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

Welcome, everyone, to the 44th Annual JPMorgan Healthcare Conference. My name is Anupam Rama. I am one of the senior biotech analysts here at JPMorgan. I'm joined by my squad, [ Rathi Pinhe ], Joyce Zhou and Priyanka Grover. Our next presenting company is CytomX and presenting on behalf of the company, we have CEO, Sean McCarthy. Sean?

Thank you, Anupam, and thanks to the JPMorgan team for the invitation to present. It really is a privilege to be here. I'm also joined by the squad. Chris Ogden, CFO; Rachael Lester, Chief Business Officer, and I see at the back, Wayne Chu, Chief Medical Officer. So once again, real pleasure to be here. Last year 2025 was a super exciting year for CytomX. We don't expect 2026 to be any different. We're working hard on building a highly differentiated pipeline, and the theme of what I'll talk about today is unmasking advances in oncology. The clicker doesn't seem to be working. While, we're doing that, I'll say that in the course of my presentation, I will be making certain forward-looking statements, and I refer you to our SEC filings. Thank you so much. So CytomX is a South San Francisco-based oncology-focused biotech company. And for the last 15-plus years, we have been developing, optimizing and applying our highly unique Probody therapeutic platform which is a novel strategy for masking antibodies and improving therapeutic window. We are the leader in this field. We have been for a long time, and we continue to lead this entire strategy. We currently are highly focused on 2 clinical programs for Varsetatug masetecan, which is our EpCAM-targeting Probody Topo-1 ADC, which we're developing in colorectal cancer and CX-801, which is our Probody version of interferon alpha-2b which we're currently developing in melanoma. We're in a robust cash position. We're funded well into Q2 2027. We completed our most recent financing last May that runway excludes any potential milestones or new business development. And we have been very active in business development over many years, resulting in a number of very high-quality partners, including BMS, Amgen, Astellas, Regeneron and Moderna. And I am privileged to work every day with 70 outstanding employees, and we have integrated R&D capabilities again at our South San Francisco HQ. So over the years, we have learned a lot about how to mask antibodies and other therapeutic modalities. And as I said, we've really CytomX has achieved every first in this field. And over the years, we have built the foundation of knowledge to allow us today to really have the most focused strategy for product development that we ever have. We are leveraging the technology to really think deeply about the right combination of what's the clinical problem you're setting out to solve? What is the target on the tumor that you're going to go after? And then what's the effective mechanism? What's the best way to actually affect cell killing in the context of that therapeutic challenge that we're taking on. And in the context of our 2 lead programs, they're both really great illustrations of this focused strategy. So first of all, the EpCAM Probody, which we now refer to as Varseta-M or Varseta that's how you'll hear me refer to it as I go through my presentation. This is a very focused strategy. colorectal cancer, EpCAM is the target. It's an antibody drug conjugate and the payload is a Topo-1 inhibitor. I'll have a lot more to say about that in a moment. The second program, CX-801 interferon alpha-2b, tightly masked to enable opening a therapeutic window for this highly potent cytokine, which really is 1 of the most powerful modulators of the tumor microenvironment, and we're developing it in a very focused way in melanoma. I'm not going to say a lot more about the platform from here on other than we really have figured out how to mask antibodies in a protease-dependent way. And the way the platform works, involves masks being removed in the tumor microenvironment, specifically and selectively by tumor-associated proteases. And we've gone very deep into this technology over more than a decade. Our platform has driven a highly differentiated pipeline. Let me just briefly lay out what we are highly focused on today as a company. With regards to Varseta-M, our EpCAM targeting Topo-1 ADC, we are expanding the Phase I study to encompass more than 100 patients. We are on track for a data update by the end of Q1 of this year. Our first data was presented, as you probably know, in May, of last year, which I'll recap briefly in a moment. And in the context of that 100-patient expansion, we're looking, of course, to further substantiate the very strong efficacy that we saw in late-line colorectal cancer with Varseta also further understand the safety profile, how to understand and manage the safety profile, how to model go-forward doses, how to plan for our first registrational study in late-line colorectal cancer, begin to move the drug into earlier lines of therapy. And in that regard, we have commenced a combination with bevacizumab. We are commencing that during Q1 and also to explore additional tumor types because EpCAM is present in many, if not all, solid tumors and really represents a remarkably large opportunity in oncology. We're also working hard to advance CX-801 to proof of concept in combination with KEYTRUDA by the end of this year. So I'll turn now to Varseta, our EpCAM-directed Topo-1 ADC, which we're developing in CRC. I don't need to tell you that antibody drug conjugates have transformed the treatment of many tumors initially hematologic tumors increasingly solid tumors. And we're seeing ADCs come earlier and earlier in the treatment paradigm and increasingly show opportunities to actually replace systemic chemotherapy in a wide variety of regimens across a wide variety of tumor types. Varseta-M is bringing the potential and the power of antibody drug conjugates to colorectal cancer. Colorectal cancer remains 1 