Pfizer Inc. (PFE) Earnings Call Transcript & Summary

Good day, everyone, and welcome to Pfizer Pflash: A Spotlight on Antibody Drug Conjugates. Today's call is being recorded. At this time, I would like to turn the call over to Francesca DeMartino, Chief Investor Relations Officer and Senior Vice President. Please go ahead, ma'am.

Thank you, and good morning, everyone. I'm Francesca DeMartino, Chief Investor Relations Officer. On behalf of the Pfizer team, thank you for joining us for our third Pfizer Pflash webcast. Today's call will be recorded and will be available for replay on our IR website at pfizer.com. As a reminder, our Pfizer Pflash series is intended to serve as an educational deep dive into our pipeline, products and leadership. Each call will give you an opportunity to hear from and interact with our business leaders. Today's session will begin with a short conversation followed by a live Q&A. As a reminder, this call is intended for the investment community, including our sell-side analysts and institutional investors. If you're unable to join the entirety of the event, you can find the replay available on our IR website. I want to note that on today's call, we will be making forward-looking statements. I encourage you to view Slide 2 in our presentation and the disclosures in our SEC filings, which are all available on our IR website at pfizer.com. Forward-looking statements on the call are subject to substantial risks and uncertainties, speak only as of the call's original date, and we undertake no obligation to update or revise any of the statements. With that, let's get started. As you know, ADCs are a key area of focus for Pfizer with a portfolio that seeks to address multiple cancer types. Today, we will provide insight into our approach to the development of ADCs that we believe have the potential to be a key driver of growth of our oncology franchise. It is a privilege to have you all with us as we delve into ADCs. This is the first Pfizer Pflash broadcast of 2025 and also the first in a series discussing Pfizer Oncology. Before we move to the main discussion, let me take a moment to introduce our speakers and my colleagues, Megan O'Meara, Head of Oncology, Early Clinical Development and Interim Oncology Chief Development Officer; Scott Peterson, Head of ADC Discovery; and Jeff Settleman, Chief Scientific Officer for Oncology R&D. Meghan, Scott and Jeff are central to our innovative work focusing on ADCs from early discovery through approval. Megan, Scott and Jeff, welcome, and thank you so much for joining today. Can you please start by introducing yourselves and giving a brief overview of your current role and experience? Megan, let's start with you.

Thank you, Francesca. I'm happy to be here today with my colleagues, Scott and Jeff, to talk about ADCs and our progress in developing potential new cancer medicines. In my role as Pfizer's Head of Early Clinical Development in Oncology and Interim Oncology Chief Development Officer, I'm responsible for clinical development of Pfizer's oncology portfolio, focusing on clinical strategy and trial execution. I joined Pfizer a little over a year ago as part of the Seagen acquisition, having previously been with Seagen for more than 12 years, where as a board-certified medical oncologist, I led both early and late-stage clinical development. And with that, I'll turn it over to Scott.

Thank you, Megan. I'm Scott Peterson, Head of ADC Discovery. I'm responsible for driving Pfizer's ADC discovery and preclinical development efforts. Like Megan, I joined Pfizer through the Seagen acquisition, where since 2018, I led advancement of innovative ADC and immuno-oncology programs through IND. Prior to Seagen, I served as Chief Scientific Officer at Cascadian Therapeutics, where I led the preclinical and translational sciences teams, supporting the advancement of the selective HER2 inhibitor tucatinib, now known as TUKYSA to a pivotal study in HER2-positive breast cancer. All told, I've been in cancer discovery research for more than 25 years. And next, we will hear from Jeff.

Thanks, Scott. In my role as Pfizer's Chief Scientific Officer for Oncology R&D, I lead all oncology research at our 2 major research hubs in La Jolla, California and Bothell, Washington. Prior to joining Pfizer in 2019, I served as Head of Oncology Research at Calico Life Sciences. And prior to that, I led Discovery Oncology at Genentech. Before joining the pharmaceutical industry, I was a professor at Harvard Medical School for 18 years and was Scientific Director of the Massachusetts General Hospital Cancer Center. With that, I'll hand it back to Francesca.

Great. Thank you all for your introductions. Jeff, to kick us off, please walk us through Pfizer's strategy in oncology, particularly where and how ADCs fit into that strategy.

