CytomX Therapeutics, Inc. (CTMX) Earnings Call Transcript & Summary

So really quickly on disclosures. So for important disclosures, please see the Morgan Stanley research disclosure website. And if you have any questions, please reach out to a Morgan Stanley sales representative. So thank you all for joining. Welcome to the Morgan Stanley Healthcare Conference. I'm delighted to be sitting with Sean McCarthy, the CEO of CytomX. Thank you for joining us, Sean.

Thank you.

And I'm Ross Cohen, and I'm an Executive Director within the healthcare investment banking team.

So maybe just kicking off, Sean, why don't you give us a quick overview in terms of history around CytomX for those of us who maybe more -- less familiar with the story.

Yes. Thanks, Ross, and thanks for having us at the conference today. Real pleasure to be here. So CytomX is an oncology-focused biologics company, developing a platform technology and a pipeline around that platform called the Probody therapeutic platform. And this is a unique antibody masking strategy that we pioneered. In fact, I refer to CytomX as the original masking company. We got this whole field going really going back as long as 15 years. And the concept of antibody masking is to improve therapeutic window for highly potent anticancer agents like antibody drug conjugates or T-cell engagers, for example, we are currently in the clinic with 2 very exciting programs, EpCAM-targeted masked ADC, we call CX-2051 and a masked version of interferon alpha-2b, we call CX-801. And just making a ton of progress. So happy to be here today and talking about our platform and pipeline.

Yes. No, great to have you in a super exciting time. So maybe just double clicking on the masking technology for a minute. Can you maybe just walk into a little bit more detail around that? And also how do you think about ADCs as being one of the better applications of that technology?

Yes, absolutely. So the way the technology works and was originally conceived of is to take an antibody or indeed other biologics, for example, cytokines, and engineer them such that they are masked with short highly specific peptides. And the mask is designed to block the ability of the biologic to bind to its target until the mask is removed. And mask removal is achieved specifically and selectively in disease tissue and in our case, specifically in cancer tissue, by tumor-associated proteases. We've known for a long time that protease biology is dysregulated in tumors. Proteases are involved in tumor cell migration, invasion and metastasis. And we take advantage of that difference in protease levels in tumor tissue compared to normal tissue where proteases are very tightly controlled to allow us to activate the drug locally. So why is this useful? Well, it allows us to go after really innovative novel targets, tumor targets that are very abundant in tumor tissue but have been difficult to drug historically because they may also be a normal tissue. So for these targets and EpCAM is a great example of this, we're able to open a therapeutic window by using the masking strategy to bias towards tumor tissue and away from normal tissues. ADCs, absolutely one of the killer applications for the technology. There are a number of proteins, including EpCAM that are very abundantly expressed in tumor tissue that would be great targets for anticancer therapy except for the fact there are many normal tissues. And so enter CytomX and that's why ADCs have become such an important focus for us.

Yes. It makes a ton of sense. And maybe on the lead ADC program, the EpCAM ADC, maybe can you just describe the design of that molecule specifically and then the unmet need within colorectal cancer that it's looking to address and maybe beyond?

Absolutely. So EpCAM is a target that's been around for a long time. It was actually first described, believe it or not, in 1979 as a highly expressed protein on the surface of colorectal cancer cells. And it's very, very abundant in CRC. It's expressed at essentially HER2-like levels. So there are millions of copies per cell. It's expressed consistently and homogeneously as far as we can tell in every CRC, just about every CRC patient. However, as the name suggests, EpCAM is epithelial cell adhesion molecule and it's present on all epithelial structures in the body. So it's present on many normal tissues throughout the body. So many have tried to target EpCAM over the years but have not succeeded because of that expression in normal tissues. And toxicities have been observed at low doses with different strategies, including pancreatitis, liver toxicity, certain GI toxicities, and that's limited the ability of anyone to bring a systemically administered anti-EpCAM drug into the clinic successfully. But there are clues from other locally administered EpCAM strategies that if you can get an empowered potent antibody to EpCAM with local delivery, it can actually be very effective. There are 2 examples of this. One drug, a toxin fusion that has been shown to be quite effective in non-muscle invasive bladder cancer, but that drug had to be given intravescicularly into the bladder. And then the second example is actually a T-cell engager, a CD3 EpCAM bispecific which has just been reapproved in Europe actually for the treatment of a condition called malignant ascites. These are epithelial structures that form in the peritoneal cavity of patients with certain GI and gynecologic tumors. This EpCAM CD3, when given into the peritoneal cavity, it's quite effective at shrinking these tumors and treating these patients who have a very difficult experience with these growths. So -- so we know that if you can get an EpCAM antibody with some kind of payload on it, if you can get it to the tumor, it could be effective. The question is how do you do that with a systemic drug, and that's what we've done with our masking strategy.

