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spk03: Good day and welcome to the Cura Oncology 3Q conference call. Today's call is being recorded. I'll now turn the call over to Pete Despain. Please go ahead, sir.
spk00: Thank you, Paula. Good afternoon and welcome to Cura Oncology's third quarter 2021 conference call. Joining me on the call are Dr. Troy Wilson, our president and chief executive officer, and Dr. Mark Grasso, our chief financial officer and chief business officer. Dr. Steven Dale, our chief medical officer, Kirsten Flowers, our chief commercial officer, and Kathy Ford, our chief operating officer, are also with us and available to answer questions. Before I turn the call over to Dr. Wilson, I would like to remind you that today's call will include forward-looking statements based on current expectations. Such statements represent management's judgment as of today and may involve risks and uncertainties that could cause actual results to differ materially from expected results. Please refer to Curo's filings with the SEC, which are available from the SEC or on the Curo Oncology website for information concerning risk factors that could affect the company. With that, I will now turn the call over to Dr. Troy Wilson, President and CEO of Curo Oncology.
spk05: Thank you, Pete, and thank you all for joining us this afternoon. I'm pleased by the progress our team has made over the past quarter, highlighted by accelerated enrollment in the Phase 1B expansion cohorts for KO539. Preclinical data highlighting the molecular mechanisms of activity for KO539 and its potential for synergistic combination with venetoclax. First clinical site activated in the Phase I-II trial of tipifarnib plus alpelisib in head and neck squamous cell carcinoma and ongoing IND enabling studies for KO2806. As an organization, we remain focused on our three main programs, our menin inhibitor, KO539 in acute leukemias, our farnesyl transferase inhibitor, tipifarnib and head and neck squamous cell carcinomas, and our next-generation farnesyl transferase inhibitor, KO2806, in solid tumors. We believe these programs have the potential to create significant value for patients, healthcare providers, and shareholders, and we believe we have the experience, leadership, and financial resources to deliver that value. Now, let's take a closer look at the progress within each of the programs, beginning with KO539. We've completed the phase 1A dose escalation study of 539, which demonstrated encouraging single-agent activity in an all-comer population of patients with relapsed and or refractory AML, including those with NPM1 mutations and KMT2A rearrangements. KO539 also showed a favorable safety and tolerability profile, notably with no evidence of QTC prolongation. We intend to conduct a comprehensive clinical development plan For KL539, both as a monotherapy and in combination. A key step is determination of a recommended phase 2 dose, which is the goal of our ongoing phase 1B study. We're currently enrolling two expansion cohorts, a lower dose of 200 milligrams and a higher dose of 600 milligrams, and each cohort is comprised of patients with NPM1 mutant or KMT2 rearranged relapsed and or refractory AML. The dose is being evaluated in a phase 1B, were selected based on the clinical activity, safety, and tolerability demonstrated in the Phase 1a study. We continue to be encouraged by the preliminary results from the Phase 1b study thus far, with evidence of activity at both doses and a favorable safety and tolerability profile. We're also encouraged by the enthusiasm of our investigators, with approximately half of an estimated 40 global sites now actively screening patients for enrollment in the study. We continue to aggressively add sites in the U.S. and Europe in anticipation of the Phase II portion of the study, and we maintain our enrollment guidance of 12 evaluable patients in each cohort of the Phase Ib study by the first quarter of 2022. Once enrolled, we will assess the patients in each cohort for safety and tolerability, pharmacokinetics, and efficacy to determine the recommended Phase II dose. The study protocol also gives us flexibility to enroll up to 30 patients in the selected cohort. This enables us to continue enrolling patients in the Phase 1b study at the recommended Phase 2 dose while we transition into a subsequent registration-directed portion of the study. Importantly, we believe data from all patients treated at the recommended Phase 2 dose have potential to contribute to the registrational patient population. Thus, our Phase 1b study not only helps us to refine selection of a recommended phase two dose, but it enables us to start our path toward registration while maintaining an aggressive development timeline for the program. We intend to provide a more comprehensive update on the phase one study, including results from the phase one A and the phase one B at a future medical meeting pending determination of the recommended phase two dose. Based on our progress, and the totality of the clinical and preclinical data to date, we continue to believe KO539 has potential to be both a first-in-class and a best-in-class Mennon inhibitor. As such, we're designing a development strategy that builds on the potential to register KO539 as a monotherapy, while giving us flexibility to get to larger opportunities in combination more quickly, including