Coherus Oncology, Inc. (CHRS) Earnings Call Transcript & Summary

Good morning everyone. It's still the morning. Thanks for joining us for another session at the 44th JPMorgan Healthcare Conference. I'm Brian Cheng. I'm one of the senior biotech analysts here at the firm. On stage, we have the team from Coherus Oncology. I will now pass the mic to Dennis Lanfear, who is our CEO, for a short presentation, followed by a live audience Q&A. Denny, the stage is yours.

Thank you, Brian, and thank you to the organizers for having us again. I'm happy today to give you an update on the progress of the company over the past 12 months since the last time we chatted with you at the organization. Let me first apprise you, of course, of the forward-looking statements and direct you to the company's SEC filings for comments specifically to LOQTORZI, Tagmokitug and Casdozo. Today, I'll talk to you about a few things, but I'll spend some time, first of all, talking about our evolution and transformation to an innovative oncology company focused on overcoming immune resistance in cancer. The cornerstone of our therapies is LOQTORZI, which is a revenue multiplier in our backbone PD-1. I'll then spend some time talking about a very, very promising asset that's in an evolving class of Treg depleters, Tagmokitug and give you a bit of a flyby on the mechanism of action and why this is such a promising new treatment paradigm. I'll also then talk to you about Casdozokitug, which is in first-line HCC in combination with toripalimab. And lastly, I'll spend just a moment underlying some of the data that we will see in 2026 in midyear across the portfolio. We anticipate a very data-rich year this year with our products, and I'm very excited to show you today. Let me first start now with a bit of a recap of the transformation that we've done with the company over the past 2.5 years. First thing, we, of course, licensed into our LOQTORZI in January of 2021 as our key product. But then we acquired Surface Oncology, and that transaction closed in September of 2023. Surface was renowned for its high science and its quality scientific advisory board. And with Surface, we gained global rights to 2 very promising products. First, Tagmokitug, CCR8 Treg depleter and then Casdozo. Directly thereafter, we initiated the complete divestiture of the biosimilar business through 2024 and 2028, which was also significantly successful. We divested the CIMERLI asset to Sandoz for about $175 million and then turn directly to the divestiture of the UDENYCA asset for $558 million, which closed in April of 2025, putting that then behind us. This is the total divestitures of about $800 million, done on a market cap of about $150 million, paying down $480 million in debt and dropping $250 million to the balance sheet to support the ongoing clinical studies that you will see today about 2 years of cash. There remains 2 milestones for the UDENYCA transaction outstanding, both for $37.5 million, one for $300 million look back 4 quarters to Q3 and one for $37.5 million look back in Q1 2027. Not included in the projections of cash, but I would say that those market opportunities are moving forward very well. And particularly in the hands of Intas, Accord, UDENYCA has achieved over 35% market share most recently. Coherus Oncology is about 3 key things: drugs, data and deals driving shareholder value creation. I'll talk to you about LOQTORZI and talk to you about our very elegant strategy to include LOQTORZI as a therapy with both Tagmokitug and with Casdozokitug. The data readouts you see in 2026 are significant and pivotal. We're undergoing perhaps 6 clinical trials with Tagmokitug across a number of cancers, GI and so forth. And Casdozokitug in first-line HCC. Deals have been a significant value driver for the company in the past with acquisitions and divestitures. We pride ourselves on our deal capability. Over 2026, you'll see additional deals, particularly as we seek to have partners with Tagmokitug, which I'll talk about in just a moment and provide you the rationale. We also have global rights to the pipeline to these 2 assets. So that means that we can do ex-U.S. deals, which not only bring in funding, but also give us partners to help offset the development cost. And of course, as you're already familiar, LOQTORZI has been subject to a couple of different U.S. supply agreements in which we put the product in the hands of collaborators. We pay for manufacturing costs, but then our partners develop product on their cost. Here is our pipeline. The key point that I'll make here is that toripalimab LOQTORZI is a revenue generator in the context of nasal pharyngeal cancer, but also our revenue multiplier in the context of combination with each of these other agents. It's indicated both with GemCis in the first line for NPC and in monotherapy for second line. And here, you see the other studies that are mostly in Phase II that I'll talk about today. This pipeline, together with LOQTORZI comprises about a $29 billion market opportunity for us, as you can see here, very broad across the pipeline, partnered indications across -- represent additional upside. And as I indicated, this does not include ex U.S. markets, which are roughly the size of the U.S. markets. Now let me just take a moment and talk to you about LOQTORZI and why that is such an important part of the strategy here at Coherus. I'm going to spend a little bit of time on the science, which I think is important for you to understand because I want you to appreciate the very high quality of this asset. LOQTORZI is a unique next-generation PD-1, which was conceived to bind the FG loop to PD-1 and do so with very, very high affinity. This results in the internalization of PD-1 from T cells. And as you can see, very, very high activity, particularly, let me focus you on the right side of the slide. And there, you will see in the low PD-L1 state, LOQTORZI having equal activity to the high PD-L1 state. This is important in the context of competition because here you see KEYTRUDA, which does not have such a label. So if you are going to combine your PD-1 with other agents such as Tagmokitug and Casdo, you want to start higher. You do not want to start lower or even even. This is really very, very important. And in particular, this esophageal data, I'll