Xencor Inc. Q1 2023 Earnings Call
Good afternoon, and thank you for standing by welcome to Zen cores first quarter 2023 conference.
Okay.
We are in a listen only mode. After the speaker's presentation there'll be a question and answer session. Please.
Please be advised that this call is going to be recorded at the company's request.
Now I would like to turn the call over to your speaker today Charles.
And the head corporate communications and Investor Relations go ahead Charles.
Thank you and good afternoon earlier today, we issued a press release outlines the topics we plan to discuss today, it's available at Www Dot Dot com.
[noise] abbreviated comments on the call is Basil Dockyard, President and Chief Executive Officer Afterward, we will open up the call for your questions and we'll be joined by Allen Yang Chief Medical Officer, John Desjarlais, Chief Scientific Officer, John Kush, Chief Financial Officer, as well as many people into Chief Development Officer before we begin I would like to remind you that during the course of this conference calls and management may make forward looking.
Including statements regarding the company's future financial and operating results future market conditions plans and objectives of management future.
Future operations, the company's partnering efforts capital requirements future product offerings and research and development programs.
Forward looking statements are not historical facts, but rather are based on our current expectations and beliefs and are based on information currently available to us the outcome of the events described in these forward looking statements are subject to known and unknown risks uncertainties and other factors that could cause actual results to differ materially from the results anticipated by these forward looking statements, including but not limited to those factors contained in the risk factors section of our most recently filed annual report on Form 10-K.
And clearly report on Form 10-Q with that I'll pass the call over to Basel.
Charles and good afternoon, everyone.
At Suncor, we use our ramp modular protein engineering tools to create a broad internal development portfolio of antibodies and engineered cytokines.
Could you not immune disease.
Target novel Biology, with our candidate designs, including C. Twenty-eight coach them by specifics more tumor selective CD three bi specifics and potency produce cytokines. This broad portfolio lets just take multiple simultaneous shots on goal in the clinic and use the proof of concept data from our early stage studies to guide, which programs, we advance which we.
In which we partner so.
So that we use our resources on programs with the greatest potential for success and they agree with our portfolio for the next wave backstopped by specifics in engineered cytokines.
You need to enroll patients in phase, one and two trials across our wholly owned portfolio for oncology and one autoimmune next mab candidates.
Last month at ACR, we presented on our preclinical portfolio of excess CD 28, co stimulatory Bispecific antibodies, which are focused on which are the focus of our research now that are very exciting new area in immuno oncology.
<unk> C D. Twenty-eight bi specifics are designed to activate T cells only in the presence of tumor antigen and thereby drive signal to activation to amplifying sustained T cell anti tumor cytotoxicity or <unk>.
Sure highlighted our platforms rapid Kennedy generation.
Opportunity for CD 28, using data from five CD 28, Bispecific antibodies targeting a variety of solid tumor targets like see a trop two and steep one.
We've initiated preclinical development of a second internal CD 28 program with a plan to file the IND next year recall that our lead clinical CD 28 program extra heartbeat away targets be seven eight screens in phase one.
Our next data presentation will be later this quarter when we expect to present data from a regulatory T cell targeting cytokines ex map 564 at the <unk> Congress on Congress of Rheumatology in Milan.
We plan to present updated biomarker data from our single ascending dose study that we initially presented in November 2022.
If my last comment I would like to welcome a new member of the leadership team at Suncor last month, we announced the appointment of Nancy Valencia, as our Chief Development Officer she'll be responsible for all of US and of course clinical activity Jordan, Our CSO, John digitally and me in the scientific leadership of the company. We are delighted to welcome Nancy to our team and look forward to benefiting from our deep expertise in developing drugs like cause either.
All of these in classifying him Libra.
She was in a unique position to see our development programs technology and people up close for the last eight months as a member of our board of directors from what she has resigned and chose to commit to work full time here.
Laborde Nancy.
Now with that we'll open the call to your questions operator.
Thank you.
At this time I'll be doing the Q&A session. After presentation. Just a question. Please press star one on your telephone and you will then hear an automated message advising that your hand is raised to.
So John a question press Star one that one again.
The first question comes from.
Mara Goldstein family.
Your line is.
Alright, thank you.
Hi, Hi, Thank you Richard support bone marrow. Thank you for taking our question I have a question on X snap five six ball congrats on getting the slot at Utah, just curious I know there'll be additional biomarker data, but it was the partner you can guide them.