of the biggest unmet needs in oncology, 1.9 million patients per year diagnosed around the world, that's going to grow to more than 3 million patients by 2040. It's the second leading cause of cancer death worldwide, and 5-year survival in patients with metastatic CRC is a dismal 13%. This is an enormous market. And in fact, colorectal can be considered the largest by far, untapped, solid tumor market after the last 20 years of innovation in many other tumor types, including, of course, the immunotherapy wave, which is really yet to make impact in colorectal. In the third line alone, we have 45,000 treatable patients in the United States, resulting in more than a $5 billion market opportunity. These numbers are very big. It's a very large untapped market. And I would say it's also an untapped market that is beginning to attract attention from large pharma after many years of really very little innovation, we are starting to see innovation and CytomX is at the leading edge of that innovation wave with Varseta. Varseta targets, EpCAM epithelial cell adhesion molecule. This is one of the most broadly and abundantly expressed tumor antigens that we know of. It's been known a long time that EpCAM is present at very high levels on colorectal cancer. In fact, it was first identified as a CRC marker. It's uniformly and highly expressed across CRC across all stages of CRC and the challenge with EpCAM has been, it's present on most, if not all, normal epithelial structures. So approaches to target EpCAM in the past have hit significant toxicity roadblocks very early in their development because of EpCAM expression in normal tissues. For example, the T-cell engager solitomab developed by Micromet and Amgen ran into significant GI and liver toxicities at very low doses and was discontinued early in development, was unable to get to therapeutically active levels of the drug. We do know, though, that if you can get an empowered EpCAM antibody to the target in a patient with local delivery, it actually can be effective, and this is illustrated very well by a drug called Korjuny, which has recently been relaunched in Europe for the treatment of intraperitoneal malignant ascites but the drug has to be given locally because systemically, it's too toxic. This is really important because it shows that engaging EpCAM can result with the appropriate empowered antibody in potent antitumor activity. So we designed and developed Varseta, a novel EpCAM targeting Probody ADC to target EpCAM systemically ultimately across a wide range of tumor types. So the molecular design is shown here. The -- this is Varseta is based on a high affinity anti-EpCAM antibody which we have masked using our protease-dependent peptide masking Probody strategy designed to minimize binding in normal tissues. The mask is removed within the tumor, allowing binding and engagement with target and delivery of the effector mechanism. The effector in Varseta being a novel topoisomerase-1 payload called CAMP59 that we licensed from ImmunoGen, it's a novel linker as well, a tri alanine cleavable peptide linker optimized for bystander effect. We have a drug antibody ratio of 8. We really believe with this drug candidate, we have the right target, the right indication and the right payload. The current standard of care in late-line metastatic CRC is highly inadequate. The options available to patients result in objective response rates in the low single digits, progression-free survival of 2 to 5 months. And these agents are really the best that's currently available for the treatment of patients after they've exhausted chemotherapy strategies. We must do better. And we are doing better. So our data that we shared last year, May 12, 2025, was a very strong start with the development of Varseta. We showed in a patient population with 4 -- median of 4 prior lines of therapy, a 28% confirmed overall response rate, 94% disease control of 5.8 months of preliminary progression-free survival, showing us very early in the development of this drug after just 12 months in the clinic that we have the potential for Varseta to become a new standard of care in the treatment of late-line CRC. We also were able to treat every patient enrolled in the study or enroll patients regardless of clinical characteristics, as I'll show you on the next slide, because EpCAM is indeed expressed at very high levels in every patient. We also demonstrated a favorable safety profile with no EpCAM toxicities, the types of toxicities that have limited EpCAM in the past. So a really exciting start. And I have to show you the waterfall plot from last May because this has excited us and a lot of other people in the oncology community and in the investment community because this is the type of waterfall that you just don't see in late-line CRC. This is essentially a fifth line CRC patient population. And you can see the depth of these responses across multiple doses. And also, I want to point out here, if you look at the bottom of this chart, we've enrolled patients, as I said, just now independent of their clinical characteristics. Over the years, CRC has become an indication where patient selection based on specific pathways or specific mutations or specific targets has become fairly typical, for example, whether or not a patient has liver metastases, whether or not a patient has a left sided or a right-sided tumor whether or not a patient has a KRAS mutation. But you can see that we have activity across the board, and this is a huge advantage for this drug once it reaches the market because it means that no patient selection should be required for the selection of patients to treat with Varseta so a really exciting start, and to position that activity relative to the current standard of care in the late line that I just showed you, we have a wide window in terms of comparing to the existing benchmarks. 