Yes. No, that's actually a very interesting point you make on the peritoneal piece of it as well because these are not uncommon in colorectal mets, right? And those tend to be some of the more challenging tumor types or...

Correct, in many tumors actually, yes.

Yes. And so do you think that EpCAM can actually have a potentially differentiated role within that specific area as well?

I think that certainly could be something else to look at with 2051 over time for sure.

Yes, that's interesting. And then maybe you guys have showed some super interesting data back in May. Can you walk us through what the data looks like on some of the early patients? And then what are the expectations going forward there?

Yes, we're just super excited about the progress we've made with 2051 so far. So first of all, let me just recap the very intentional design of this drug. So obviously, EpCAM as we've discussed, is the target, very abundant in CRC. The masking strategy essential to localizing the drug into tumor tissue and mitigating the previously seen systemic toxicities with EpCAM therapies. And then thirdly, and really importantly, the effector on CX-2051. Of course, it's an ADC, and the effector mechanism is a topoisomerase-1 inhibitor payload. And the reason that we selected topo-1 inhibitor is, of course, because topo-1 inhibition is a central component of standard of care in earlier line settings in the treatment of colorectal cancer and specifically irinotecan. So we designed this drug very intentionally, the right target, the right payload, the right tumor type, using our masking strategy to really deliver in -- initially in late-line colorectal where the unmet need is just enormous. I mean it just -- and we can talk more about that later. But there's so much need in this field. So the Phase I study that we conducted, we focused entirely in CRC which was, I think, a bold move. It's a tough patient population for sure. But we decided to be -- we designed the drug to be evaluated first in CRC, so that's what we did. And in May this year, we reported our first clinical experience from the first year in the clinic, but only a year, the program has actually moved really very quickly. We had 18 efficacy-evaluable patients across 5 dose levels beginning at 2.4 milligrams per kilogram up to 10 mg per kg, the drug administered every 3 weeks. A late-line patient population, median number of prior therapies of 4. So this is essentially a fifth line CRC patient population. So very heavily pretreated. And we were just delighted to see really robust clinical activity in this very-difficult-to-treat patient population. First of all, confirmed objective responses in 28% of those 18 patients. And to put that in perspective, the current standard of care in the fourth line has a response rate of between 1% to 2%. So a huge step forward, we think, for the field, a very active drug, but in addition to the objective responses, most patients, in fact, just about all patients benefited from drug with a 94% disease control rate which translated into an initial assessment of progression-free survival of 5.8 months. Again, to put that number in perspective, the current standard of care in the fourth line has a PFS of 3.5 months. So a very competitive profile emerging for the drug in this first dose escalation. The drug looks to be performing exactly as we designed it. It's translated very effectively from our preclinical studies into the clinic. And on the safety side, we're very encouraged there as well in terms of what we've seen so far. This is the first in-human evaluation of the payload, we call it CAMP59. It's a payload that we licensed from ImmunoGen. So we are learning as we go with this particular topo-1 inhibitor, but we've seen an attractive safety profile with actually no dose-limiting toxicities during dose escalation, manageable hematologic tox with low rates of Grade 3 anemia and neutropenia. And in terms of other toxicities, generally well tolerated with perhaps the AE to watch going forward being GI. We've seen a little bit of GI tox, upper GI in the form of nausea and vomiting, which is fairly typical for topo-1 inhibitors, particularly topo-1 ADCs. And we saw a reasonable amount of Grade 3 diarrhea in patients about 20% across the 25 safety-evaluable patients. And that's something that we continue to learn about as we move forward, and we'll continue to understand and look to take steps to manage and mitigate. But overall, we're just so thrilled with this first look, the first year of development and just so excited now to push this drug forward as fast as we can.

Yes. No, really, really exciting data, and it's great to see. And so -- and then you briefly touched on that in terms of what comparator data could look like per se. But I guess, when you think about what a comparator in late-line CRC looks like, what are you really comparing to? And what are the typical results in the efficacy side? What are the things that they're also focused on from a safety perspective?