In terms of why we should pay attention to and then on an ex snap 564.
I'm just curious if it competitors dataset in development, including Nektar square Peg and Amgen compiled I'll give you a pause on it mechanically and why atopic dermatitis and so the rises are selected as an indication for the match study. Thank you.
Any other questions that was about four.
That's all.
Great.
Let's get started.
So.
So they kind of biomarker data that we're going to present as really an elaboration in more detail on the phenotype of the T cells that.
The regulatory T cells in particular that were amplified in our single ascending dose study that we presented in November so really characterizing how those look in more detail I think we would you liberate the punch line in November .
Markedly durable with sustained T Reg increases out to 21 days.
And.
We're excited by the opportunity to try to extend the dosing interval beyond what sort of the class has gotten too which is every two weeks.
So we're really quite enthusiastic about the mechanism I think the data from the competitor that you mentioned it has to be put into context up there.
Less than ideal selectivity for CD 25.
You know John do you have anything to add to that.
No I mean, just based on our in vitro comparisons you know looking at various molecules and what's what's been available in various posters.
We like our selectivity profile better.
Little bit more surgical engineered to you.
You have preferential binding exceeded 45 positive T regs.
And very carefully potency reduced to maximize that.
Farmer, Connecticut.
Pharmacodynamic effects.
So so we're still quite enthusiastic about the potential of the mechanism of action I think it is really about making sure you have engineered what you think is the right molecule to attack that M O N.
Now you asked about our indication selection in our phase one multiple ascending dose study we also started.
Treating patients in in November of last year, and we picked a atopic dermatitis and psoriasis and Theres two goals that you want us to rapidly determine.
A good dose and schedule with multi dose.
And we wanted to pick indications that we could rapidly enroll that we can also directly view clinical outcome quite easily. So these skin autoimmune diseases allow you to do that look at actual clinical response correlate that the T regs and in your safety profile, we think in particular for atopic dermatitis. The remains a strong opportunity for good agents that can have long desk.
The interval through good safety.
Got it thank you.
Thank you the next question.
Comes from the line of Edward cannot Hypersound that your line is open.
Okay, great. Thank you.
Okay.
Yeah.
Yeah, Hi, guys.
Great. Thank you so I apologize if I missed this but what is.
If anything are you guys can be showing at <unk>.
Get the next modality.
Okay.
Yeah, we're not presenting any new data at <unk>. This year you recall, our tempo of presentation is usually falling towards the late in year conferences.
And we'll guide on that specifics on that as we get a little further out into the year and closer to whatever data updates we're going to do we're not we're not guiding full year data.
We're really doing it a little closer like we did just now for about 564.
Awesome guys.
There you are.
Take care guys.
Thank you. The next question comes from the line of Brian Cheng from Jpmorgan go ahead, Brian .
Hey, guys. Thanks for taking my question maybe.
Maybe just one question on five six for your IL two F C.
So you previously mentioned that psoriasis is a great starting point for you to get some proof of concept.
As we look forward to some data early data in psoriasis.
Early next year I'm, just wondering how do you think about the market opportunity for this molecule.
Given that this may not be the ultimate market for you to move forward, where 564 and any guidance on you know just from an analyst standpoint, how should we think about the.
The Tam here 4564, thank you.
I'm sorry, how should we think about the what for 564 I missed that word that total addressable market for 564 got it got it Tim sorry.
So.
I think we made a point of adding atopic dermatitis into the phase one be mixed and we will be dosing patients in cohorts there as we as we step up a little bit in dose because we do think a D has still a significant unmet need both for.
The breadth.
Of the number of severe patients as well as the need for longer acting agents, we know that theres a lot of exciting about libra kismet coming on with a monthly.
Which is better than.
<unk> Mab, which is every two weeks and is really bound by the target mediated clearance. There. So we think there is we tried to be thoughtful about adding things that can both have proof of concept as well as.
A meaningful potential for differentiation into our phase one b, but remember that this goes to your total addressable market. There is a wide range of indications that you can potentially reach with a broad autoimmune drug.
We know that some of our competitors are developing also with colitis.
Development come and gone and other kinds of.
Diseases like type one diabetes like in.
And just a wide range for total addressable market I think.
You can you could be sort of incredibly broad right now where you could wait to see how we define it further as we pick up additional indications as we come out of this phase one later say in 2024.