28% overall response rate, 94% disease control, 5.8 months of PFS. Of course, too early to comment on overall survival that will come over time but a highly competitive profile for further development in late-line CRC. On the safety side, the safety profile that we presented is encouraging, the -- rather remarkably, we have not seen any evidence of the classic EpCAM toxicities of pancreatitis and liver enzyme elevation, strongly suggesting that masking is delivering. This is the first time that a systemic anti-EpCAM antibody therapeutic has successfully demonstrated antitumor activity and it's an ADC to that. So we're a long way ahead now in terms of being the only -- not only the only anti-EpCAM therapeutic antibody but also the only anti-EpCAM ADC. So we've really broken through, we believe, on the target. In terms of the safety profile, we're encouraged so far. AEs generally manageable and reversible most grade 1, grade 2. As I said, no signs of pancreatitis or serious liver tox. No evidence of ILD, which has been a challenge for a number of Topo-1 ADCs, as you know. An attractive hematologic profile, low rates of high-grade anemia and neutropenia, which may be attractive for future combinations. The most common treatment-related adverse event we saw in the Phase I study so far is diarrhea with a 21% to 22% rate of grade 3 diarrhea. That is something that we're laser-focused on understanding more of as we expand to this 100 patient data set, including evaluating prophylaxis of patients to try to prevent or reduce the incidence of high-grade diarrhea in these patients. And that's really the 1 safety signal that we have with this drug to really learn more about. In terms of where we are and where we're going, we're currently expanding the Phase I at 3 dose levels, 7.2, 8.6 and 10 mg/kg. Those together, those expansions will reach 100-plus patients by the end of Q1. Our goals with the expansion update, which we'll give by the end of Q1 will be, of course, First question, does that level of efficacy replicate in a larger patient population across these different dose levels? And secondly, how much more have we learned about the AE profile and specifically the GI toxicities and the role that prophylaxis can play in managing patients through their course of treatment. I also anticipate that in this upcoming update, we'll have a preliminary assessment of progression-free survival at each of the 3 doses, which will be very important in helping us pick our doses or dose for moving into a potential registrational study, which is our -- really our top goal as a company today is to move Varseta as quickly as we possibly can into a late-line colorectal registrational study. There's a very broad development opportunity for Varseta in metastatic CRC. Of course, we're beginning in late line, and that's where we believe this drug can first be registered and where it makes the most sense to run that first registrational trial. But we're very motivated to bring the drug into earlier lines. And as I said, we've already initiated the combination with bevacizumab with the goal of bringing the drug into the third line, potentially even into the second line, where our vision is to replace the irinotecan component of combination chemotherapy. This is very consistent with what we're seeing across the board with ADCs and solid tumors coming earlier and earlier in the treatment paradigm and beginning to replace components of chemotherapy in earlier lines. Beyond colorectal, EpCAM is expressed in just about every other solid tumor. This is why there have been so many attempts to drug EpCAM in the past that unfortunately have failed. Given that we've broken through in CRC, in a way, I think you can argue fairly strongly that we've done the hardest experiment first. It's a very, very difficult-to-treat tumor type, and we have remarkable levels of activity in that patient population. But shown here is just a few examples of solid tumors where EpCAM is highly expressed. And in the second half of this year, we aim to start work in non-CRC indications. And over time, you could see how an anti-EpCAM ADC could potentially move towards a pan tumor agnostic label, a little bit like ENHERTU has, for HER2. It's going to take a little bit of time to get there. But it absolutely is on the horizon. So the multiple layers of value creation that we see for CytomX that are unlocked by Varseta are shown here. First of all, get the drug approved in late-line CRC, get the drug launched. And in third line plus more than 35,000 patients in the U.S. alone, this is a significant, as I said earlier, more than $5 billion market opportunity that we can tap into by getting the drug registered in that late line. Move to combinations to replace chemotherapy in the first and second line and then expand into additional EpCAM indications. And the patient numbers get very large, as you go from left to right on the slide. And accordingly, the commercial potential is really very, very big. So quickly, mindful of time, I'll move to our interferon alpha program, which is a novel immunotherapy focused in melanoma. A little bit like EpCAM, interferon alpha-2b is an old friend. It's been around a long time. It actually was the first immunotherapy to be approved in 1986. It's fallen out of use because it's severely toxic, patients do not tolerate interferon alpha very well at all. It does have single-agent activity in multiple tumor types but it really has receded into the background in the context of clinical oncology because it's just so difficult to use. But interferon alpha is a very potent and multifaceted modulator of the tumor microenvironment, the immune microenvironment, it does a lot of different things to the immune system. It can activate antigen presentation, can modulate NK stromal cells and vascular cells and also has direct antitumor cell killing ability as well. So it's a very differentiated cytokine from IL-2, IL-12, IL-15, very potent. And if we can harness its activity. We were very encouraged a number of years ago by the data with the gene therapy Adstiladrin that showed that local