earlier lines of therapy. Efforts are already underway to support some of these additional development activities. For example, encouraging preclinical data has been generated through a research collaboration with Dr. Kapil Bala at MD Anderson, highlighting the molecular mechanisms of KO539 and its potential for synergistic activity in combination with venetoclax in KMT2 rearranged and NPM1 mutant AML models. These data have been accepted for presentation at the upcoming American Society of Hematology annual meeting. The abstract was published earlier today and is now available on the ASH website. We look forward to Dr. Bhalla's presentation next month and to sharing our progress with you as we continue to drive toward a recommended phase two dose for KO539 next quarter. Turning our attention now to farnesyl transferase, we continue to view farnesyl transferase inhibition as a potentially valuable therapeutic and commercial franchise one with potential to deliver multiple opportunities in oncology. For example, earlier today, an abstract was published with the final results from a Phase II study of tipifarnib in patients with relapsed or refractory peripheral T-cell lymphoma. Although we paused continued development of tipifarnib in T-cell lymphoma in early 2020 to focus on our programs in head and neck squamous cell carcinoma and AML, the Phase II trial continued. The final results will be presented by Dr. Thomas Witzig hematologist at Mayo Clinic, and a studies lead investigator in an oral presentation at ASH. This abstract can also be found on the ASH website. The clinical benefit demonstrated in patients with certain subtypes of T-cell lymphoma, including an overall response rate of 56.3% and a median overall survival of 32.8 months in patients with angioimmunoblastic T-cell lymphoma, underscore the potential to target farnesyl transferase to drive clinical benefit in patients. As most of you know, our most advanced effort with tibifarnib is focused on patients with head and neck squamous cell carcinomas, or HNSCC, which carry mutations in the HRS gene. Tibifarnib has been awarded Breakthrough Therapy designation from FDA for the treatment of patients with recurrent or metastatic HRS mutant HNSCC. The Breakthrough Therapy designation was based upon data from our Phase II RUN-HN trial, which was published earlier this year in the Journal of Clinical Oncology. We continue to be motivated by these data and remain focused on our AIM-HN registration directed trial of tibifarnib as a monotherapy in patients with HRAS mutant HNSCC. In addition to addressing an urgent unmet need for patients, we believe the opportunity for tibifarnib in HRAS mutant HNSCC provides a beachhead to the development of rational combinations and the expansion to larger genetic subsets. Just last month, a review paper was published in the journal Cancers, highlighting the rationale and preclinical and clinical data that support the potential for farnesyl transferase inhibitors in combination regimens in squamous cell carcinomas. Among these potential combinations, we've identified as a priority the combination of tipifarnib and a PI3 kinase alpha inhibitor. Our preclinical data suggests that HRAS and PI3 kinase alpha are codependent oncogenes in HNSCC, and that combining tipifarnib with a PI3 kinase alpha inhibitor has potential to provide meaningfully better antitumor activity relative to inhibiting either target alone. We believe this combination has the potential to increase the total addressable population for tipifarnib to as much as 50% of patients with HNSCC. This past quarter, we announced a clinical collaboration with Novartis to evaluate the combination of tipifarnib and the PI3 kinase alpha inhibitor alpelosib in patients with HNSCC. Alpelisib is approved to treat patients with PIK3CA mutant breast cancer, and it has demonstrated encouraging evidence of clinical activity in patients with HNSCC. We're now actively preparing for a Phase I-II study of tipifarnib in combination with alpelisib in HNSCC, which we call the current trial. The initial cohort will include patients who have PIK3CA-dependent HNSCC. These patients can be identified using next-generation sequencing, which should allow us to identify a recommended phase two dose for the combination. We've now activated the first clinical site, and we're on track to begin dosing patients in the current trial by the end of this year. Meanwhile, through our own internal efforts and our network of academic collaborators, we've identified some exciting opportunities for farnesyl transferase inhibitors in combination with other targeted therapies in large solid tumor indications, opportunities that we believe represent significant potential value creation. Last quarter, we nominated KO2806 as the lead development candidate in our next-generation farnesyl transferase inhibitor program, a compound with improved potency, pharmacokinetic, and physical chemical properties relative to tippy farno. Our next-gen FTI program is designed to target innovative biology and to address large solid tumor indications of high unmet need through rational combinations with a focus on delaying the onset of drug resistance. We're very excited about this emerging opportunity, and we look forward to sharing more information in the months ahead. With that, I'll now turn the call over to Mark Grasso for a discussion of our financial results.