Sure. Our oncology strategy can be described along 2 dimensions. In the first dimension, we have a portfolio of programs that each fall within 1 of 3 core therapeutic modalities for which we've developed deep technical expertise and extensive capabilities. First, there are the small molecules where over many years, we have established truly world-class drug discovery and medicinal chemistry expertise that's delivered several important cancer medicines. We also have core strengths in large molecule biologics enabled by our excellent capabilities in protein engineering and antibody design. And with the acquisition of Seagen, we now have an industry-leading platform and know-how to deliver ADCs or antibody drug conjugates, which occupy a special place at the intersection of small molecules and biologics. And following the successful development of several important ADC medicines, we're now focused on the next generation of potentially even more effective and safer ADCs, leveraging new targets and with improved conjugation technology and highly differentiated anticancer payloads. And in that regard, we see a great opportunity to find synergies between our small molecule and antibody discovery capabilities and the legacy Seagen know-how to potentially deliver many new breakthrough medicines. And the second dimension of our strategy relates to the specific cancer indications that we're prioritizing. We continue to build on Pfizer's established presence in breast cancer, genitourinary cancers, hematologic malignancies and thoracic cancers, and we're constantly working to expand the reach of our medicines to unmet medical needs across the care continuum within each of these cancer types.

Thanks, Jeff. It's clear that ADCs represent an important component of Pfizer's oncology portfolio and that they leverage the expertise developed over many years by both Pfizer and Seagen. Briefly, why did Pfizer choose ADCs as the right opportunity for the future rather than other technology platforms such as mRNA vaccines in oncology or cell therapy approaches such as CAR-T?

Well, we're always looking at new science and technology with the potential to advance the future of cancer treatment. Cancer vaccines and cell therapies are both exciting areas, each with their own unique complexities. Cancer vaccines, including those based on mRNA are still an emerging technology, and it will be important to see how the early promising clinical data in that space translates in ongoing clinical studies. Cellular therapies are highly personalized treatment options and scalability is certainly a consideration. In contrast, ADCs are both modular and can be broadly deployed. They're modular in the sense that ADCs consist of 3 key components that are assembled in different combinations to address different cancers and patient populations and their potential for broad deployment means that a single ADC can potentially be used to treat large segments of the patient population. So we believe that we can be more successful and reach more patients with ADCs that is currently feasible with those other modalities.

Terrific. Thank you. Following up on that, Jeff, what are the 3 key parts that make an ADC?

Right. So ADCs consist of 3 key components. There's an antibody, a payload and a linker. The antibody is directed against the cell surface target that's highly enriched in tumor cells versus normal cells. Payload is the active part of the molecule that kills cancer cells once the ADC is internalized within the cancer cell. And the linker tethers the payload to the antibody. And for each of these 3 components, there have been significant advancements made in recent years. So for example, using advanced technologies in single-cell genomic analysis and proteomics, we're able to identify novel tumor-enriched antibody targets for ADC development. There's also been good progress in the design of new drug linkers and conjugation technology that can improve the stability and performance of ADCs and simplify the manufacturing process. And we're finding opportunities to engineer new payloads with differentiated mechanisms of cancer cell toxicity. So there's a lot of new technology and learnings being applied to the discovery of the next generation of ADCs that could potentially deliver even greater impact for patients.

Thank you, Jeff. Scott, let's dive a little deeper. How do the components of an ADC come together to provide antitumor activity?