cite later when we talk a little bit about Tagmokitug. Now this data in NPC has very good effect. I would just point out to you that last month in December, the 5-year survival data. The 5-year survival data, just take a look at this for LOQTORZI was disclosed. And this has gone from 65 months to about 34 months. So a patient on chemotherapy survival of 34 months versus a patient on chemo plus LOQTORZI, 65 months. This sort of data has earned as top ranking in NCCN guidelines, as you can see in the right portion of the slide. And here, I'll just take a moment to show you how our commercial team is very successfully converting this in the market. Here, you see the growth on the left panel. This is demand growth quarter after quarter. Now there's 2 ways to look at how much LOQTORZI the market is using. The first is demand. That's actually going from the distribution centers to the physicians and being used. So this is probably the most relevant metric of utilization. And you can hear 16%, 19%, 12%, 15%. We've guided the street to 10% to 15% growth per quarter, and we exceeded that in 2025. The results you see now on the right side, is a doubling of revenues from 2025 over 2024, estimated $40.8 million versus $19 million. If you take the guidance of the 10% to 15% revenue growth per quarter, and you project that, we will arrive at our target of $150 million to $200 million by mid-2028. Let me now take a moment to talk to you about Tagmokitug, our highly selective best-in-class Treg depleter. Let me just take a step back. There's been really substantial progress, of course, in the past 10 or 15 years in immuno-oncology with PD-1s in treating patients. But 70% of these patients remain not to be treated. They are T cell deserts. These are places where either there is low or absent PD-L1 expression, there's a high infiltration of Tregs or there's low T cell infiltration. Many, many cancers then remain untreated, liver, prostate, colorectal, pancreas, as you can see. And this is where we are going to focus with Tagmokitug in the context of Treg depletion. This is the key to turning gold tumors hot and particularly to get CD8 positive T cells into the tumor microenvironment. Now CCR8 Tregs present a real problem in treating cancer and are predictive of lower survival in solid tumors. And on the left side of this panel, what you see here is that when you have high levels of Tregs, then you have lower survival outcomes. And on the right panel, what you see is this delicate balance. Tregs enforce immunological homeostasis systemically. But this creates a problem in tumors, particularly in the tumor micro environment. You must deplete the Tregs in order to allow CD8-positive T cells to infiltrate. And this has been the key focus of these Treg depleters, and this is some of the key data that I'll talk to you about now today. I would just lastly add at the importance and therapeutic potential of Tregs was underlined by the awarding of the Nobel Prize just this past year. Now Coherus prides itself on a scientific leadership as a small company in the Treg depletion space. And there's 3 key things I want you to take away from on this slide that are requirements for success with Treg depletion. First of all, you have to have significant Treg depletion from the TME and not in normal tissue. It has to be selective. It was discovered in 2016 that Tregs in the tumor micro environment have on their surface CCR8, a receptor. And if you were able to bind the receptor and use it as a place where you could then induce depletion of these cells, that would be very advantageous therapeutically. And you can see that here with the graph. We have successfully demonstrated such. The second thing you need is subsequent T cell infiltration. And thirdly, what you need is the activation of these T cells. Here's the surface of the CCR8, as I just talked to you about a minute ago. It's a very -- it's a GPCR receptor. So it's a very small amount of real estate that you have there. And the folks at Surface Oncology were very diligent and careful in bringing this forward. This particular asset was screened against 5,280 surface cell proteins in the proteome. The result, Tagmokitug is that it only is the only known selective CCR8 binder that has been disclosed. Unlike the comparators, which you see at the bottom of the center panel, where we take a look at some of the other competitive molecules have significant off-target binding. Tagmo has best-in-class potential. First of all, demonstrated proof of mechanism, significant depletion in the tumor of CCR8-positive Tregs. And it's the only one to show remodeling in the immune system. Secondarily, high selectivity and last, very strong pharmacology, high affinity, high potency with enhanced ADCC and excellent PK. This is really some very, very significant data that we disclosed last year at AACR. And on the left side of this panel in the green, what you see is the depletion of CCR8, which are in the greens, which you can see here. And you can see pretreatment, the green, and you could see post treatment with Tagmo, the almost complete depletion of these CCR8. What is really significant in what was hoped for, but not expected was the infiltration of CD-positive T cells. And you can see that here in the top panel, the red. And you can see how many enhanced T cells show up in this bottom panel. This is in a monotherapy patient in head and neck. So this is in a fourth line patient for head and neck. On the right panel, you can see in another arm of this very same study, a patient who received Tagmo, but also received toripalimab. And you can see a large 2.8 centimeter tumor in this patient's lung. So this is a head and neck metastases in the lung, which is then over 3 or 4 months by follow-up 3, almost completely decreted. This is a partial response. This is the first time such data has been shown where you have seen CCR8 depletion, T cell infiltration and subsequent diminution of a lesion. This data, of course, warrant an expansion of our program with our CCR8. And you can see here, we are prosecuting a very broad set of indications in 2026. First of all, as I pointed out, and I started, there is a significant issue with Tregs in the GI track, whether it's gastric esophageal and colorectal. And so we have programs in gastric. And I would say in all