delivery of interferon alpha-2b in nonmuscle invasive bladder cancer can be very effective in shrinking that particular tumor type. That gave us the impetus and the rationale for making a masked version of interferon alpha that by localizing into the tumor could potentially unlock the potential of using interferon alpha as a centerpiece of immunotherapy to turn cold tumors hot. That's essentially what we're trying to do with this drug. So we've applied our protein engineering strategies and our masking strategies to make a very tightly masked version of interferon alpha-2b. It actually has 2 different masking strategies that we're leveraging. First of all, protease-dependent peptide masking on the cytokine domain at the top of this cartoon. And then an Fc domain, which is a steric mask, which serves to not only lock down the systemic activity of the drug but also increase the half-life to more antibody-like which we think could be a big advantage. Both of these masks are protease cleavable. We are focused in melanoma and our dose escalation, and the reason for that is that there is still significant unmet need in the late-line melanoma setting. Obviously, immunotherapy and checkpoint inhibitors, specifically have made a huge impact in the treatment of melanoma. But once patients progress on checkpoint inhibitors, they have very few options available to them. So we're initially evaluating 801 in the post checkpoint inhibitor setting, where rechallenge of these patients results in single-digit response rates. So there's a real opportunity here to bring the power of interferon alpha to melanoma and specifically in combination with KEYTRUDA. So we're in the clinic. We are currently escalating with KEYTRUDA. We presented at SITC last year data from the first 5 patients treated with CX-801 monotherapy, and that initial dose escalation experience in monotherapy allowed us to open up the combination last year. The combination will be the drug the drug here will be 801 plus KEYTRUDA, at least initially in melanoma. That's what we're very focused on. But I do want to show you some of the data from the SITC presentation, which we think is really quite honestly, super cool. So what we did with these first 5 patients, we were able to get on treatment patient biopsies, so we have pre- and post-treatment biopsies, really looking within the microenvironment that how this powerful cytokine is modulating the immune microenvironment. Shown here are 2 single cell images showing potent induction of interferon-regulated genes within the tumor microenvironment by 801. So this is strong evidence that the drug is being unmasked in the tumor, and that it is engaging with interferon receptors and inducing interferon regulated gene expression. And importantly, some of those interferon-regulated genes are indeed checkpoint inhibitors like PD-1, PD-L1 and LAG-3, setting the stage for the combination with KEYTRUDA. I should also say that we were very encouraged in dose escalation to have not seen any dose-limiting toxicities across the first several doses that we've evaluated monotherapy and we've already exceeded the clinically approved dose of Peginterferon alfa. So far, so good on safety. It looks like the masking in the periphery is really working to shut down the systemic toxicity. And in the tumor, we're seeing exactly what we want to see, which is activation of gene expression. And that actually extends the activation of an inflammatory microenvironment within the tumor. And this is one of my favorite slides as my team knows, showing here the dynamic induction of cytotoxic T cells into the tumor bed, you can see in the top right hand of this panel, you can see a blood vessel. And you can see that T cells have been extravasating from the vasculature into the tumor. And that's been driven by the induction of a potent T-cell recruiting cytokine CXCL10, which is in and of itself, at interferon-regulated genes. This is just 1 example of the powerful immunobiology that interferon can stimulate if you can get it to the right place at the right time. So very excited about that, and our goal for the program is now to really study the combination as we move through 2026. So let me wrap up on milestones and outlook, and then we'll go to some Q&A. So first of all, with Varseta-M laser-focused on this 100-patient Phase I study. We are on track for an update by the end of Q1. And we also anticipate presenting additional updates as that 100-patient study matures over the course of the year at major medical meetings, of course, focused in CRC. As that data matures, we will be going to the FDA to discuss our registrational design, including, of course, dose selection for that study and really looking forward to those discussions. Also with Varseta-M we're initiating Phase I with the bevacizumab combination to enable earlier lines of treatment, and we anticipate initial safety and efficacy data early -- in the early part of 2027. We're also planning to initiate other tumor types with Varseta-M where there's a multitude of choices, we'll have more to say about that in the second half of this year. Right now, we are continuing to be very focused in CRC because we really want to pin down this huge opportunity in colorectal, where this drug is behaving exactly as we have designed it. 801 with that foundational work done over the last 18 months, including this really exciting PD data that I just showed you, we're now highly focused on executing dose escalation with KEYTRUDA in melanoma, and we plan to have initial data for the combination also by the end of 2026. So an action packed year ahead, not that 2025 wasn't action packed. I really want to thank the CytomX team for doing just such an incredible job. Well, I thank the patients and our investigators for participating in our studies, and we've never been more excited about what we're doing at CytomX for patients and would like to thank you all for your interest and support of the company. Thank you very much.