Yes. So in the fourth line, I mean the field has evolved a little bit over the last few years. We've seen approval of the tyrosine kinase inhibitor fruquintinib, specifically in the fourth line. That is now 1 component of standard of care, is 1 option for patients. And as I mentioned, fruquintinib was approved based on 2 placebo-controlled studies with a PFS of 3.7 months, an ORR of low-single digit, 1% to 2%. So fruquintinib doesn't really efficiently shrink tumors, but it does give a modest PFS benefit. Other options in the late line include LONSURF, which is trifluridine and tipiracil, monotherapy or in combination with bevacizumab, the anti-VEGF antibody, that's typically used in the third line. So by the time patients get to the fourth line, fruquintinib or maybe the other TKI regorafenib are options for patients. Our additional data with 2051 really has the potential to transform this field because we're so far our ORR and our PFS are so much better than current standard of care. We think that a potential fourth-line study that will compare ourselves to the current options in the fourth line could be executed very quickly, could be enrolled very fast, would have a, we think, a very high degree of probability of technical success based on what we already know about 2051. We're going to know a lot more by Q1 of 2026. We've already completed enrollment into expansions of 3 dose levels, 7.2, 8.6 and 10 milligrams per kilogram. Each of those 3 dose levels showed activity in the dose escalation with confirmed PRs at each of those levels and an impressive disease control. So we've expanded. We now have about 20 patients at each of those dose levels enrolled into the study. We'll have that data moving into Q1. And that's going to be really helpful to us and essential to understanding dose response, dose relationships as it pertains to adverse events, the degree to which adverse event management strategies that we've implemented in the expansion phase are helping us with the overall AE profile and integrating all of that into selecting our doses for this go-forward study that we plan to initiate in 2026.

Yes, no, makes a ton of sense. And I guess just shifting back to maybe the EpCAM point, you mentioned kind of the rationale for why EpCAM makes so much sense in CRC and the expression. But I guess as you look across the different lines of therapy within CRC, do you expect to see consistently high levels of EpCAM expression?

Yes, we do. We've done some work on this actually. So if you look in the public databases, there's a lot of information on EpCAM out there. It's been -- the target has been worked on by so many people for so many years. You can see in the expression data that EpCAM is highly expressed in all stages of CRC and it doesn't change as colorectal cancer advances. It's expressed in sort of stage 1 through 4. It's expressed at similar levels in primary tumors and metastatic tumors. And we've also begun to do some work within our Phase I study, looking at the kinetics, if you like, of how EpCAM expression looks over the course of treatment. And our data is still quite preliminary, but we're encouraged to see that so far that EpCAM levels are maintained as patients are maintained on drug. So it's a very stable antigen, we believe, which I think makes it another reason why it's such an attractive target. One other thing that I should mention about why we think EpCAM is such a great target for CRC is that in our Phase I study to date, we've confirmed that in every patient for whom we have an evaluable sample, EpCAM expression is indeed very high. So we haven't selected patients coming into the study for EpCAM expression. We don't think any selection will be necessary. This really does have the potential to be an all-comer drug. We also observed in this first data set in May that the activity that we've seen is across all clinical characteristics. It's independent of some of the typical clinical characteristics that can be used to segment the CRC population. So for example, whether patients have left or right-sided tumors or whether they have liver mets or not or whether they have KRAS mutations or wild-type KRAS. We see activity across the spectrum. And again, this has the potential to be an enormous advantage for this drug candidate because -- and this is how our investigators are seeing that they can bring any patient onto the study without having to spend time sub-categorizing them into specific clinical subsets. So we think that ultimately, commercially, this will be a great advantage and it's one of the great hallmarks of EpCAM as a target for CRC.

Yes. No, it makes a lot of sense. And so -- and then on 2051 on safety specifically, maybe -- and you walked through a bit of the initial safety profile, but if you can touch on that again and also focus more so on what -- how are those indicators in the masking technology might be working on your EpCAM ADC versus what you've seen in another situations?