of these, we are combining Tagmo, our CCR8 with toripalimab. The rationale for this gastric is very compelling data in the hands of others on a background of toripalimab, I would add, positive clinical data in CCR8. So we feel very bullish about this particular indication. Two indications, both second line and first line in esophageal. And then colorectal, we're currently exploring fourth-line colorectal with -- in a non-liver met setting, and we'll be spooling up the liver met setting subsequent to that. And we are proceeding now, of course, with the head and neck study so on. Each of these data will read out during the course of mid- to late 2026. We got started in the colorectal little late, just in later 2025. That will probably read out near the end of '26 or early '27. Most of these, though, are mid-2026. Now let me take a step back because I've talked a lot about Tagmo or CCR8 in the context of toripalimab, a PD-1. But the important point to take home here is that it is not just of use in such a setting. Our strategy is to broadly develop Tagmo as the CCR8 Treg depleter of choice with partners across treatments. So as a small biotech company, what we were able to do is put our products even like LOQTORZI in the hands of others. And as they develop their products, we get that label also. We will pursue a similar construct with Tagmo because there are a number of therapies that other companies are developing, whether they be ADCs, T cell engagers, CAR-Ts or even radiation, where the proliferation of Tregs is problematic in stunting the efficacy. So there's a number of indications here. And let me just talk about one of these, which is T cell engagers. And here, you see it here. So yes, you have the depletion of the CCR8 Tregs and yes, you have infiltration of these C8-positive T cells. That is what you need, but you must have these T cells in the tumor microenvironment for the T cell engager to latch onto and to bring in proximity of the tumor cell. So this is a particular promise. We're exploring a number of these collaborations. You'll hear more about this over the next year or so as we go forward with these. But this is really the take-home message is that these sorts of applications are very, very broad, and we will not take a parochial view to it. We will take a very broad view. Let me talk a little bit about now Casdozo. And while Tagmokitug, we believe, is a best-in-class asset, Casdozo is a first-in-class IL-27 antagonist. Now IL-27 has some very interesting functionality. It's a cytokine. Cytokines, of course, regulate the immune system. But IL-27 has 3 key functions. First of all, it upregulates these various checkpoint receptors, PD-1, LAG-3, TIGIT and so forth. This is, of course, is very negative for immune response in the tumor microenvironment. The second thing it does is it downregulates all these pro-inflammatory cytokines. And thirdly, it constrains the behavior of natural killers cells and all the talk of T cells and so on, natural killer cells are sometimes forgotten. They are very, very important. And IL-27 does all 3 of these things. It's a response actually to pathogen invasion in barrier tissues, such as liver, lung, kidney, et cetera. And it plays a key role in those tissues. So this is data that we have just generated in HCC. And I'll just walk you through the waterfall plot on the left side of this, where you see 5 complete responses and 11 objective responses in this data. This is a 38% overall response rate and a 17% complete response rate. Equally impressive is the duration of the response, which you see on the right panel. The spider plot showing more than 2 years of duration for these patients. Keep this in mind as you see the trajectory here of the duration because this is something as we go ahead and we do the next part of this study and build on this, I won't build your expectations for how long they take this duration to develop. But this is very, very impressive. And here, you can see its comparison to the other standards of care, whether they're atezo/bev or various TKIs. And you can see how the overall response rate of 37.9% compares very favorably with, for example, atezo/bev, lenvatinib, TKIs and so on and also the complete response rate. Here's a study of my team is currently conducting. And this we will use, for example, toripalimab and bev instead of atezo/bev, we're exploring 2 different doses of Casdozo in this. This, again, is first-line HCC. The first patient was dosed last year, and we expect to see this data start to emerge in mid-'26, and then we will watch the duration expected to deepen as we go on further in the year. We're confident in using toripalimab for this. Toripalimab has shown significant efficacy. I talked about its mechanism of action being unique, significant efficacy earlier in the HEPATORCH study. We're compared very, very favorably against TKI. So before I take the questions, let's just have a recap here of our progress. The value proposition, our drugs, LOQTORZI, our cornerstone product, a very active next-generation PD-1, particularly active in low PD-L1 states in esophageal, we're subsequently exploring with Tagmokitug. Tagmo, which we believe is the best-in-class CCR8 antibody being developed across a number of indications in our hands in conjunction with LOQTORZI. But also, we will reach out during 2026 for collaboration agreements with others in which we will put it in their hands and also get further development. And then Casdozo, a first-in-class asset that is moving forward, I think, very successfully in hepatocellular carcinoma. This data all will reach readout in mid 2026 and beyond. And then lastly, I'd again just mention a few things to the deals. Our deal efficiency, I think, is quite good in terms of acquisitions, divestitures, collaborations and so on, you'll see more of these, these are all value creation exercises for our investors. In particular, as the data evolves from these clinical trials, you'll see us do ex U.S. licensing exercises, which will actually help us offset long-term development costs for the global programs. And with that, I'll just stop for just a moment, and thank you for your attention, and then we're happy to take some questions from Brian and just introduce my Chief Scientific and Development Officer, Dr. Theresa Lavallee. Thank you.