Sure. I'll start with a brief description of the mechanism of action of ADCs, first with a vedotin ADC as a case example, and then I can circle back and discuss other payloads. The primary mechanism of ADCs is direct tumor cytotoxicity. The first step is antigen binding in which the antibody binds to the target protein on the surface of cancer cells. This antibody antigen complex is then internalized into the cell by the lysosomal pathway. As this complex moves further through the lysosomal pathway, the linker is cleaved and the payload, in this case, MMAE is released. MMAE escapes the lysosome and very potently leads to microtubule disruption, cell cycle arrest and cell death. But the payload can also exit the target cell and enter adjacent tumor cells, repeating this process and killing additional cancer cells. This is called the bystander effect. And then there is a third very interesting effect that some payloads such as MMAE can induce. Here, the intracellular stresses can lead to the release of immune stimulating molecules that induce the infiltration of T cells and innate immune effector cells and to the display of tumor antigens on the surface of the cancer cell where they can be recognized by T cells. These alarm cells can recruit, activate and enlist the immune system in the tumor destruction process in a way that's called immunogenic cell death, or ICD. The ADC landscape is dominated by 2 payload classes -- payload mechanisms of action. Many of the approved ADCs deploy payloads that target microtubules, including the vedotin payload MMAE. The other main mechanism of action of ADC payloads is the induction of DNA damage, principally using potent inhibitors of topoisomerase 1. Blocking topoisomerase 1 inhibits DNA replication and transcription resulting in tumor cell death. While both the microtubule and TOPO1 targeted payloads have been a component in many important approved ADC medicines, we feel the future of ADCs requires us to look beyond these 2 payload classes to identify new mechanisms of action. One area that we're particularly interested in exploring is the use of protein degrader payloads. Protein degraders can be designed to target many essential tumor cell functions, potentially resulting in novel mechanisms of cell killing. In addition, we believe protein degraders may enable the design of ADCs that are even more selective for cancer cells, potentially providing improved efficacy and enhanced safety profiles for patients.

Great. Thank you so much. Megan, I'd like to come back for just a moment to the immunogenic cell death or ICD mechanism of action that Scott mentioned. Can you elaborate on the clinical relevance of ICD?

Sure. Immunogenic cell death is a very important part of the ADC mechanism of action, though not all ADCs appear to be equally adept at inducing ICD. Interestingly, vedotin ADCs in particular, seem to be quite proficient at eliciting ICD. The MMAE induced cancer cell death leads to release of immune activating molecules. These pro-inflammatory signals are capable of recruiting T cells to the tumor microenvironment and thereby enlist the immune system to fight to eliminate those cancer cells. But we know that cancer cells also have the ability to shut down T cell activity, for example, through the PD-1, PD-L1 access. However, when this interaction is blocked, for example, with an anti-PD-1 antibody, then the T cell can be activated and kill the tumor cell. This would suggest that an ADC with strong ICD activity could be a powerful combination partner with, for example, an anti-PD-1 antibody, one of the class of medicines referred to as immune checkpoint inhibitors. And in fact, this is exactly what we see. For example, when we compare objective response rates and duration of response in patients treated with an ADC regimen versus that ADC regimen in combination with an anti-PD-1, we see additional potential response benefit with the ADC plus anti-PD-1 combination. Examples are shown for PADCEV and TIVDAK. Of course, we would want to see this translate also to higher quality and depth of response and improved survival. And with a very recent example here is seen an updated results from our EV-302 study presented earlier this month at ASCO GU, which show that PADCEV plus pembrolizumab, an anti-PD-1 antibody, outperformed chemotherapy in metastatic urothelial carcinoma. We see this in the overall survival in which the PADCEV plus anti-PD-1 combination demonstrated median OS of more than 33 months versus less than 16 months for chemotherapy, corresponding to a reduction in the risk of death by nearly 50%. These results provide an opportunity to think about PADCEV plus anti-PD-1 combination as a future potential foundational treatment option in metastatic urothelial carcinoma treatment. These are just some of the recent data that highlight the opportunity for potentially improved clinical outcomes when ADCs and immune checkpoint inhibitors are combined.

Thank you very much, Megan. Scott, of the 12 ADCs currently approved by FDA, 6 of these were developed by Pfizer and/or Seagen or leverage their technologies and one additional Pfizer ADC product is approved in China. All of this underscores this deep institutional knowledge. How does this expertise inform preclinical development for novel ADCs?

Yes. Over the years of ADC research at Pfizer and Seagen, many lessons have been learned about the design of ADCs and the factors that influence both safety and efficacy. While ADCs are conceptually simple, the underlying reality is much more complex. To successfully bring truly next-generation ADC technologies to patients requires a deep understanding of past successes and challenges in the field. This includes all aspects of ADC design from antibody target selection, antibody design and engineering, drug linker design, conjugation technology and the evolution of payload features. It also requires expertise on how to test ADCs in preclinical efficacy and toxicology studies and importantly, how to interpret and translate those findings into the design of clinical studies. Lastly, it is very important to use the learnings from our ADC clinical studies to inform our ongoing ADC bench research. The importance of reverse translation of clinical findings just can't be understated. The only way we can successfully innovate to bring new ADC technologies forward is to integrate our clinical data from both successful and unsuccessful ADCs.