Great. Thank you.
Thank you. Our next question comes from the line.
David.
One question you can't just go ahead David.
Hey, Thanks for taking my question I just had a quick one on the cotton 63, just with.
The way the ovarian cancer market is evolving kind of where you would see it slop and potentially I know, it's early stages, but I was curious on that thanks.
Oh, that's a tough one.
I think.
It's a market in flux, but still even with the agents that are coming on.
Even the response rates are still not that dramatic in people relapse fairly quickly, we think with the distinct target.
That you would be aiming to be the first time that patients see anything hitting this target I think you are going to start with the the later line in the clinic, but try to move forward pretty aggressively.
Nothing that slammed the door, certainly and I think that a cytotoxic agent like this.
Could have a lot of a lot of potential and I know that theres, a competitive landscape with adcs with other CD threes, but.
I still think theres, a wide a big unmet need.
I'll add with with a completely different mechanism of action and some of those other molecules I don't think theres.
Any emerging resistance against those therapies will really read too much on alto <unk> III.
Could you remind remind me at least maybe not all of us on the phone but is there a.
Hum.
Alright.
That's a requirement or a likely requirement for testing of our expression here or is it probably express I just can't remember off the top of my head.
We think it's definitely going to be prudent to very closely monitor for card Cisco suppression, Okay got it.
Some heterogeneity.
Yes.
Thank you.
Thank you. The next question comes from the line of Dana Leoni.
Raymond James.
Hi, Thanks for taking my questions.
Good luck.
Based on where you see that.
Barb.
Program.
Thank you.
Alright, Dan you were choppy.
Kelly for did you say, it's still a port PD one.
PD one.
In terms of clinical updates and progress.
You know as we said earlier, we're not guiding specifically on data timing until we get a little closer to events.
You know we've traditionally.
<unk> done that program late in the year, but we're not saying anything definitive yet we are enrolling well and our both of our phase twos are combination chemo phase two as well as our monotherapy phase II.
The first being in prostate only the second gen prostate as well as gyn tumors. So.
Well, we will update our well, we'll give guidance on data data timing a little bit later.
Okay. Thank you.
Thank you. The next question comes from the line of.
Cadbury Pullman.
B T I D.
Tahira Your line is open.
Hi, good afternoon, and thanks for the update and for taking my question just for IL to Al How do you think about that.
Given that there have been some disappointment in this space can you tell us about your approach and how it could be different from others.
And my second question is regarding with Allomap.
If you could provide more color on your trial amendment toward chemo combinations of course the RPC.
And you are enrolling 20 patients per cohort four different update can you tell us what you would like to see from these cohorts you lose all right. Thank you.
So maybe for the IL 12 question, John if you want to address our differentiation there yeah, yeah, well first of all I mean in terms of disappointments are all we have as you know.
Something about.
Assets being moved around.
I actually don't have any of the data from that study yet so it's really hard to interpret what that means.
But you know our molecule is very different.
It was.
Specifically designed following off of what we learned from our IL 15, and IL two programs. It was designed to have reduced potency.
To the tune of around 100 fold reduce potency and.
What we've seen in our preclinical studies very similar to what we've seen in the human studies for the IL 15, and IL two programs does that pose a reduction actually gives you a dramatic improvement in pharmacokinetics seems.
Seems to also impact Tolerability, and we hope it'll it'll positively impact therapeutic index.
Definitely saw evidenced in the nonhuman primates that we have a much more gradual dose response of the pharmacodynamic activity with our IL 12 than for instance, compared to a wild type IL 12, let's see so.
So we think we'll have a lot more flexibility in phase one to really zero in on the best.
Does that gives you the highest therapeutic index.
And I don't know if theres a lot of noise around other programs that weren't actually engineered cytokines being injected systemically things that are very complex like anaclitic viruses and localized delivery programs.
I just don't think there was a relevant comparator is I don't think those teach you anything.
Now onto your food Allomap question number two about the more on the trial amendment to the chemo as well as what we think the bar for success is roughly maybe Alan if you want to touch on that yes, sure. So just to remind people on the 700 704 study. The design remember we had several groups in there we had an aggressive variant group we had eight.
Naive margus recombination deficient groups August recombination deficient are treated group MSI High group and then a biomarker negative group. So it's really dependent on the group that several of the groups have chemotherapy and so depending on the chemotherapy regimen, you would expect a response rate of about 40% to 50%. So.