Great. Thank you for joining us. [Operator Instructions] Just to kind of kick off the conversation here. As you think about last year, you have done a lot of move to really reposition yourself. How do you think about 2026? Where do you think 2026 is going to lead Coherus Oncology? There are multiple data catalysts ahead of us that are spread across 2026. What are you most excited about?

Thanks for the question, Brian. I think we're very bullish on 2026. I think things are really coming together very nicely. Let me first just make a comment about LOQTORZI and how pleased we are that the sales are very, I think, systematically marching up towards our target in 2028. That gives us assurance that we'll have very strong financings as we go forward. But I think with respect to the 2 products, and I'll let Theresa chime in just a little bit. I think that we are following the science with respect to where the T regulatory cells really are present and where they are a problem. It's substantiated, I think, by all the data. And I really like the data in Casdozo. So as I look forward, I'm very excited about the gastric cancer study with Tagmo. I think that's -- that has already been done once. And so I think there's a very strong, probably, a success there. But I also like HCC with respect to Casdo. Theresa?

Yes. No, I agree. I think it's a data-rich year for us, and it's an exciting progression from the pipeline. So for Tagmokitug, I mean, I think the studies designed are very intentional to really learn where is the best setting. I mean, the data we've seen to date with the CCR8 depletion has shown this is a good drug. Now we need to figure out the best setting and the risk combination to advance it into more mature studies. And these studies will really inform us, including the dose selection. So dose optimization is a key aspect and development. The Casdozokitug study, I mean, we're just trying to build on the very nice preclinical, so strong translation to high expression in liver cancer, preclinical models showing selectivity in 3 different models where we see activity when the tumors in the lung or the liver, not in other locations and then that translation to humans with a very nice safety profile that CCR8 stands out in all treatments in liver cancer. And the safety profile is so important in this disease where these patients are so beat up. So that readout -- a positive readout from the randomized study that's ongoing now would set us up for a pivotal study. So I think a lot ahead.

