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spk06: Thank you for standing by. Welcome to the Q3 2021 Heroes Pharmaceuticals, Inc. Earnings Conference Call. At this time, all participants are in a listen-only mode. After the speaker's presentation, there will be a question-and-answer session. To ask a question during the session, you will need to press star 1 on your telephone. Please be advised that today's conference is being recorded. If you require any further assistance, please press star 0. I would like to hand the conference over to your speaker today, Courtney Solberg with T-Rose. Please go ahead.
spk00: Thank you. This morning we issued a press release with our third quarter 2021 financial results, along with anticipated future milestones and recent accomplishments. This release is available on the Investors and Media section of Cirrus's website at www.cirrus.com. We will begin the call with prepared remarks by Dr. Nancy Simonian, our Chief Executive Officer, Dr. David Roth, our Chief Medical Officer, Kristen Stevens, our Chief Development Officer, and Jason Haas, our Chief Financial Officer. We will then open the call for questions. Dr. Eric Olson, our Chief Scientific Officer, and Conley Chee, our Chief Commercial Officer, are also on the call and will be available for Q&A. Before we begin, I would like to remind everyone that statements we make on this conference call will include forward-looking statements. Actual events or results could differ materially from those expressed or implied by any forward-looking statements as a result of various risks, uncertainties, and other factors including those set forth in the risk factors section of our annual report on Form 10-K, our quarterly report on Form 10-Q that were filed this morning, and any other filings that we make with the SEC in the future. In particular, the extent to which the COVID-19 outbreak continues to impact our operations and those of the third parties on which we rely will depend on future developments which are highly uncertain and cannot be predicted with confidence. Any forward-looking statements made on this call represent our views only as of today and should not be relied upon as representing our views as of any subsequent date. We specifically disclaim any obligation to update or revise any forward-looking statements. I would now like to turn the call over to Nancy.
spk01: Thank you, Courtney. The third quarter of 2021 was extremely productive for Cirrus as we continue to execute towards our three strategic priorities that we laid out in the beginning of the year. We are leveraging our leadership and expertise to build a synergistic portfolio where success in one program can inform and benefit efforts in another. We believe we are well on our way towards achieving our goal of becoming a fully integrated biopharmaceutical company that has the potential to provide profound benefit for patients with cancer and monogenic diseases. This quarter, we made two new strategic hires, adding additional strength to our experienced leadership team as we prepare for two expected NDAs in 2024. In September, we appointed Conley Chee as our first Chief Commercial Officer, bringing 20 years of pharmaceutical sales leadership, marketing, and strategy experience. In October, Jason Haas joined Cirrus as our new chief financial officer, bringing more than 25 years of healthcare investment banking and corporate finance experience. We are excited to have them on board. Importantly, as David and Kristen will review shortly, we made tremendous progress across both our hematology and CDK7 portfolios. In September, we dosed the first patient in our Select AML-1 Phase II trial of Tamiberitone and Rara-positive unfit AML patients, and the first patient in our dose confirmation study of SY-2101 in newly diagnosed APL patients. These milestones showcase our team's commitment to quickly advance medicines that have the potential to offer new standards of care for patients with hematologic cancers. Furthermore, at ESMO, we presented encouraging Phase I data for SY5609, our highly selective and potent CDK7 inhibitor, which showed single-agent clinical activity at tolerable doses. We believe 5609 has the ability to attack cancer in multiple ways and could therefore become a transformative targeted therapy. With that, I'd like to turn the call over to David, who will review our progress across our hematology and CDK inhibitor programs in more detail.