For most regimens you would want to see numbers above that however, some regimens like the aggressive variant or the PARP experience group the bar will be much lower.
Got it thank you.
Our next question comes from the line.
As Charles <unk> of Guggenheim Charles Your line is now open.
Hi, This is Edward on for Charles just a question on 56 four please.
How strong is that the mechanistic link between sort of inducing T. Reg levels as you've shown pretty clearly to actually having.
Sort of a beneficial effect on the disease.
There's two sets of data that read on that one fairly recent coming from actually one of our competitors. The raspberry program that Lilly presented last year showing.
Clear and convincing activity at reducing psoriasis as well as atopic dermatitis science.
Signs and symptoms and in particular, a really profound durability post end of treatment.
I'd say the other line of of evidence comes from really the last decade, and a half of work with low dose IL, two wild type <unk>, which sort of mimics a CD twenty-five selective molecule because of the debt. The high expression density and selectivity for T regs or very low doses about modest selectivity and theres efficacy that's been shot.
Hone in in.
Prior intractable autoimmune disease.
Ulcerative colitis like type one diabetes like <unk> like lupus like lots of other.
Indications. So those are the two threads of evidence at all as you know just going back to two real basics remember theres that disease, Aipac's, which were paid.
Patients have a defect of the Fox P. Three G, which is critical for producing T regs and that will all array of various autoimmune type diseases from having that disease. So from a very basic perspective.
Regs are critical for preventing autoimmunity.
Great. Thanks, So maybe just a follow up if I can on the one off for the PD. One class I think you mentioned in the press release that you were going forward with the <unk>.
Colorectal MSS stable expansion I'm. Just wondering are you also considering other potential expansion cohorts and kind of what pushed you to focus on that one at least for now thank you.
Right now, we're focusing on the MSS colorectal cancer.
Really looking for a larger number of patients than we had in our expansion cohorts to see if we have the kind of activity that would suggest a relevant path forward in MSS CRC.
You know what what so we don't have other indications right now we're focusing on on the CRC will disclose specifics at a later time, but we saw we saw in our expansion cohorts things that suggested MSS might be viable for this agent in particular in combination with linear map, which is how the study is designed in these.
Additional sets of patients and so we're eager to enroll it and gather the data and see.
Great. Thank you very much.
Yes.
Thank you. The next question comes from the line of Gregory Zhao.
From RBC capital markets go ahead Gregory.
Hi can you hear me okay.
Yes.
Great Hi, this is Neil on for Greg.
That's on the progress and thanks for taking my questions, maybe just on a high level just with your current cash position I'm wondering how are you thinking about business development as we have seen M&A heating up in the space.
How would you balance internal innovation and capital preservation in this cash cost Jamie on macro environment.
You.
Yes, we really do try to focus on having a high bar for putting molecules into the clinic.
Because the clinic is where the spend really hits you read our research is incredibly efficient on it both cost and people basis, and that's what's been able to drive so many partnerships. So many license agreements over the years.
But right now it's about being stringent about the molecules we put in the clinic and then getting even a even better more aggressive and faster about making quick decisions from our early clinical data to either advanced quickly or too to stop the spend by partnering I think you can see from our promote about deal a year ago that program is still progressing but now that's really in Jan.
Since hands.
So we try to balance that.
Holding onto the commercial rights for molecules of our own. So we can build the value of the company with the spend and we just wanted to be as fast and as nimble and as quick about the decisions we make because it is a as you write a capital constrained environment.
Partnerships have sustained us over many years the partnership's acquire another party involved and so that's unpredictable.
So I think it's we're being doubly stringent and strict about advancing programs and the design of our studies to be really efficient.
Yeah.
Thank you. The next question comes from the line of <unk> from band Brad Go ahead. Your line is open.
Yeah.
Yeah.
Your line is open.
Okay.
Maybe we'll go to the next question and see if we can circle back with him later.
The next line excuse me on stage is going to be Jonathan Chang from SBB Atlanta go ahead Jonathan.
Hey, guys. This is Matt copper on for Jonathan Thanks for taking my question I suppose just to piggyback on that last question on cash noticed that your R&D burn was a little higher this quarter I was just wondering if that's something we could expect.
Going forward as you sort of launched these early stage.