And I guess just maybe switching gear and looking at Tagmokitug, your CCR8 asset. It's interesting that there are other CCR8 that are out in the space and others are running really large studies, too. Where do you see yourself differentiating in this space? And can you talk about just a molecule itself? I mean, how much do you know now in terms of differentiation?

Sure. Like pharmacologically, we do have differentiation, the most notable being the selectivity in the potency. So from the screen, I mean, it's well known that GPCRs are druggable. 1/3 of FDA-approved drugs are against GPCRs. But there's only like 5 antibodies approved because it's tough, right? Dennis showed you the structure of the molecule, getting that -- there's a small amount of the protein exposed and the confirmation to get that selective binding is really hard. And we saw that in the screen even for lead identification. We were -- the molecule we advanced to the clinic was the only selective binder. Others have shown that they have off-target binding. We have characterized some and identified off-target binding. Off-target binding obviously can complicate development with toxicity, PK, those issues that can show up during development. The potency is also a standout, both from the affinity with the binding and the picomolar range as well as being ADCC-enhanced. Not all molecules have that enhancement. Shionogi showed really nice data at ASCO with a CR and PR in colorectal cancer, MSS, CRC, super exciting. They are a wild-type IgG-1. So I think those features as well as the commutation with toripalimab and looking at novel combinations will really set us up to differentiate and advance this competitively.

The other point that I would make to complement Theresa's remarks is that when it became known that the CCR8 was the ideal binding target for Tregs in the tumor micro environment, many team rush to the fore to bring products forward into development. Some of those teams now are having trouble. For example, there's teams that have dropped out. And if you take a look, they had inadequate PK really to support a therapeutic indication or cross reactivity. And so I think with something like this, it's more important to be very deliberate and careful with your development than it is just to go fast and sort of just do a lot of patients. Big pharma can afford to do thousands and thousands of patients and throw the spaghetti on the wall, but that's not -- that's really not a strategy that we endorsed at all. I think we're quite deliberate. We have to really just follow the science, and we think that's the best way to be best and not really to be first.

There was this one slide that I find interesting is you see Tagmokitug being -- you're positioning it as the depleter of choice, right? So how do you leverage partnership over time to get you there? Can you talk about perhaps for some of the ideal modality that you should shoot for? And then -- and also where are you in the process in lining up these additional partnerships to make sure that you will be the CCR8 of choice?

Let me -- I'll let Theresa handle the back half of that question, but let me handle the first half of the question. I think that it's first very important shows strong data, and we have been at the forefront of producing data. We are the first U.S. team that show CCR8 depletion and then subsequent T cell infiltration and then a response. So in that regard, that generated a lot of interest in pharma. And so we're having conversations with a number of teams. But I think that the Tregs are -- that's an approach that is very broadly applicable through a number of modalities as you can see here on the slide. I would probably manage your expectations that over the next 6, 12 and 18 months, you will see these kind of agreements come forward. As a small company, as I indicated in my earlier remarks, we can do these sorts of arrangements collaboratively and so on, where I think perhaps larger companies are less willing to do so. But there's certainly sufficient scientific rationale to have conversations with a number of folks, perhaps Theresa wants to make some additional remarks.

Yes. I think that looking at the T regulatory cells that have been studied for years as poorly prognostic, a resistant sector, I mean, Tregs are upregulated with wound healing, so chemotherapy radiation. I mean it's well characterize that PD-1s and radiation are compromised in efficacy due to upregulation of Tregs. So that's a rational combination science-driven. I mean, as Denny showed in the immunofluorescence slide, having that many CD8s in the tumor poised to be activated really lends itself to strong scientific evidence to combine with the T cell engager. The bane of development for those in solid tumors is really getting enough T cells in the tumor because they are limited by the ability they have to tickle the tumor on one side to bind and then tickle the T cell on the other. Well, if it's not -- if the 2 aren't closed, they can't activate. I mean we've seen phenomenal efficacy with T cell engagers in heme malignancies and starting in solid tumors. So really improving on that is something exciting. CARs are another example that have had real challenges getting into solid tumors. And then even bispecific molecules could be very exciting. So we see broad applicability and are energized to really explore those combinations from safety and efficacy.