spk06: Thank you, Troy, and good afternoon, everyone. I'll provide a brief overview of our financial results for the third quarter of 2021. along with reiterating our guidance for the full year 2021. I invite you to review our TEN-Q file today for a more detailed discussion. Research and development expenses for the third quarter of 2021 were $22.4 million, compared to $16.6 million for the third quarter of 2020. The increase in R&D expenses was primarily due to increases in clinical trial costs, development and manufacturing activities related to our KO539 program, clinical trial costs related to our registration-directed trial of tibifarnib, non-cashier-based compensation, personnel costs, and other expenses. General and administrative expenses for the third quarter of 2021 were $11.3 million, compared to $7.6 million for the third quarter of 2020. The increase in G&A expenses was primarily due to increases in personnel costs, professional fees, and non-cashier-based compensation. Debt lost for the third quarter of 2021 was $33.4 million, or 50 cents per share, compared to a net loss of $23.8 million, or 42 cents per share, for the third quarter of 2020. As of September 30, 2021, we had cash, cash equivalents, and short-term investments of $543.4 million, compared with $633.3 million as of December 31, 2020. We continue to anticipate our operating expenses for the full year 2021 to be in the range of $130 million to $140 million. We continue to expect our net cash used in operating activities for the full year 2021 to be in the range of $105 million to $150 million. Based on our current plans, we continue to believe that our cash, cash equivalents, and short-term investments will be sufficient to fund current operations into 2024. With that, I will now turn the call back over to Troy.
spk05: Thanks, Mark. Before we jump into the question and answer session, let me lay out our anticipated upcoming milestones. Dose the first patient in the current Phase I-II study of tipifarnib in combination with alpelicib by the end of 2021. Complete enrollment of 24 evaluable patients in the COMET-001 Phase I-B expansion cohorts by the first quarter of 2022. Determine the recommended Phase II dose of KO539 by the first quarter of 2022. And submit an IND application for KO2806 by the end of 2022. With that operator, we're now ready for questions.
spk03: Thank you. To signal for a question, please press star 1 on your telephone keypad. Also, if you are using a speakerphone, please make sure that your mute button is turned off to allow your signal to reach our equipment. Once again, it is star 1 at this time for questions, and we'll pause to give everyone the opportunity to signal.
spk02: We'll take our first question from Jonathan Chang with SVB Lyric.
spk04: Hi, guys. Thanks for taking my questions. First question, can you provide any more granular color on comments in the press release indicating evidence of activity at both doses and a favorable safety and tolerability profile?
spk05: Yeah, Jonathan, as we said, we're enrolling both of the lower dose cohort and the higher dose cohort. And we are encouraged by what we're seeing in terms of clinical activity. Unfortunately, at this point, given that this is a Phase 1b study that's where patients are randomized as to dose, we can't be any more granular at this point, but I think we're encouraged, very encouraged by the direction that we're going by enrollment, and we look forward to providing additional qualitative updates. We also think, Jonathan, as we said in the prepared remarks, that we're on track to hit the goals of full enrollment, and determination of the recommended phase 2 dose by the first quarter of 2022.
spk01: Got it.
spk04: Understood. Second question, what is your latest thinking on whether KO539 or other MENIN inhibitors will show comparable or different levels of activity in NPM1 mutant patients versus KMT2A rearranged patients?
spk05: Sure. Thanks for that. Jonathan, let me just press pause. I realized I neglected to answer the safety and tolerability question in your last question. To this point, we've seen, we continue to see what we're characterizing as a very favorable safety and tolerability profile, you know, very much consistent with what was seen in the Phase Ia. So I just wanted, I had neglected to mention that in my last answer. With regard to activity against two genetic subtypes, we haven't seen any, you know, clinically or preclinically, actually, any basis for believing that there is a difference in dose between those two genetic subtypes. And, you know, nothing that would convince us that those two populations should respond any differently. I think whether you're looking at our trial or at the trial of our, you know, one of our competitors, We're talking about small numbers, very small numbers, and, you know, a response here or there can skew the balance. At this point, you know, we believe, based on what we have today, we believe that the recommended phase 2 dose that we determine in the phase 1B will be sufficient, you know, to support activity, safety, and tolerability, both in the KMT2A and the NPM1 mutant populations.