Megan, how does that same depth of institutional knowledge influence clinical development of novel ADCs?

What Scott said actually applies equally well for clinical development. The deep understanding that accompanies years of hands-on learnings with ADCs cannot be understated. With every trial we conduct for each ADC in our portfolio, we continually expand our knowledge across the many areas that are critical to the design of future successful studies. This includes a wealth of data for both antibodies and payloads, experience with dose levels and dosing frequency, efficiency in our interactions with health authorities and the list goes on. I should also point out the importance of Pfizer's global footprint and scale for our clinical trials, manufacturing and commercial activities. All of this allows us not only to design and conduct early-stage clinical trials that can speed our progress toward pivotal studies, but also once approved, to get new medicines to patients faster.

Thank you both. Megan, let's talk for a moment about Pfizer's ADC products as well as the mid- to late-stage pipeline. What are some of the key data and programs and what is coming up in 2025?

Sure. Our approved ADCs include ADCETRIS, which recently received its eighth approval in hematologic malignancies, TIVDAK for recurrent and metastatic cervical cancer and PADCEV for locally advanced and metastatic urothelial cancer. As also Polivy, an ADC for the treatment of DLBCL, which is out-licensed to Roche. Our mid- and late-stage ADC pipeline includes both new molecular entities as well as approved ADCs that are being tested in additional patient populations. PADCEV, for example, has ongoing pivotal trials for cisplatin-eligible and cisplatin-ineligible muscle invasive bladder cancer, which we anticipate will read out in the second half of this year. Another ADC in the genitourinary focused pipeline portfolio is disitamab vedotin, or DV, which is a novel HER2-directed ADC being tested in frontline HER2-positive metastatic urothelial cancer. Exciting novel ADCs in our thoracic cancer pipeline portfolio include sigvotatug vedotin or SV, a potentially first-in-class integrin beta-6 directed ADC and PDL1V, a potentially first-in-class PD-L1 directed ADC. SV is currently being tested in a Phase III study of second-line plus metastatic non-small cell lung cancer with a second Phase III study in frontline metastatic non-small cell lung cancer that we expect to initiate imminently. Later in 2025, we could also see a potential Phase III start for PDL1V in metastatic non-small cell lung cancer as well as a potential Phase III start in head and neck cancer. We look forward to sharing more data and details for PADCEV, DV, SV and PDL1V later this year. We also anticipate sharing updates on multiple exciting early-stage ADC programs at upcoming 2025 conferences, such as 35T, our investigational CD30-directed TOPO1 ADC.

Thank you, Megan. Definitely some exciting times ahead. Scott, we've talked about the past and the present. What are some of the approaches being taken to shape the future of ADCs?

Yes. We are laser-focused on how we can advance ADC technologies to improve patient outcomes. Unmet needs still exist to improve tolerability, enhance efficacy and to address resistance mechanisms that emerge with the current payload classes. One way we're aiming to do this is through the evolution of our existing auristatin payload and drug linker technologies to improve ADC tolerability. For example, 35T is an investigational ADC that employs a new drug linker, which we found could increase the tolerability of MMAE in preclinical studies. We're conducting clinical trials to validate whether these modifications may also provide an improved therapeutic index in patients and whether these modifications may potentially improve the therapeutic index of ADCs compared to our vedotin technology. We're also working to create a next-generation auristatin payload that improves tolerability of MMAE while maintaining the key features of ICD. Finally, we're exploring new conjugation technologies that may potentially increase the tolerability of existing ADC drug linkers. All of these efforts are made possible by the breadth and depth of institutional knowledge, as we discussed earlier. It's clear that the clinical successes have driven a significant expansion in ADC development. There are more than 150 ADCs in development across the pharmaceutical and biotechnology industries. But there's really less diversity than that number would suggest. Many ADC programs are pursuing the same targets and/or use the same payloads. In order to reach the next frontier for ADCs, I think it's important to pursue novel targets that leverage the latest biologic data and potentially offer greater precision. And there's also a real need to push the scientific boundaries of our existing ADC payloads and bring forward next-generation payloads to diversify beyond microtubule and DNA damage mechanisms of action. As we spoke about earlier, I'm particularly excited about the opportunity here to explore new cytotoxic payloads that also incorporate tumor immune modulation mechanisms of action, such as immunogenic cell death, and this potentially synergize with immune checkpoint blockade. We believe this bright future for ADCs could hit the mark and potentially achieve 3 important things for patients, improve tolerability, enhance efficacy and address resistance mechanisms.

