan you want to take the I'll take the first one so it will be IV not the sub Q form.

Got it.

John Kuch: Yeah, as far as the spending, the spending we have in the next two to three years anticipates these trials basically as an early look into the potential, but we do not have large multi-, So 200 patient-type trials budgeted at this time. So it doesn't include the cost for the initial running of these, but we've not, at this time, budgeted larger trials.

On the spending were to take that one Jeff yeah as far as the spending.

Spending we have in the <unk>.

Next two to three years anticipate these trials.

Basically early look into the the potential but we do not have large multi national tomorrow.

<unk> type trials budgeted at this time.

So it doesn't include the cost for the initial run it for these but.

We've not at this time budgeted larger trials.

Got it awesome. Thank you.

Got it.

Etzer Darout: Awesome. Thank you. Your next question comes from the line of Zhizhang Zhu from Berenberg. Your line is now open.

Your next question comes from the line of Jean Charles Zhou from Barron. Your line is now open.

Zhizhang Zhu: Great, thank you. Good afternoon. I want to ask about the new program you're going to put in the clinic, A19. I guess, what gives you the confidence in this program in RCC? Any valid targets that you want to highlight here? And, broadly, for this program to succeed in the indication, any thoughts around combination approaches later on? That was two questions. That wasn't your first question.

Great. Thank you good afternoon.

I wanted to ask you about the new program, you're going to put in the clinic.

I guess, what gives you the confidence that this program in RCC.

Sure.

Target that you'd want to highlight here.

I guess broadly for this program to succeed in the indication any thoughts around combination.

Purchase laid out that's the first question.

That was two questions that wasn't your first question.

Yes.

Yeah.

So I'll, let John take the one on confidence may be the mechanistic and the historical confidence yeah.

John Deserlay: So I'll let John take the one on confidence, baby, the mechanistic and the historical confidence. Yeah, sure. So, you know, there was, in fact, an Estellus agenda, the ENPP3 drug conjugate program, and we had also independently identified the target really just from bioinformatic analyses of, you know, different targets that are overexpressed in various cancers, and ENPP3 emerged as one that is very nicely, selectively overexpressed in renal cell carcinoma, to some extent in papillary as well, but we're going to focus on clear We see, you know, really nice bright standing in renal cell carcinoma.

Yes sure so.

There was historically there was in fact, an astellas agendas E&P three drug conjugate program.

And we had also independently identified the target really just from bioinformatics analyses of different targets that are over expressed in various cancers in E&P three emerged and one that is one that it's like very nicely selectively over expressed in renal cell carcinoma.

To some extent in papillary as well, but we're going to focus on clear cell.

Other than that we've also done immuno histochemistry analyses, we see really nice bright stating in renal cell carcinoma. We've also talked to various academics that are working with RCC cells and they say, it's E&P P. Threes, one of the cleanest markers of that tumor population. So.

Alan Yang: We've also talked to various academics that are working with RCC cells, and they say that ENPP3 is one of the cleanest markers of that tumor population. That's what's driving most of our confidence in this, is that it was sort of safely targeted with a drug conjugate coupled with the overall expression pattern and high expression and getting, And I would just add from a clinical perspective that now there's clear proof of concept data that these T-cell engagers work in solid tumors. There is AMG-757 in small cell lung cancer, as well as AMG-509 as early data.

That's what's driving most of our confidence in this is that that was it was sort of safely targeted with a drug conjugate coupled with the overall expression pattern and high expression.

Kidney cancer.

And I would just add from a clinical perspective, you know I think now there's clear clear proof of concept data that these T cell engages with work in solid tumors. There was AMG 757 in small cell lung cancer as well as AMG 509, because early data.

And so I think we're clearly going to work in solid tumors as well I would remind people that in renal cell cancer. It is responsive to immunotherapy checkpoint inhibitors are the standard of care in frontline.

Alan Yang: And so I think we're clearly going to work in solid tumors as well. I would remind people that in renal cell cancer, it is responsive to immunotherapy. Checkpoint inhibitors are the standard of care and the frontline. On the second part, in terms of combinations, I think we have to wait to see the data. I think for kidney cancer, combinations are sort of the game with a checkpoint inhibitor and a TKI for frontline therapy, but, you know, we still need early data.

And the second part in terms of combinations I think we have to wait to see the data I think for kidney cancer combinations as sort of the game with a checkpoint inhibitor at Teekay.

For frontline, but we still need early data.