spk04: Understood. And just last question for me. Did you guys get a chance to review the competitor ASH abstracts today? And if so, I'd love to hear your thoughts on any learnings that you got from that as it applies to the Mennon space. Thank you.
spk05: Yeah, thanks for the question. So yeah, we did see the ASH abstract from one of our competitors. I would say You know, we continue to be very encouraged by the clinical activity that they're seeing, both in the KMT2A and in the NPM1 mutant populations. You know, they're seeing a very encouraging response rate. They're seeing a rate of CRCRH that's perhaps on the lower bound of the guidance that we've given of 20% to 30%. But I'll just remind everybody, you know, it's early, both, you know, These data are being gathered and they're maturing in real time. We continue to believe, Jonathan, that there's potentially an opportunity to register at least 539 in both NPM1 and KMT2A. What I think we didn't see, and this isn't a criticism, is we didn't see clarity from that abstract in terms of the recommended phase two dose. So at least as far as when that abstract was submitted, They're very much where we are, or they were where we are, which is determination of the right going forward dose. And I think as far as what we're doing with KO539, our hope and expectation next year when we show the full phase one data is you'll have a very clear picture on the safety and tolerability and the efficacy at the specific recommended phase two dose. and real clarity as to then how does that read through into an ultimate registration-enabling study as a monotherapy, or how will it play in combination with other agents in earlier lines of therapy. That's, I think, the thing that we found missing, and perhaps they'll provide more color on that in the days and weeks ahead.
spk02: Got it. Thank you. Sure.
spk03: Moving on, we'll go to Tiago Faust with Credit Suisse.
spk07: Okay, thanks for taking the question. Perhaps just a follow-up on your competitor's update. They did provide some early duration of response data for patients that achieved CR-CRH, which seems to be lower than some other targeted agents. But again, I wanted to get your thoughts on how to interpret those data in the context of this particular relapsed refractory patient population. and what you think is a reasonable benchmark for that metric specifically. And then a quick follow-up on just on TP4NA, but I know it's difficult to predict enrollment, but for the AIM-HN trial, just any updates there on when we could see some data would be helpful. Thanks. Sure.
spk05: So, let's take those questions in turn, Tiago. on the bar, the hurdle, if you will, for median duration of response. We continue to guide that we think it's approximately six months. If you look at the data from that abstract from our competitor, they still have 13 patients on study. In our experience, that duration of response is likely to get longer. Again, I will refer you to them to speak to their data, but I wouldn't get overly exercised about that duration of response. It's also, you know, it's very early days, and I just want to stress a point that I stressed to Jonathan before. This was all done in the context of dose optimization, right? So, I think the needle is deflecting in the right direction. Clearly, you want to see, you know, longer duration is always better. I think we, you know, on balance, we came away, I think this index update was a good update. It was an encouraging update. In terms of the enrollment around AMHN, we're not at a point, Tiago, to give you an update on that. That study continues to enroll patients. We are, as we indicated in the prepared remarks, we should very imminently be dosing the first patients in current, and we've taken pains to make sure that The current study doesn't cannibalize the AIM-HN study. That's part of why we're starting in the PIK3CA mutant population, which by any estimate is, you know, anywhere from three to five times larger than the HRAS mutant. So AIM is ongoing. Current will start here certainly before the end of the year. And I think that, you know, that's going to build on the clinical data that we've already seen thus far, the very encouraging data for TIPI as a monotherapy.
spk01: Got it. No, perfect. Thanks a lot for the answers. Sure.
spk03: And next we'll go to Peter Lawson with Barclays.
spk09: Thanks for taking my questions. I guess as we think about kind of enrollment and recommended phase two dose, just how should we think about when that data comes out and how much data that we should expect to see next year, Troy?
spk05: Yeah, so it's a good question, Peter. So As far as the Phase 1B is concerned, as we've indicated, you know, the goal is to, in fact, the requirement is to enroll at least 12 valuable patients in each cohort and then to be able to compare those two cohorts to one another. So, from the Phase 1B, you'll have at least 24 valuable patients. Now, some of those may be very early on because they'll be relatively, you know, later in enrollment. But I think that's a good, meaningful update as far as the Phase 1B is concerned. And those patients, unlike the 1A, those patients will all be either KMT2A or NPM1. In terms of where those patients are, you know, our expectation is for, you know, to present that data at a medical meeting probably mid-year. So, you know, you'll have some maturity data. you know, of anywhere from, you know, three to six months to longer, depending on when they've come on the study, just to kind of help calibrate the quantum of data from the 1B and the timing. And from everything we can tell, Peter, you know, enrollment is tracking to what we would have expected, and we're on a good course. So, I think we're feeling good about, you know, delivering on those milestones next quarter.