Any questions from the audience? I guess as you think about the upcoming data readouts, can you give a sense -- a sneak peek into what to expect? What would be good data for you to move into the next stage of development? What should we be expecting?

Yes. No. So I think what we're looking for is, again, I want to recap what we've shown to date. We've shown strong pharmacokinetics impressive pharmacodynamics, proof of mechanism that full depletion of Tregs in the tumor. So we have the right dose. So defining that and further characterizing the safety profile, which has shown an absence of dose-limiting toxicities to date and really acceptable safety and convention with toripalimab. So now looking for efficacy, we've seen response. We've reported a response from the safety cohort in head and neck. Now do we have sufficient activity to reach benchmarks. We're aware of the field. We're watching the competitive landscape with IO and other bispecific molecules and ADCs. And so I think that this -- overall, what we'll see from these studies is where is the tumor type that really lends itself to overcome PD-1 resistance because that's what we're asking. We're taking patients who have progressed in head and neck and gastric and esophageal on PD-1, given a PD-1 again with a new drug. So our T regulatory cells the primary resistance mechanism to that be a therapy in that line of therapy. We're also looking at combination with chemotherapy to show safety so we can advance to the frontline setting. So we're looking for where is the fastest development and the best efficacy to really pursue in larger studies.

And turning to Casdozo. There's going to be HCC data coming up in the first half. Can you talk about just -- I guess, the response, whether -- how confident are you that you already saw some response with atezo plus bev combination. How confident that the response that you saw there will also translate to your current combo work with tori and bev?

Yes. I think the strength of the data from the mechanism and the preclinical and the clinical data, tori, bev, I mean, we've seen PD-1 VEGF inhibition, PD-1, CTLA-4 translate very nicely across the class in first-line HCC. Now we're looking to advance beyond that with the triplet. So seeing initial ORR. So I'll remind people that Casdozo data when we first looked at it in June of 2023, the ORR was 27% and 0 CRs. So what we're looking for in the initial data set is maintaining that safety profile, no added new or added toxicity to PD-1 plus VEGF, a comparable ORR. 6 months later, we saw an improvement in both depth of response and ORR, 38% response rate and 3 CRs. A few months later, 5 CRs that continue over 2 years. So the initial data set, we want to see benchmarked activity for PD-1 VEGF and patients to stay on therapy to look for that improvement in depth and ORR.

Got it. Maybe just in the last couple of minutes we have. I also want to touch on your LOQTORZI franchise. Denny, can you talk about where we are in terms of sales trajectory? I'm curious if you can give us some color in terms of the adoption dynamics that you see on the ground. How confident are you that you can get to that $150 million to $200 million goalpost?

Thanks for the question. We're very confident. I think we have a very firm understanding of the market at this point. We understand the market drivers and what goes on. Regarding the NCCN guidelines, having such preferred positioning has been very, very helpful. So when that first occurred in November of 2024, it resulted in an immediate and substantial increase in penetration, particularly in the academic setting in Q1, which then went into Q2. This year, I think that the survival data out to 65 months from 34 months will be equally impactful. So we're looking forward to that educational process with the physicians. However, I would make the point that the -- in academia, the physicians are very proficient regarding NCCN guidelines and standard of care and evolving practices. This is a rare disease forever, there's only 2,000 patients. So that means that the community physicians see perhaps a patient every 1 or 2 years. The rest of the time, they're seeing breast cancer, lung cancer and all these more common cancer patients. So it is more difficult to have the opportunity to educate the community physicians. So we have to reach out to them. So what we have done is put in place a sophisticated system of alerts. Last year, we were able to detect about 30% to 35% of the alerts and the patients that are diagnosed by receiving data on the diagnosis codes. This year, we just completed a project in which we grow up to 65% or 70%. We've also enhanced our team with additional head count to reach each of these physicians as they get a patient. And then lastly, as per the label, we're able to put patients on LOQTORZI who have already started chemotherapy. So you saw us march up 10% to 15% per quarter, as I showed you earlier on the slides, we feel very confident we can do that. We do that. We'll go ahead and we'll hit the midpoint of the $150 million to $200 million by mid-2028, just mathematically. But overall, I think the table is set, the strategy is sound, the people are in place, and I think we understand the market very well.

Great. Thank you so much for your time today. It's a great pleasure to have you guys. Thank you.

Thank you, Brian.