Alan Yang: You know, T cell engagers do have CRS, but I think they're more manageable in solid tumors, so we'll have to see how good that data is. And then whether we combine it with something that accentuates the T cell engager or just empirically has activity, like a TKI, has to be seen until we see the phase one data. Great, that's helpful. I guess maybe a third question for me, given I asked two, either for Baz or John, in terms of capital allocation, now you have $600 million in the bank. It's very comfortable in today's market, I guess. How would you think about spending the money?

T cell engages do have Crs, but I think they are more manageable in solid tumors. So we'll have to see how good that data is and then whether we combine with something that accentuates the T cell engaged or or just empirically has activity like the teekay has to be seen until we see the phase one data.

Great that's helpful.

Maybe.

The third question for me.

That's too bad or John in terms of capital allocation now you have a $600 million of bankers.

We're comfortable in today's market I guess, how would you think about spending the money.

Zhizhang Zhu: Obviously, you have a lot of programs, a lot of 2-plus-1 format detail engagers in pretty close stage, but you also have mid-stage assets like the dual amount. How would you think about either pushing the mid-stage to the finish line or kind of pushing more quick link or assets into the current area? I don't appreciate any color here.

Obviously, you have a lot of programs a lot of two plus one format.

T cell engages in particular stage, but also you could do.

<unk> assets like but how.

How would you think about either to push the mistake to the finish line or more kind of pushing more quick clinical assets in Brooklyn.

In color and care.

Bassil Dahiyat: We look at the data. If we think the data that we see so far in a clinical program merits us putting down the money to go forward all the way to the finish line ourselves, to try to get approval ourselves, we'll do it. We'll continually feed programs into phase one, you know, the exploratory phase, and see whether they merit further advancement. And we're gonna judge every program against what exists in our portfolio at that time. But it's all gonna be data-driven.

We look at the data if we think the data that we see so far in the clinical program merits us putting down the money to go forward all the way to the finish line ourselves you could try to get an approval ourselves we'll do it we will continually feed programs into the into the phase one.

Exploratory phase.

And see whether they merit further advancement in there we're going to judge every program against what exist in our portfolio at that time, but it's all going to be data driven and we do want to be thoughtful about making sure. We have something that we really truly believe has a competitive profile before we put all our chips down. So for example, do down the Mab the phase two studies, we're doing now we're actually fairly.

Bassil Dahiyat: And we do wanna be thoughtful about making sure we have something that we really, truly believe has a competitive profile before we put all our chips down. So, for example, Vudalumab, the phase two studies we're doing now are actually fairly contained and modest in scale relative to something that would be registration, because we're still looking for how we now fit in the complex prostate cancer combination treatment landscape. So we're gonna be data-driven.

Contained in modest in scale relative to something that will be registration because we're still looking for how we now sit in the complex prostate cancer a combination treatment landscape. So we're going to be data driven we're not at the point of committing to Registrational studies, but when we do we will tell you and I would also say that we.

Bassil Dahiyat: We're not at the point of committing to registrational studies, but when we do, we'll tell you. And I would also say that, you know, we're very careful and thoughtful about managing our cash because money's never easy to come by, even in the so-called easy times.

We're very careful and thoughtful about managing our cash.

Because money.

Money is never easy to come by even in the so-called easy times.

Great. Thank you very much.

Zhizhang Zhu: Great, thanks very much. Your next question comes from the line of Dalvin Wu from Raymond James, and the line is now open. Hey guys, this is Bowen on behalf of Dane.

Your next question comes from the line of <unk> from Raymond James Your line is now open.

Hey, guys. This is calling on for Dan Thanks for taking our questions and congrats on the pipeline progress so far.

Dalvin Wu: Thanks for taking our question and congratulations on the pipeline progress so far. On 306, can you kind of guide when we could see kind of the comprehensive data from the Phase I trial, maybe a presentation or publication? And on the combo trials for 306?

Three O six can.

Can you kind of guide.

And when we could see kind of a comprehensive.

Data from the phase one trial, maybe presentation or publication.

On the combo trial for 306.

Dalvin Wu: You know, you mentioned that you're interested in NK cells and T-cell mediated, but kind of curious if you can squeeze any additional color on any potential guidance for the COMPO trial? And then lastly, on 564, kind of what are you looking for in the Phase 1 Healthy Voluntary Trial that could kind of shape the MAD trial initiating thing? Yeah, so first on the 306, it really has to be agreed between Genentech and us when we present.

You mentioned that you're interested in NK cell and T cell mediated but kind of curious if you can create any additional color what colors left there on in.