spk09: Thank you. And then just when you hit the recommended phase two dose, what the plan is to broaden that development so you start thinking and start running combination trials, just your process there, is that partnerships or you just start running them yourselves or is it ISTs? What's the plan?
spk05: Yeah, so that's a good question. And that probably, you know, that could be a much longer discussion. We definitely see an opportunity in frontline. We also see an opportunity in the earlier relapse setting. And as you're aware, there are, you know, several standards of care depending on the genetic makeup of the patients. We'd like to, Peter, provided again that the recommended phase two dose supports it, we'd like to go as aggressively as we can into both of those populations. In terms of strategically and tactically how you do that, it's important to us that we maintain control of the design of the trial, that we maintain control of operational execution of certain of the trials. That's part of what we've been working on behind the scenes. There will be clearly opportunities for ISTs, but everything is predicated on getting a recommended phase two dose. So we're doing the work, both the preparatory work and the preclinical work to support the combinations, and we will move with the absolute greatest urgency we can into those combinations as soon as we have a recommended phase two dose that will support the submissions to begin the phase one combination studies.
spk01: Great. Okay.
spk02: Thanks so much, Drew. Pleasure.
spk03: And next we'll go to Ren Benjamin with JMP Securities.
spk11: Hey, good afternoon, guys. Thanks for taking the questions. I guess, Troy, just starting off, when we think about KO539, at what point do you have any sort of metrics that you might be able to throw away in terms of a go-no-go decision or any sort of hurdles that internally you want to meet before you decide you know, make the commitment to a registrational study and a path forward.
spk05: Yeah, Red, thanks for the question. So, we do have go, no-go criteria. I don't think we've articulated what they are, but, you know, they are, would certainly be sufficient. These are obviously, these are 12-patient cohorts, so you're not going to get statistical power, but you would want to see a level of CRCRH that's enough to give you confidence that a properly powered trial is would hit its endpoint of 20% to 30%, you know, CR, CRH. And so that's the way to think about those go-no-go's. And I don't think that's of any great surprise to anyone.
spk11: Got it. And then when we're thinking about, you know, the broader developmental strategy, you know, not only as a monotherapy but also as a combination, you know, can you maybe just take us through that? I mean, it seems like venetoclax is a natural – strategy in the future, but what other sort of combinations are you thinking about and where else do you want to go and explore?
spk05: Yeah, thanks for that, Ren. And, you know, one of the ways in which 539 we think is differentiated from the competition is, you know, we're expecting and hoping it should have a equivalent to superior efficacy and a better safety and tolerability profile, particularly in our ability to combine. And when I made the comment earlier in the call about the safety and tolerability is consistent, I just want to emphasize we've seen it is a very, very well-tolerated compound. There was one incidence back in the 1A of pancreatitis. We've seen no additional evidence of that. Really, no toxicities at all that we think would limit the ability either to develop the drug or to combine it. When you think about combinations, you know, the combinations depend on the genetic subtypes. So in the front line, you principally have venetoclax and azacitidine in the patients who are unfit. You have 7 plus 3 in the patients who are fit. And then you have to figure out how you work with the FLT3 inhibitors, because there are different algorithms depending on which patient population you're in. As you move to the patient populations that are earlier relapse, then you look at, you know, you look at patients who have failed one of those frontline options. You may see things like flagida. You may see, again, FLT3 combinations. And we're doing a lot of work, Wren, to figure out how can you cover as much landscape as possible with these different genetic subtypes, but also move as efficiently as possible to get to the market. You know, you... Ideally, you're setting up trials where you're able to take as many patients as possible, and then they just get slotted into sort of different arms or different combinations. All of that work is going on. Obviously, we're keeping a lot of that close to the vest because this is a super competitive field, and everybody, I think, recognizes the value of moving, both clinically and commercially, moving to those earlier lines of therapy. And, you know, I think it's highly likely there are opportunities for registration as a monotherapy. But if you want to do the best for patients and you want to drive the greatest value, you need to move with as much urgency as possible into combinations. And we're doing a lot of work behind the scenes to do just that. So I hope that gives you a little bit more color.