Thank you, Sean. I'm going to ask the first couple of questions, but to the extent there are any questions on the audience, I'll prompt you and just raise your hand, and we'll get your question answered. Sean, I was wondering if you could expand a little bit on the Varseta-M Phase I dose expansion data that we're going to be getting here in 1Q. I mean I got to ask if you can give more granular time lines, which you'll probably just reiterate 1Q. But if I could just hear that from you. And then the size and scope of the data, I was interested because you said you'll give us a PFS update as well, right?

Q1, yes. In terms of size and scope, we gave a couple of updates last year on how enrollment was progressing in August. Our update was that we reached 73 patients and achieved our initial target of 20 patients at each of the dose levels. And then in our -- at our earnings call in November, we further updated that we had decided to further expand the Phase I study to 100 patients with the goal of having 100 patients enrolled by the end of Q1. So the data update in Q1 will be somewhere between 70 to 100 patients. And we do think that there'll be sufficient data at each of those dose levels that have at least a preliminary assessment of PFS.

And then how are you defining a win scenario on ORR specifically, the dose escalation part that we got last time was around 28%, but the high dose was had a 4 handle on it. like what's the win scenario there on ORR?

Well, we've got a lot of room to maneuver, we believe, when you look at the benchmarks with current standard of care in the late line setting, having very, very low single-digit response rates. So we've really broken through 28% is a great number. I think that there's a lot of room to maneuver around that number. and have a very, very competitive drug. So we'll see where it lands. I would also emphasize that as we get deeper and deeper into the development of Varseta, it's really PFS and OS that will be the most meaningful endpoints. And that's why these preliminary assessments of PFS in this upcoming data release, I think will be very helpful for investors.

And then maybe if we could dig into the safety side, specifically on that diarrhea AE, and you talked about the use of prophylaxis now in the study. the prior data was all grade 78%, grade 3 was 22%. So with prophylaxis, what does that diarrhea profile look like that would get you excited?