spk03: Thank you, Nancy. To start, I will discuss the designs of the TAMI Baratine Select AML-1 Phase 2 and the SY-2101 Dose Confirmation Phase 1 trials in AML and APL, respectively, as well as the unmet need of each indication. Our select AML-1 randomized phase two trial is now ongoing and aims to evaluate the triplet combination of tamibaratine, venetoclax, and azacitidine in RARA-positive newly diagnosed unfit AML patients. The trial begins with a single arm safety lead-in, followed by a randomized portion, which will evaluate the safety and efficacy of the triplet regimen compared to the combination of venetoclax and azacitidine in approximately 80 patients randomized one-to-one. The primary endpoint of the trial will evaluate the composite CR rate, and we expect to announce initial data in 2022. There remains a tremendous unmet need in AML, despite recent advances in the field. Nearly one-third of patients do not respond to the standard of care and have poor prognosis, and a majority of those with initial response ultimately relapse. A new treatment option that provides durable benefit and is well tolerated and convenient is what patients are looking for and need. Additionally, in September, we dosed the first APL patient in our dose confirmation study of 2101, which is our novel form of arsenic trioxide, or ATO. The study is expected to enroll up to 24 newly diagnosed APL patients and aims to evaluate the safety, tolerability, and pharmacokinetics of 2101. Patients will be enrolled during the consolidation phase of their APL treatment for PK assessments of single doses of 2101 in a fasted and a fed state to evaluate absorption effects on PK, as well as IV ATO to compare oral to IV directly. Patients will then have the option to enter multiple dose cohorts to provide additional steady-state PK and safety data. We expect to report dose confirmation and PK data in the first half of 2022, and we expect to initiate a Phase III trial in 2022. There are approximately 2,000 APL patients diagnosed annually in the United States and Europe. Thus, an oral treatment presents a significant market opportunity. The IV formulation of ATO in combination with ATRA is approved for use in newly diagnosed APL and is curative in more than 80% of patients. However, there's a tremendous treatment burden associated with the standard of care, requiring up to 140 infusions over the 10-month course of induction and consolidation treatment. Offering a new therapeutic option that is oral delivers similar clinical benefit and dramatically reduces the treatment burden has the potential to provide a tremendous benefit to these patients and improve their quality of life. Now turning to our CDK inhibitor portfolio. We recently presented at ESMO our updated phase one dose escalation data of 5609. Patients were treated in cohorts exploring continuous daily dosing, as well as intermittent dosing regimens. As a reminder, the trial is enrolling patients with advanced breast colorectal, lung, ovarian, and pancreatic cancer, as well as other tumor types with RB pathway alterations. As of the July 6th data cutoff, 54 patients were treated with single agent 5609 and were evaluated for the safety analyses, and 45 were evaluable for clinical response analyses. The majority of adverse events were low-grade and reversible. The most frequent treatment emergent adverse events were GI-related, fatigue, thrombocytopenia, and anemia. And across the study, there were low rates of discontinuation due to adverse events. Tolerability was optimized with the seven-day-on, seven-day-off dosing regimen, which had the lowest rates of treatment emergent AEs. And this regimen also demonstrated clinical activity consistent with that of other regimens. These data support the advancement of the seven-day-on, seven-day-off regimen in future studies. We were very encouraged to see single-agent clinical activity, particularly given that our study enrolled heavily pretreated patients, many with tumor types that are commonly refractory to treatment. In total, 13 of 45 response-available patients achieved stable disease across multiple tumor types. Of these 13 patients, Six had tumor regressions of up to 20%. Stable disease was observed in patients treated with both the daily and the intermittent regimens, including the seven-day-on, seven-day-off regimen, at doses as low as three milligrams per day. Notably, we observed the strongest clinical activity in pancreatic cancer patients. Five of 13, or over 38%, of responsive, valuable patients with pancreatic cancer achieved stable disease, including two with tumor shrinkage. Additionally, decreases were seen in clinically relevant tumor markers that are typically used in the clinic to monitor disease progression, including decreases in three of four or 75% of the pancreatic cancer patients with serial tumor markers. Nearly all pancreatic cancer patients are highly refractory to existing therapies, which makes these data particularly compelling. Across all patients in the trial, we saw the highest level of clinical activity in patients with KRAS mutations and in patients with RB pathway alterations. KRAS mutations are potent stimulators of cell signaling and transcriptional programs for cell cycle progression and are nearly ubiquitous in patients with pancreatic cancer. Knowing this, along with our data, further supports our mechanistic understanding of how CDK7 inhibition works, as well as our go-forward plan to focus next steps in the expansion phase of the trial in patients with pancreatic cancer. Additionally, as part of our ongoing study, we analyzed the degree of PolR2A induction, which showed high correlation between target region response as assessed by resist criteria. This data is important as it demonstrates the value of PolR2A as a PD biomarker of clinical response to CDK7 target inhibition with 5609. Additionally, we observed sustained PD effects to the desired target levels that lasted at least three days after dose suspension, showing that CDK7 target coverage can last long after the time when the drug is not taken. This supports our confidence that we have a critical biomarker that is associated with anti-tumor activity. Additionally, the data supports the use of intermittent dosing schedules to optimize tolerability, setting the stage for long-term administration in our go-forward combination plans in various indications. I'd now like to turn the call over to Kristin to discuss our planned next steps for 5609.