Potential guidance.

The combo trials.

And then lastly on 564 on kind of what what are you looking for in the phase one healthy volunteer trial that could kind of shape.

That trial machining.

Yeah. So first on the 306.

It really has to be agreed between <unk> and us when we present I think a natural point would be when the phase one is done and we go to a medical conference.

Dalvin Wu: I think a natural point would be when phase one is done and we go to a medical conference. Though phase one we are hopeful is wrapping up soon, I can't imagine we'd have a publication ready given Genentech's timeframes for that thing this year. So I'm hopeful for next year, but I can't even guide on that.

So the phase one we are hopeful is wrapping up soon I cant imagine we'd have a publication ready given genentech's timeframe for that thing. This year. So I'm hopeful for next year, but I can't even got on that we'll give you guidance on when but it will be when the phase ones wrapped up and that's that's that's gonna be discussion was gentex.

Bassil Dahiyat: We'll give you guidance on when, but it would be when phase one's wrapped up, and that's going to be a discussion with Genentech. You know, on the combo trials, I really can't offer any more color until we announce them, unfortunately.

On the combo trials.

Really can't offer any more color until we until we announce them.

Bassil Dahiyat: I do think that the NK cell boosts we saw were remarkable, notable for their magnitude, their durability, and the kind of control that that suggests we can have by varying doses and varying schedules. So that's that there. For 564 on the SAD, what can we get out of these healthy volunteers in this IL2 Treg space to guide the MAD? Well, I think the key there is the durability of our Treg expansion and how that helps us select the dosing frequency in the MAD.

Unfortunately, I do think that the NK cell boost we saw were remarkable were notable for their their magnitude. The durability. The kind of controls that that suggests we could have by varying dose at varying schedule. So that's out there for 564 on the S. A D. What we get out of that healthy volunteers.

As in this Iot T Reg space to guide the <unk> I think the key there is the durability of our T Reg expansion.

And how that helps us select the dosing frequency and the M D.

Bassil Dahiyat: Right. Longer is better. And I know that our competitors seem to be settling in on every other week, and we're going to be looking hard at how well we do in frequency. I mean, that's the biggest impact on the MAD.

Right longer is better and I know that our competitors seem to be settling in on every other week and we're going to be looking hard at how well we do it.

In frequency.

I mean thats the biggest impact on the S E T.

Dalvin Wu: Thanks, guys. Thanks, guys. Your next question comes from the line of Mike King, from H.C. Winwright. Your line is out. [inaudible] Hey, good afternoon, guys. Thanks for taking the questions. First, just a financial question.

Got it great. Thanks, guys.

Your next question comes from the line of Mike King from H C. Wainwright. Your line is now open.

Good afternoon, guys. Thanks for taking the questions.

Mike King: I just wanted to see if you guys would be willing to give more color on the spend out to 2025 with the drivers of the burn. I don't know if you'd be willing to talk about the different components of spend, you know, on the particular programs. No, because we budget pretty carefully, I'd rather not carefully, balls budget carefully; we budget pretty specifically in the near time frame of the next year or two when we have clarity on what the clinical trials are going to be, and then we keep placeholders for next stage trials depending on which program we decide to promote.

Just a financial question at first I just wanted to.

See if you guys would be willing to give more color on.

The spend out to 2025 with the drivers of the burn I don't know if you'd be willing to talk about the different components of spend.

You know on particular programs.

No because we we budget pretty carefully I'd, rather not carefully bulbs, but it carefully we budget pretty specifically in the near time, Fred the next year or two when we have clarity on what the clinical trial is going to be and then we keep placeholders for next stage trials, depending on which program. We decided to promote I think that's about as much as we could say in terms of granularity.

Mike King: I think that's as much as we could say in terms of granularity. I think that's as much as we could say in terms of granularity, I think that's as much as we could say in terms of granularity. Okay. Sorry, on vacation with the fam, and they just came back to the room.

Okay.

Alright.

No.

John Kuch: I wanted to also explore five, six, four, a little bit more. Can you just talk about... Have you compared the molar activity of IL-2 with a native IL-2? Because, you know, we've talked a lot about your competitors. NECTAR has basically been dosing at similar levels to what the tolerable levels of native IL-2 are. So is there any difference between 564 and native IL-2 or the NECTAR 358 program? There's a marked difference, in fact.

On vacation with the family and they just came back to the room.

I wanted to also explore a five six for a little bit more can you just talk about.

Have you compared.

The molar activity against.