Programs and then second question is just I was wondering if you could provide any mechanistic rationale for the development of <unk>.
<unk> three <unk> in multiple myeloma.
Maybe John do you want to talk about the mechanistic rationale through six in myeloma.
Yeah, I mean it.
There's actually two components.
Gordon early good as we disclosed what about a year ago.
At expanding natural killer cells and so the.
The combination with their tumor mab.
Turns out that there are two of them have actually takes out some of the NK cells as it's as it's working and so that was sort of a natural idea genetics part too.
Try to explore the combination with X, Matt three or six months to expand the NK cells further to.
To sort of mitigate that sort of fratricide effect, hopefully it'll go beyond that and even further potentially a day or two of them out.
And then the other combination with the CD three engage your Savasta mab.
That's also just motivated by some of our preclinical work.
Recall natural killer cells are generally more sensitive to IL 15, because they express higher amounts of IL two receptor beta.
But it turns out we also were able to see pre clinically that when you activate T cells, such as with a T cell engaging <unk>.
You also up regulate IL two receptor beta and so it's really a natural question.
We admire the fact that genetic whatsapp.
<unk> hundred six with multiple different kinds of modalities to see where we.
It has the most utility.
And maybe on the cost question I wouldn't read too much into that quarterly fluctuations of the reported R&D spend.
I mean, John I think can you guide on our cash use this year cash is pretty consistent to address your question. It can be lumpy. The early stage R&D I mean, theres preclinical studies, but.
It's not going to be consistently increased court or to the extent that it was over the previous year.
Got it thanks for taking my question guys.
Thank you. Our next question comes from the line of Boris <unk> from TD Con go ahead Laura.
Great. Thanks for taking my question. This is Nick on for Boris I, just have a quick one on North America.
So you guys mentioned in the press release.
<unk> announced the phase III study initiation. So I was wondering if you guys are expecting potential milestone payments from this phase III like whether it comes to the end or whatnot and then also will you potentially receive royalties from this additional indication if it is approved.
We received royalties on any indication from any country that theres valid patent claims worldwide, regardless of the mode of administration IV sub Q.
And sorry, what was your first question on their phase III I missed that.
Yes.
Potentially receive any milestone payment from the phase III no theres no more clinical milestones left theres only a sales milestone left which.
We could get this year, we'll see.
Okay, great. Thank you very much.
Thank you. The next question comes from the line of Michael Kaye from ESI go ahead Michael.
Hey, guys. Thanks for taking my question most of my asset specific questions have been answered I, just wonder if John might.
Give us his thoughts on.
<unk> 28 versus <unk>, three by specifics, especially as applies to solid tumors and you know what are the odds of success and.
Solid tumors are going to be.
Greater fluid, one or the other or no real biology to predict.
You know what might succeed and what might not.
Yes, you asked me my favorite question in fact, I almost anticipated that this morning thinking about it.
Yes.
Easy the glib answer is we don't really know yet because there haven't been enough CD three's versus CD 20, eights and Theres, certainly hasnt been any sort of head to head studies against the same tumor associated Jen, there's nice validation of Cds reasons in solid tumors.
You know in a couple of different programs and there's really nice validation recent validation of preceding 20th of solid tumors.
But really to answer your question the way I think about how a differences might emerge. So a CD three engage was basically it's going to take any T cell that it can find either in the periphery or the perceived the tumor.
We don't know if those T cells or tumor reactive they could just be by standard T cells and it's going to utilize those that are at it yeah. It takes advantage of having all of those T cells around CD 28 really has to build off of an existing signal one.
And so if youre doing a combination with say a checkpoint inhibitor with the CD 28, the signal one actually come through the T cell receptor recognizing neo antigen peptides MHC complex is on the tumor cell.
So I'm guessing and that's just pure speculation.
That CD 20, eights would have potential for for longer durability.
Of response, just because youre actually building up a memory T cell response, you're specifically expanding those T cell tumor reactive T cells.
Okay. Thanks for taking the question John .
Thank you. Our next question comes from the line of Peter Lawson from Barclays Go ahead Peter.
Hi, This is Jerry on for Peter Thanks for taking our question. So just quickly first about <unk>.
So for the second study and the gynecologic tumors and high risk prostate could.
Could you maybe speak to us a little bit whether you're thinking of just Christine monotherapy or is this also going to be ultimately combo therapy.