spk05: Thanks, David. As we've previously mentioned, we plan to pursue a three-pronged combination strategy for 5609, focusing on indications with high unmet need as well as where there is strong rationale based upon available mechanistic preclinical and clinical data. As David alluded to earlier, pancreatic cancer represents an area of tremendous unmet need, as the only approved second-line therapy offers a progression-free survival of just three months. We plan to initiate our expansion trial with 5609 in combination with chemotherapy in the fourth quarter of this year. The trial is designed to include two arms, both of which will enroll patients with metastatic pancreatic cancer who have progressed following first-line treatment with fulfurinox. One arm will explore the doublet regimen of 5609 in combination with gemcitabine, and the other arm will explore a triplet regimen of 5609 with gemcitabine and nabpaxil-paxil. The endpoints for the study are safety and tolerability, as well as efficacy measures including disease control rate and progression-free survival. Next, I would like to discuss our second combination strategy in mantle cell lymphoma, a subtype of B-cell non-Hodgkin's lymphoma affecting approximately 10,000 patients in the US and EU. This is a tumor that is driven by overexpression of cyclin D, an RB pathway regulator, and dependent on B-cell receptor signaling and NF-kappa-B transcriptional programs for survival and growth. Most patients will eventually relapse after their first-line treatment, and the median survival is three to five years. BTK inhibitors offer a non-chemotherapy option for second-line patients, but with reduced activity after first-line treatment. Most patients relapse, at which point they will have very limited treatment options, and face poor outcomes. We expect to initiate our Phase 1B trial in mantle cell lymphoma in the first half of next year. This trial will begin with a safety evaluation of 5609 as a single agent, after which we will move into a safety lead-in in combination with a BTK inhibitor. This will set the stage to move the combination with a BTK inhibitor into an expansion phase in second-line mantle cell lymphoma patients who have not previously been treated with a BTK inhibitor. The endpoints for this study include safety and tolerability, as well as efficacy measures such as complete response rate, overall response rate, and progression-free survival. Additionally, at the upcoming December ASH meeting, we will be presenting preclinical data of 5609 as a single agent, as well as in combination with a BTK inhibitor in mantle cell lymphoma cells. Finally, I would like to discuss colorectal cancer, or CRC, which is one of the leading causes of mortality and morbidity in the world. Although early diagnosis has significantly improved outcomes, many patients aren't diagnosed until the cancer is always metastasized to other parts of the body, making it very difficult to treat. Adding to the complexity is that different genetic mutations cause CRC to grow. Mutations in the BRAF gene are found in about 10% of metastatic CRC patients and are associated with a particularly dismal prognosis and a median survival of less than 12 months. As we announced in August, we recently entered into an agreement with Roche to explore 5609 in combination with atezolizumab in patients with BRAF mutant CRC. Under the terms of this agreement, we will supply 5609 for a combination dosing cohort in their ongoing Phase 1, Phase 1B intrinsic trial. This marks the first clinical investigation of a CDK7 inhibitor with an immunotherapy that has the potential to demonstrate significant and broad opportunity for combinations of 5609 with immunotherapy and other important indications. We believe that these three studies provide a solid foundation for us to explore the full potential of 5609 in indications where patients need better treatment options than those that are currently available. We look forward to providing additional updates as we progress in the clinic. I'd now like to turn the call over to Jason Haas, our Chief Financial Officer, to review our third quarter financial results.