spk11: Yep, that's great. One last question for me. Regarding the phase two study of TIPI in AITL, that 32.8 months median overall survival looks really impressive to me. And I was wondering if, if you can either, you know, just maybe put that in context for me as well as does, do these final results potentially cause you to revive the program or potentially partner the program, you know, going forward? Yeah.
spk05: Yeah. Great, great question. And thank you for that. So I think, Like you, we were very impressed by both the response rate in AITL and the overall survival. And there's a lot more work to be done. I mean, we're looking forward. You know, Dr. Witzig is the PI. Dr. Witzig and Dr. Foss, who's at Yale, are really, you know, two of the thought leaders. They're both super excited about this data. The interesting thing about it, Ren, is because of the high level of activity in AITL, there isn't a requirement for a companion diagnostic. So we're doing some work internally. We need to meet with the KOLs. And obviously, we need to get some regulatory guidance. And that's something that we're planning on doing to understand what are the next steps for the program. But, you know, AITL is an ultra-orphan indication. PTCL is a little bit larger. but this is really meaningful activity, and we want to make sure we do our due diligence to understand what's that opportunity versus what we're doing in head and neck, what we're doing in AML, what you're hearing we're going to be doing with the next-gen FTI as far as large solid tumor indications. We view this as a high-class problem, and I think we'll be able in the next months to come back to you with more color on on what, if any, are the next steps for this program, for the T-cell lymphoma program with tippy farnet.
spk11: Perfect. Thanks for taking the questions, guys.
spk01: Sure.
spk03: And next, we'll go to Joe Pantginnis with H.C. Wainwright.
spk10: Hey, guys. Good afternoon. Thanks for taking the question. Most of my questions have been answered, but I wanted to focus on... corporate question. So you guys are obviously very busy with current studies you're about to start, you know, additional studies as well. So a lot going on here. And I'll pose the question this way. Have you had to anticipate or adapt in any way due to the global supply chain issues that the world is looking at right now for, you know, any of your activities?
spk05: Yeah, Joe, that's a good question. The short answer is no. I mean, well, the short answer is we haven't been impacted. The longer answer is, you know, we have a very strong cross-functional team that looks at, you know, clinical operations, clinical supply, you know, site activation. You know, there are still challenges in the system. Some sites you know, are unable to take on new studies because they're still kind of digesting the, you know, the fallout from the pandemic. But we really haven't seen much of an impact now in terms of the comet study, the current study. It appears that as far as supply chain and just, you know, clinical development activities generally that we're, you know, I don't know if we're an outlier. We're fortunate that we have small molecule orally available drugs that can be given on an outpatient basis. You know, so that actually works to our advantage. But I think at this point, you know, there's relatively little, if any, impact from either the pandemic or the supply chain challenges around it.
spk01: Great to hear. Thanks, Troy. Pleasure.
spk02: And moving on, we'll go to Eva Privatera with Callen.
spk12: Hi, thank you for taking my questions. Luckily, many of them have been addressed. So just a quick one. How is duration of response counted in your trials? Are patients censored when they go on to receive a transplant?
spk05: Yeah, Eva, thanks for the question. Let me actually invite Dr. Stephen Dale, who's on the phone here with me, to answer your question about how duration of response is measured. particularly with respect to transplant. Steven, do you want to take Ava's question?
spk08: Yeah, sure. Thank you, Troy. Hi, Ava. Thanks for the question. Yeah, so in very, very simple terms, you know, when patients go into transplant, so a patient who responds, tracking duration of response up until the point of transplant, the data are then censored. They're always censored at that point because if they're not, then the data become confounded because you can't distinguish between transplant and the active agent. The answer is yes, data are censored at that point.
spk02: Great. Thank you so much. Thank you, Eva.
spk03: And now I'd like to turn the call back to Troy Wilson for any additional or closing comments.
spk05: Great. Thank you, Paula. And thank you all again for joining our call. We'll be participating in the Credit Suisse Virtual Healthcare Conference next week. Look forward to speaking with many of you then. In the meantime, if you have any additional questions, please feel free to contact Pete, Mark, or myself. Thanks again, and have a good evening, everyone.
spk03: Thank you, and that does conclude today's call. We'd like to thank everyone for your participation. You may now disconnect.
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