Yes. Well, any time you take a new ADC into the clinic, you hold your breath a little bit. I think in particular with this one, given how broadly and widely EpCAM is expressed and what's been seen before with serious toxicities with previous approaches. So what were we on the lookout for? We were on the lookout in particular, for pancreatic toxicity because, as I mentioned, that was the roadblock that the first EpCAM strategies ran into. I'm very pleased to say that not only have we not seen any pancreatitis to date, we haven't seen any modulation of pancreatic enzyme levels either. So that, I think, is strong evidence that masking is delivering and keeping the drug masked and quiet, if you like, in systemic normal tissues. I think additional evidence that masking is working comes from the liver toxicity profile. So we've seen EpCAM agents in the past have significant liver tox in terms of elevating liver enzymes. We haven't seen a signal there either. And so I think the evidence that masking is working, I think, is really quite strong.

Yes. And I guess, how is that GI tox compared to irinotecan and other topo-1 ADCs?

Well, when irinotecan was first studied many years ago, it was first being used, it had a very high incidence of high-grade diarrhea. It was a very difficult drug to use. That's been optimized with different dosing strategies and regimens over the years, as you know. And is -- I mean, there still is significant GI toxicity with irinotecan, but it's -- oncologists have learned a lot about how to use it and how to dose it over the years. But it's a really important point that topo-1 inhibitors in general, whether the chemotherapy itself or in the context of antibody drug conjugates, they do induce significant GI toxicity. So we were on the lookout for this in our Phase I study and the fact that we've seen some GI tox is not a surprise at all. So the -- and as I mentioned, this is the first human experience with this particular payload, and one topo-1 inhibitor is not same as the next. They all have their own unique profiles in terms of how the toxicity emerges. Some have significantly more heme tox, for example, than ours does. But overall, I would say we've not been surprised by the tox profile, and we continue to take steps to learn more about it.

Yes. And then what have been some of the learnings maybe from most of the -- probably the oncology community as well and clinicians, but around mitigating some of those GI tox with other ways, too?

Yes. So this, of course, is not the first drug to have GI toxicity and specifically diarrhea as a signal. And there is a lot of precedent of strategies being used to manage and mitigate and in some cases, even use prophylaxis to treat patients early in their treatment cycle to minimize these types of adverse events. The types of strategies that have been used previously include anti-motility agents, like loperamide, steroid approaches like budesonide. And I'm thinking of drugs like neratinib, the HER2 inhibitor, which has a fairly high rate of Grade 3 diarrhea, those are some strategies used there. There's a study called the PRIME study, which was performed on TRODELVY, looking specifically at the ability of prophylactic loperamide to reduce Grade 3 diarrhea. And that actually was quite successful. It reduced by about 40% to 50%, the incidence of Grade 3 diarrhea for that particular topo-1 ADC. In terms of what we're doing in April this year, as we initiated our expansion cohorts or the expansion phase of the study, we decided to implement loperamide prophylaxis. So we asked our investigators still with a level of discretion because it's really up to them to manage every patient, to use loperamide where indicated upfront, to try to, yet again, get ahead of this fairly predictable AE of diarrhea.

Yes. And then final question on safety, I promise. But I think for last month, there was the Grade 5 event that you announced and so maybe can you just walk us through some of the details that you can share?

Yes, it was a complicated situation that we had seen a Grade 5 treatment-related adverse event going back a couple of months. This was a patient who experienced some GI toxicity and unfortunately, advanced to acute kidney injury and for various reasons, including other confounding clinical factors, including the fact that patient had donated a kidney earlier in their life, so had a solitary kidney, the patient ended up unfortunately not making it. And in reviewing the patient's clinical history with our Safety Review Committee very quickly after learning of this event, the Safety Review Committee felt that while this was likely an outlier event, the kidney injury, most likely secondary to the GI toxicities that we're seeing, and this can happen that patients with nausea, vomiting, diarrhea can become dehydrated that could put pressure on the renal system, and in this particular case, this patient having a solitary kidney, that renal pressure -- the pressure on the renal system was -- ended up just being too much. And again, other confounding features unfortunately contributed to this patient situation. So our investigators were of the view that, okay, this looks like an outlier case, study continues, no changes, except to more proactively monitor patients to ensure that we don't enroll patients that have donated kidneys previously, but no other significant changes to enrollment criteria. We felt that they were all fine. The challenging situation we found ourselves in was receiving or being notified by a few of our investors that there was a patient blog that they had come across that actually included some very specific details of this particular case at one of our clinical sites and so we -- which quite honestly, shouldn't really have happened, but we don't need to get into the details there. But it put us in a tough situation where we were getting a lot of inbound questions from investors. There were a number of other comments made in this blog that quite frankly, were inaccurate relating to study being paused, study being on hold, investigation with FDA. And so we quickly -- we quickly decided to issue a press release to lay out exactly what happened with this particular patient case and also set the record straight that the study was ongoing, that everything had been reported appropriately to FDA in a timely manner. And we had a lot of very constructive conversations and follow up with our investors over the following 24 to 48 hours, and I think everybody appreciated that transparency. It does I think, highlight in a way, kind of a new challenge that we all have to deal with as drug developers running public companies, which is that this public narrative that can appear in blog posts could be very, very difficult to deal with. And we're, of course, not in the business of responding to these comments. Typically, in this case, we felt that it was important to because there were just some real specific details shared and we were getting a lot of inbound inquiries. I think we made -- I'm 100% confident we made the right decision to disclose at that time. So in totality, though, as unfortunate as this case was with this particular patient, this adverse event is not out of -- it's not completely out of scope in terms of what we've seen with the drug already in terms of originating from some lower grade GI toxicities. And we know that's something we need to learn more about and manage with 2051 moving forward.