A native IL, two because we've talked a lot about your competitors and.

Nektar has basically been dosing at similar levels to what the tolerable levels saw native IL. Two are at so is there any difference between 564 and native IL two or the nektar.

Finally program Mark in fact, so.

John Deserlay: So as we learned with our XMAP-306 program, the IL-15, this class of cytokines, IL-2 and IL-15, and to a large extent, most of the cytokines, when they signal, they get internalized. And so there's an inverse relationship between their potency and their exposure. So we found out that basically the way to make these cytokines into really good drugs is to actually reduce their potency dramatically. So 564's potency was reduced by about at least 100-fold compared to native IL-2.

As we learned with our R X map through a six program the IL 15.

This class of cytokines, IL, two and IL 15 and to a large extent most most of the cytokines when they signal they get internalized and so there's there's an inverse relationship between their potency and their exposure.

So we found out that basically that the way to make turn these cytokines into really good drugs with facts to reduce their potency dramatically.

So five six wars potency reduced by about at least 100 fold compared to native IL. Two however, it actually last.

John Deserlay: However, it actually lasts at least 100-fold longer in terms of exposure, so you've got it sitting around a lot longer. It makes it a more tolerable drug, and it can do its job longer than the native.

At least 100 fold longer in terms of explode right. So.

You got it sitting around a lot longer it makes it a more tolerable drug.

And it could do its job longer than the native kit.

Mike King: Okay. And I know we recently launched you guys, but you have a tremendous amount of scientific data to process. So, remind me if there are two questions I would have, I guess, one is the selectivity for the alpha receptor on the Treg versus the T effector cell, number one. And number two, I don't believe there are any modifications that would keep it away from endothelial cells in the periphery, but I guess your response to that would be you're detuned, so you wouldn't have the same kind But could you just go into that in a little bit more detail?

Okay, and I know, we recently launched a new guys, but you have a tremendous amount of scientific.

Additive process, So remind me if.

There are two questions I would have I guess there is one is the selectivity for the alpha receptor on T Reg versus T effector cell number one and number two.

Don't believe there's any modifications.

Modifications that would keep.

Keep it away from endothelial cells in the periphery, but I guess your response to that would be your D. Tuned. So you shouldn't have the same kind of setup.

Outside of kind of released syndrome, but you wouldn't have the petro liberally about that yeah.

Periphery, but could you just go into that a little bit more detail yeah yeah.

John Deserlay: Yeah, yeah. So, we basically did – we engineered it so it has a slightly higher affinity for CD25. We want it to be CD25 biased in its activity. And so, most of the potency reduction comes from the IL-2 receptor beta reduction. So that, again, that helps with selectivity.

We basically did we.

We engineer it so it has a slightly higher affinity for <unk> 25, we want it to be seeded twenty-five biased in this activity.

So most of the potency reduction comes from the IL two receptor beta.

John Deserlay: You know, based on what we've seen in our own assays and, you know, looking at making other people's molecules and characterizing them, we're pretty much top of the class in terms of Treg selectivity versus effector T cells. And so, you know, we think overall we've got a great profile in terms of Treg selectivity as well as potency tuning and the long half-life. Okay, great guys. Thanks so much for taking the questions.

Reduction.

So that again that helps us to selectivity.

Based on what we've seen in our own assays in and looking at making other people's molecules characterizing them.

Pretty.

Pretty much top of the class in terms of T regs selectivity versus effector T cells.

And so we think overall, we've got a great profile in terms of T Reg cell activity as well as the.

The potency tuning in the long half life.

Okay, great guys. Thanks, so much for taking the questions.

John Deserlay: It's great to have you covering us after all these years of knowing each other, Mike. It's a pleasure. There are no further questions at this time; I'll turn the call back to Basil Dahiyat. Thank you very much and thank you everyone for joining us today. We look forward to updating you more over the course of the year, and have a wonderful evening. This concludes today's conference call. Thank you for participating, you men. A A A A A A A A A A A A A A A A A A A A A A A A A A A A A A A A A A A A A A A A A A A A A A A A A A A A A A A A A A A A A A A A A A A A A A A A A A A A A A A A A A A A A A A A A A A A

That's great too great to have you covered us after all these years of knowing each other Michael it's a pleasure.

There are no further question at this time I'll turn the call back to Basel.

Thank you very much and thank you everyone for joining US today, we look forward to updating you more over the course of the year and have a wonderful evening.

This.

Today's conference call. Thank you for participating you may now disconnect.

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Yes.

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