And for that piece of an H day by specific could you maybe speak to where you see the highest chance of success in solid tumors and whether that might be prostate based on teradata and how you may see that fitting into such a competitive space. Thank you.
Okay.
I think it was the Dow lab, we expressly ran the state's two monotherapy, because we think there could be potential monotherapy.
In those gotten indications and in that slice of CRP C. I think Alan.
Alan can address some of the data we got an expansion cohorts are about why we believe that.
Yes, I was just going to add that so remember this is a 71705 study. So it's our second shot on prostate as a mono therapy, we defined the high risk prostate group clinically as opposed with molecular markers and then we're looking at guidance signals at an early marker in the expansion. The one thing is that we're looking at cervical endometrial as well as overall.
<unk> cancer, which is not unmet need and checkpoint inhibitors have shown activity and there hasnt been a lot of activity I will also add one of the neat things about the <unk> five studies that studies are a better dose and schedule. So we're doing a flat.
Dose every three week schedule as opposed to every two weeks and then the other question was around <unk> 780 <unk> III.
I'll take that yeah.
So yeah.
Yeah. It's a great question about a <unk> 73 for X mapping, a week, which solid tumor indications where he most excited about prostate for sure. It is right right at the top.
Theres, certainly nice validation targeting DCF at age three in prostate cancer and of course, we've got nice validation of CD 28 by civics actually working in prostate cancer.
Other histology step.
Would certainly think about would be small cell lung cancer based on some some proof of concept data, they're targeting PS seven H three.
But you know somebody squeeze expressed across a lot of different solid tumors and we're going to we're going to go to want to take a look at a lot of.
Great. Thanks, so much.
Thank you. The next question comes from the line adhesion.
Go ahead.
Great. Thanks.
Thanks very much for taking the question I also wanted to ask a question around on your CD 28.
Portfolio, obviously present, some clinical and preclinical data in H E. R. I wonder.
Your criteria in terms of selecting the other targets for your future molecules and also how you decide to move one or more targets into the clinic.
So the criteria is really based on.
Where we think CD 20, it could have the biggest impact we think thats in tumors that had been cold.
For immune checkpoint therapy, we think the example, given by the PSM ACD Twenty-eight data presented by Regeneron last year suggest that this CD 28 pathway could turn onto response tumors that would be cold. They did that in prostate cancer, albeit in a very small number of patients and so there's a huge unmet need.
And a lot of patients that would be ecstatic, if you could turn on.
Turn on tumors that are nominally pretty cold like small cell lung cancer like colorectal cancer like ovarian ovarian cancer like I mean, there's the list is longer than the list of tumors that actually respond well to immune checkpoint therapy, even the ones with some labeled checkpoint inhibitors are pretty pretty weak right like gastroesophageal.
Gastric H D C et cetera. So so we're focusing on targets, where there is that's a big big Delta possible.
It looks cole to checkpoints.
And where you could really maybe maybe change the landscape, but also where you could clearly see a signal early in clinical development. If you start seeing response. So I think that's important because we don't want to be lost in a in a sort of a swap of trying to deduce whether it's the checkpoint or it's the.
<unk> 28, driving the activity like you might be if you were enrolling patients in melanoma or RCC, which are pretty warm tumors.
Got it and just a quick follow up on the on the tech or technology side of things.
It appears all your CD 28 in Q3 by specific year ago Youre using.
Two plus one format.
Is it as to possible on your preferred format to going to go to other targets as well, whereas to decrease in 2008.
Yes, I would I would say is that two plus one as a tool.
It's just one of the tools in our tool kit.
Every targets different right theres, all kinds of considerations like density how.
How different is the expression on tumor cells versus normal cells.
We liked the two plus one for the <unk> because it gives us a little bit more we believe a room for it to.
Design in the therapeutic index to preferentially kill tumor cells versus normal cells, CD 28, sort of a little bit different and so where we think we want or need the two plus one we'll utilize that but.
One plus ones are also on the table for the <unk>.
Great. Thanks very much.
Okay.
Thank you for your questions I would now like to turn it over Q basal body hat for closing remarks.
Thanks, very much and thanks, everybody for joining us. This afternoon, we look forward to give you further updates later in the year.
Goodbye.
Thank you for your participation in today's conference. This does conclude the program you may now disconnect.
Okay.
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Okay.
Yeah.
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