Yes. No. It makes a lot of sense. And so now that you've basically fully enrolled all 3 expansion doses, what is -- what do you view as the key criteria for now selecting a dose and next steps?

Yes. So really very interested to see a number of things from this -- what will be at least a 70-patient update. So we've enrolled 73 patients as of the last update. And that's consistent with guidance we've given since our May disclosure that we would have 70-plus patients of data in Q1, and we're absolutely on track, because enrollment went so well in Q2. And by the way, one of the other things you can see from these patient blogs is that people want to come on our study. These patients have very few options and they want to be on 2051. And even the patients who put all these details out there was frustrated and disappointed that they haven't been able to get on the study themselves. So enrollment went great. By Q1, we're going to have, I think, pretty significant follow-up on the majority of those patients in terms of follow-up on clinical activity. We'll have obviously an update on the response rate across the 3 dose levels of 7.2, 8.6 and 10. We'll have, I think, preliminary estimates at a dose by dose of PFS, which I think will be really important in helping guide us to the go-forward doses. And we'll also have an analysis of exposure dose response and exposure dose AE relationships. And I think that will all go into an analysis then of which dose or doses we're taking into our next study that, again, we hope to launch in 2026.

Yes. And just a quick follow-up to that point is how many patients do you expect there? And maybe how much follow-up do you anticipate to have?

Yes. So the expansions have all been enrolled to about 20 patients at each of the dose levels. And given that enrollment was complete as of August 13, our last update, we're going to have I would think 6 months of follow-up on the majority of patients which I think will be great. So we'll see -- we haven't decided exactly when in Q1 we'll disclose. We're keeping our options open at this point. But I think we're of the view that communicating data that's more mature rather than less mature will be most helpful for everybody. But we're still working through exactly when that communication will be.

Yes. And in terms of the benchmark that you're looking to hit as a driver for success there, how do you think about that when you're presenting?

Well, we think the numbers that we delivered in May were a great starting point. And obviously, we're -- we'll be very excited if those numbers remain in that ballpark. I think the 28% overall response rate across the first 18 evaluable patients, efficacy evaluable patients is a terrific start. I think there's room -- there's quite a lot of room on either side of that number, quite frankly, for this to be a very competitive drug. So we'll see how it shapes up. I think the 5.8 months of PFS again, if that is maintained, we'll be very happy, if it happened to improve a little bit, we'd be even happier.

Yes. And then do you expect the registrational pathway to require a randomized controlled study? Or could a single-arm study suffice? And maybe walk us through how you're thinking about the next set of studies?

Well, I think in the CRC space, we're not setting any expectations at this point for a single-arm accelerated approval. That's been a really tough bar with FDA in colorectal for a multitude of reasons. But we also feel that the time line to execute a randomized study, given the -- unfortunately, given the speed with which patients advance in this late-line setting, that study could be executed very, very swiftly. So one way that we're thinking, no decisions made yet, is that the next study could be absolutely a randomized study against physicians' choice or against fruquintinib, for example, in the fourth line, maybe 2 doses initially of 2051 because we really don't want to rush dose selection. I think it's an ADC, we need to be thoughtful. Perhaps we take 2 doses forward. Depends on what we learn from the expansions. If the expansions give us the answer, then we'll be taking 1 dose forward, but probably 2 or leaving our options open for 2. And that would be -- I think that study could very well have a basis for accelerated approval based on a PFS endpoint. That's how our current thinking has evolved. So -- but again, all these decisions about the design and structure of our next study will be highly informed by our data and will be data driven.