Thank you so much. There's definitely a lot to look forward to. Thank you, Scott, Megan and Jeff for a great discussion. We'll now begin the Q&A session with Megan, Scott and Jeff. As a reminder, our Pfizer Pflash series is designed as an educational deep dive into our pipeline programs. I'll therefore, kindly ask participants to keep questions focused on ADCs and the programs discussed today and to avoid those that would require us to provide forward-looking financial projections. While we're happy to clarify any information shared during the presentation, we will not be offering estimates beyond what has already been communicated. Thank you for your understanding. With that, we're ready to take the first question. Operator, if you could please assemble the queue.

[Operator Instructions] And we will take our first question from Chris Schott with JPMorgan.

This is Ethan on for Chris Schott. Just as you look at lung, can you speak to how you think about the evolving competitive landscape and maybe specifically the role that Trop-2 will play in the space and then how you think about how the potential success of the VEGF PD-1 bispec would impact the positioning of your integrin beta 6? And then can you also just remind us on the timelines of the integrin beta 6?

Sure. I can take that. This is Megan. It's -- great questions. Obviously, the non-small cell lung cancer space is a dynamic landscape that we're following closely. And we're familiar with data from potentially competitive programs. I'm not going to focus on that too much today, but I can say that we're certainly enthusiastic about our sigvotatug vedotin program, which would be a potentially first-in-class integrin beta-6 directed ADC and hopefully, a potential future standard of care in non-small cell lung cancer. I can comment a little bit, integrin beta 6 specifically is expressed on a very high proportion, more than 90% of tumors, lung cancer tumors and is associated with a poor prognosis. And so really, we designed this with high target selectivity to integrin beta 6 and limit binding to other integrins to avoid potentially off-target toxicity or normal tissue binding and provide a favorable safety profile as well as the potential to leverage the vedotin immunogenic cell death potential. And so in terms of timelines for our SV program, we have an ongoing Phase III in second-line plus non-small cell lung cancer. And we're imminently about to start a frontline PD-L1 high expressing metastatic non-small cell lung cancer study combining sigvotatug vedotin with pembrolizumab. And so that, again, will start in the first half of this year. And then with regard to the PD-1 VEGF space, obviously, we're following that very closely. It's a very interesting target that bispecific combination of targets that we're interested in. And I'm sure you may have noticed earlier this week that we announced a collaboration with Summit to combine our vedotin ADCs with their PD-1 VEGF bispecific. And this includes opportunities for us to evaluate the safety and activity for EV, DV, SV and PDL1V. So we're really planning ahead for the -- for potential future options for these programs.

And we will take our next question from Geoff Meacham with Citi.

I just had a couple. So I know it's not either/or, but if you had to prioritize R&D dollars in this area, would it be to improve the linker or payload or just to increase the number of assets in the ADC pipeline? And then the second question is, what's the ability to link other elements to deliver? I've seen platforms that include nucleic acids or molecular switches, et cetera. But I wasn't sure if that's a focus for Pfizer or if it's scalable.

Yes. Thanks. This is Jeff. Maybe I can take the first question to start with. I would say that each aspect of the ADC technology, all the components that we described requires still attention to optimize the components to generate the best next generation of ADCs. I don't think we view it as a trade-off between optimizing each technology and having more programs. At the same time, we're not just taking lots of short-term goals with different combinations to empirically determine what's the best ADC. So it's a mix of being very strategic and thoughtful about addressing the most significant unmet needs with novel ADCs, but at the same time, taking the learnings from our prior experience as we were describing earlier with ADCs to ensure that each new molecule has potentially optimized features that leverage what we've learned from previous experience. And then the second question, if you can repeat that.

The second question is -- yes, go ahead.

No, no, Geoff, I was going to ask you to repeat it. Go ahead.

Yes. So the question is the ability to link other elements that you can deliver besides a payload, besides the toxin. I've seen other platforms that link antibodies, nucleic acids, molecular switches. I wasn't sure if the next-gen technology for that is a focus for Pfizer or whether it's scalable or whether that's a priority.