Yes. So at the end of the day, with Varseta the balance between the efficacy and the safety profile will be evaluated in the context of overall risk benefit in this patient population. And this is a patient population with very few options that progresses incredibly quickly for which new treatments are desperately needed. So the initial assessment of grade 3 diarrhea in the low 20s is something that we're coming to understand a lot more about and it's hard to put a number on it really at this point. It's really too early. I think we have to understand a lot more about the clinical benefit. And that, again, will be reflected in this next update in terms of ORR and PFS. We are working very hard to understand more about the etiology of the diarrhea in these patients. We have a lot of discussion with investors around where does it come from? Does it come from the payload? Is there a target-mediated component. And our view on that is to the extent that we know, which we don't, is that the fact that masking has allowed us to avoid the classic on target EpCAM toxicities like pancreatitis. It suggests very strongly that masking is working. And masking has to be working for us to get to this remarkable level of antitumor activity. So in the context of the masking delivering, it tends to, we think, tip the balance towards the GI toxicity being more payload driven, and we know that irinotecan, SN-38 or the Topo-1 inhibitors. In fact, even on the Topo-1 ADCs do induce GI toxicities. All that said, the most important thing, we believe, is to really understand the clinical course of the GI tox in patients and evaluate strategies for continuing to get ahead of it, so that we can deliver the maximum risk benefit for our patients.

Questions from the audience? Sean, I was interested in if you could expand a little bit more on in the back half of the year, you're going to be talking about additional EpCAM indications. Like when you look at the whiteboard of indications that you could possibly choose, like what are the push/pull levers in choosing? And maybe you could walk us through how you got to CRC, maybe that might help us as well.

Yes. That's a great question. Beginning with CRC, it was an interesting decision that we had to -- a very important decision that we had to take in focusing Phase I dose escalation entirely in metastatic CRC. It was a decision we discussed that with investors going back a couple of years. I think it was viewed as bit of a risky strategy because of the large number of drugs that have just failed in that setting. But we really had conviction that the drug -- the target is so abundant in colorectal and we were confident in our preclinical data. And we really felt that it was the right time to do the absolute killer experiment to demonstrate once and for all that this technology can deliver. And so we committed and we generated this data set, and we're obviously super excited about that decision. I mean, the other way to go would have been to do a more typical multi-tumor solid tumor all-comer study go looking for signals and then pursue those signals and expansions. That's the more conventional strategy, but we decided not to do that. And I'm very glad that we did. In terms of other tumor types, I mean, there really is a multitude of opportunity. We look at some of the other GI tumors as being great opportunities, but the target is so broadly expressed. I think for us, it's taking -- going to take a bit more analysis including thinking about potential combination strategies as well because in every solid tumor field, now including colorectal, nothing stands still, right? I mean these fields are evolving very, very quickly. There's so much innovation, so we've got a bit more work to do before we settle in on exactly where we go next.

Questions from the audience? Maybe just switching gears in the last few minutes here. When you think about the SITC update for 801, what do you think the Street is missing here? And then just walk us through for the combo later this year, what's going to be the size and scope and what would get you excited?

I'm not sure, the Street is missing a whole lot at the moment. I think that there's so much focus on Varseta understandably that we do need to remind, we do need to remind investors and quite frankly, sometimes we need to remind ourselves about our second child. And -- but the second child is growing up. And that's why we put that data out in November. We intentionally wanted to get some early results out there to provide a foundation for conversations with investors about what's coming down the road. And I mean, 801 has the potential to be just as big as Varseta, I mean really, the number of tumor types that interferon has been shown to be active in and the unmet need in post immunotherapy -- the post-immunotherapy solid tumor setting is enormous, and we really see 801 as potentially becoming a new centerpiece of combination immunotherapy and everything that we showed in that SITC update demonstrates in our view that we're just right on track with that biology. Again, back to the T cell recruitment, I think about on the -- as an example, one of the biggest challenges with developing a wide range of immunotherapies, including T cell engagers, is that you're dependent upon a T cell effective function to actually bring about the tumor cell killing that you need. And that's a very -- that's complicated pharmacology to be dependent upon T cell biology as your effector and a subset of T cells at that will be reactive to the appropriate neoantigens in the context of each tumor cell, it's asking a lot. So an agent like 801 that has this ability to dramatically stimulate the tumor microenvironment and bring T cells into it offers terrific opportunities for combinations, we think, with a wide range of mechanisms. We're focused initially, just like we are with Varseta, we're focused in melanoma. We're focused on the PD-1 combination, to get to an initial proof of concept but that really is just the beginning. So I don't really think investors are missing a whole lot. I think they'll -- we'll certainly be talking more about it as the year goes on. And I'm sure that it will continue to grow in their minds, as an important part of our story.

Okay. Thank you, Sean.

Thank you very much.