And then as you think about combinations such as bev, how do you fold those in over time?

So obviously, the late line is just the place to start with 2051 and represents, by the way, a major commercial opportunity. Even in the fourth line, we can see this being a multibillion-dollar drug. There are 12,000 patients at least in the U.S. treated every year in the fourth-line setting. And fruquintinib actually has done quite well in its first couple of years on the market with those numbers that I mentioned with 3.7 months of PFS. So we see the late line is a terrific opportunity, but we're highly motivated to bring 2051 into earlier lines of therapy where the numbers get very big very quickly. Yes. So third line, we will want to do some initial combination work with bevacizumab bringing the drug into the second line. We'll want to do some combination work with chemotherapy because the vision of the drug ultimately is to use 2051 in place of irinotecan to make a superior second-line therapy to currently the irinotecan containing chemo strategies. So it will be a progressive build over time. with combinations really being very, very important. And as we learn more about the safety profile, I think we'll learn more and more about the combinability of the drug in the earlier lines.

And then maybe more broadly, how do you -- what other indications do you think 2051 could work in beyond CRC?

Well, EpCAM has got so much potential. It's present in just about every solid tumor at some level including many tumors that are known to be topo-1 sensitive. So multiple places to go, including other GI tumors, certain gynecologic tumors, lung cancer. And so really, the ultimate vision for the drug is for 2051 to become a pan-tumor treatment. And so we look at the way that ENHERTU gained its pan-tumor label in HER2-positive solid tumors. In our mind, there's no reason why we couldn't go there with 2051 over time.

Yes. And then maybe shifting gears a little bit to CX-801, interferon alpha-2b, what should investors expect to see in the preliminary mono data update in the fourth quarter?

Yes. So we're really excited about 801. It's obviously, a different concept altogether. It's an immunotherapy, and it's designed to turn cold tumors hot and to restore responsiveness to checkpoint inhibition. We're conducting a very focused Phase I study in melanoma with 801. And again, just to remind everyone, it's a masked version of interferon alpha-2b which we know has some monotherapy activity in melanoma. So we're making good progress. We've advanced through several monotherapy escalation cohorts. The drug has been well tolerated. That's all gone fine. That allowed us to open up the combination arm with KEYTRUDA. We dosed our first patient with KEYTRUDA in Q2. And our goal for this year is to share some translational biomarker data on paired biopsies in the monotherapy arm, looking at regulation of interferon responsive genes, modulation of different cell populations in the tumor microenvironment by the masked interferon. So looking at -- our goal is to demonstrate that the drug is mechanistically doing what it should be doing, getting unmasked, activating the right cell types, inducing interferon responsive genes, really setting the stage for the combination to be effective, combination data, clinical data we'll plan to present sometime in 2026. So this update this year will be very translational biomarker, not planning any response data or safety data from the study. It will be very, if you like, sort of molecular evidence of performance of the drug in the early stages of dose escalation.

Yes. No, makes a ton of sense and that's super exciting. And so maybe we probably have time for 1 more question. And so maybe just taking a very quick step back. How are you kind of thinking about the next 12, 18 months? You obviously have a number of catalysts coming up as you kind of think about your financing strategy around that, as you think about nondilutive options around that. Maybe just walk us through a little bit your thinking.

Well, we've got a lot of work to do, that's for sure. We've got a really, really exciting drug on our hands in 2051. Top priority is now to get this expansion data and use it to formulate our next steps in clinical development in CRC to begin combination work to get the drug ready to come earlier in the treatment paradigm for CRC to evaluate which tumor types to potentially initiate additional work in other tumor types in the not-too-distant future. And all the way along, carefully consider our financing strategy. We were very, very pleased to be able to finance in May this year in conjunction with our data disclosure. But we've got a big program here that's going to have significant capital requirements. And so we're thinking carefully about what that future capital formation strategy will be. And of course, also thinking about when might the right time be to consider a partnership for 2051 because it does have the potential to become a very broad program very quickly. And I do feel confident that there will be a lot of interest from strategic parties in potentially collaborating with us. So a lot of work ahead of us. It's been an exciting year so far. And again, thanks for having us today.

No, of course, not. And thank you for joining, Sean. Congratulations on all the success. And we're looking forward to the next several months here, as always.

Thanks a lot, Ross.

Thank you.