Yes. Good question. I mean we certainly view the platform as having the potential to use antibodies or antibody-like biologics to deliver a variety of payloads and not just for oncology, I think there are potentially other non-oncology indications where the idea of delivering specific payloads to target cells of interest, whether it's disease cells or immune cells to modify disease, that would be seen as an opportunity for us as well. The focus has been on delivering new payloads for cancer indications, payloads that, as we talked about earlier, go beyond targeting tubulin and topoisomerase, which is still where a lot of the focus is. As Scott mentioned, protein degraders and rationally selected payloads is also going to be a very important opportunity for us. And we're putting a lot of our emphasis right now on delivering the next generation of payloads that are highly differentiated from what is currently being most actively pursued in the clinic. Conjugating nucleic acids is certainly something that could be a scope, but it's not currently a priority or other types of payloads. But we think that between targeted protein degraders, molecular glues, other rationally targeted inhibitory molecules or agonists, immune agonist, for example, could be all in scope for us for the ADC platform.

And we will take our next question from Mohit Bansal with Wells Fargo.

This is Trina on for Mohit. I wanted to ask about a potential biomarker strategy for SV. I mean it seems like this is something that is being considered for other ADCs. But as you mentioned, IB6 is highly expressed in non-small cell. So I was curious if you think this is a potential strategy going forward?

Sure. This is Megan. I can answer that question. It's a great question that we think about across our ADC pipeline is the expression response relationship. And it's fascinating that, for example, particularly with vedotin ADCs, we tend to see responses even in tumors with very low expression of antigen in some cases. And so we try to collect the data to really understand case by case what the expression response relationship is and then make data-driven decisions to design our randomized trials effectively. In the case of sigvotatug vedotin or SV, as you mentioned, integrin beta 6 is expressed on a very high proportion of non-small cell lung cancer. However, we're interested to understand if the higher expressed same tumors with IB6 might have a better chance of having deeper and more profound responses. And so we're continuing to evaluate that within the Phase I trial. The current Phase III study in second line -- second to third-line non-small cell lung cancer is not prospectively selecting for IB6 high tumors, but we are retrospectively evaluating that. And I won't go into details of the statistical analysis plans, but there are opportunities for us to evaluate not only the all-comer population, but also the IB6 high population for the efficacy endpoints. And I will also say for our frontline lung cancer study, again, we're selecting for high PD-1 expression in the -- or PD-L1 expression tumors, not IB6, but again, we'll be evaluating the biomarker for expression response.

And we will take our next question from Steve Scala with TD Securities.

Two questions. First, I'm curious how AI or machine learning is being used in the research or development of ADCs? Where has it already been used successfully and where might it be used in the future? Some of you came from other companies. So what is Pfizer doing that is unique relative to those other companies? So that's the first question. Second question is, how do you view AstraZeneca's QCS scoring system for employment when -- in their clinical studies of ADCs?

Yes. So -- this is Jeff. On the first question about AI, obviously, we don't have detailed insights into what every other company is doing in this space. But certainly, we're doing many of the same things, which is just looking at the potential application of AI across pretty much everything we do, including how we organize and interrogate our data, both internally and as far as publicly accessible data, but also how we design our clinical studies, how we access real-world information and incorporate that into our next-gen programs. And then at the level of ADC discovery, for example, how we optimize antibody sequences and how we discover new payloads. So AI is being deployed pretty much across the spectrum of everything that touches our ADC platform, including our clinical trial plans.

Sure. And I can take the QCS question. I think there are a lot of different ways to look at target expression, and it's exciting to see how the field is advancing and that sponsors are looking at novel automated solutions for this approach. Historically, for kind of global approaches to cancer selection and treatment, standard immunohistochemistry has been employed and it's typically something that can be globally feasible. So I think it will be interesting to see how the QCS approach pans out, but we're following closely and looking at different options for our programs in the future as well.

And it appears that there are no further questions at this time. I will now turn the program back to Francesca for any additional or closing remarks.

Great. Thank you to our speakers and my colleagues for joining today and for everybody that was able to dial in. We recognize that there's a lot of interest in our oncology pipeline. And as I mentioned at the beginning, this will be the first of many series that we'll host throughout the year, particularly as the scientific conferences start approaching, we'll consider relevant follow-on discussions related to any presence we have there. So stick with us. There's more to come, and thanks for dialing in, and have a wonderful rest of the week.

Thank you. This does conclude today's presentation. Thank you for your participation. You may disconnect at any time.