spk09: Thank you, Kristen. Working in partnership with the team over the past month, I have already experienced firsthand the passion and shared commitment that drives the team every day. I could not be more excited to join them in ongoing efforts to develop new medicines that have the potential to provide profound benefits to patients. Now, turning to our third quarter financial results. Cirrus continues to operate from a position of financial strength. We entered the third quarter with $166.7 million in cash, cash equivalents, and marketable securities. compared to $174 million as of December 31st, 2020. This reflects the cash used to fund our operations during the first nine months of 2021, partially offset by gross proceeds of $75.6 million that Cirrus received from our January 2021 public offering. Based on our current plans, we believe we have sufficient capital to fund our planned operating expenses and capital needs into 2023 beyond multiple expected value drivers. We recognized revenue of $5.7 million in the third quarter compared to $3.8 million in the third quarter of 2020. This consisted of $5.6 million in revenue under our collaboration with Global Flood Therapeutics and $100,000 under our collaboration with Insight. In the third quarter of 2020, we recognized $3.5 million in revenue from our collaboration with GBT and $300,000 from our collaboration with Insight. R&D expenses were $27.3 million in the third quarter of 2021 compared to $17.7 million for the same period in 2020. This increase was primarily due to the continued advancement of Cirrus' clinical and preclinical programs and an increase in employee-related expenses. DNA expenses were $5.3 million in the third quarter of 2021 compared to $5.2 million for the same period in 2020. Finally, we reported a net loss for the third quarter of $26 million, or 41 cents per share, compared to a net loss of $19.5 million, or 43 cents per share, for the same period in 2020. With that, I will turn the call over to the operator for questions.
spk06: As a reminder, to ask a question, you will need to press star 1 on your telephone. To withdraw your question, press the pound key. Please stand by while we compile the Q&A roster. Our first question comes from the line of Ted Tentoff Piper Sandler. Your line is now open.
spk08: Great. Thank you very much, and thank you for taking my call, and congrats on all the good updates. I wanted to focus on 5609 and the compelling data that you demonstrated at ESMO. How quickly do you think we could actually start to generate data from that And I think it was very astute to kind of follow the data here. But are there other indications or from preclinical results, is there anything else that might represent future opportunities? And then just last question here, with a focus on hematology, does 5609 ultimately represent a partnering opportunity? Thanks so much.
spk01: Thanks for the question, Ted. Kristen?
spk05: Yeah, Ted, thanks for the question. So we believe that 5609 has broad potential in a large variety of unmet need cancers. You know, that being said, we are taking a very focused approach in three distinct populations, pancreatic CRC and mantle cell. So that's where our first area of focus is and could lead to a broad number of potential opportunities. Beyond that, you know, we always remain open to partnering to answer that question. However, you know, we're continuing to progress forward the plans that we have in place.
spk08: Great. That's very helpful. It makes a lot of sense, and I'm excited to see continued progress.
spk01: Thank you. Thank you, Ted.
spk06: Thank you. Our next question comes from the line of Phil Nadeau from Cowling Company. Your line is now open.
spk02: Good morning, thanks for taking our questions. A couple from us. First, on the SelectAML1 trial for timibaratine, you indicated data will be out next year. Is that initial data from the safety lead-in portion of the study, or will the initial data also include results from the randomized portion?
spk03: Thanks for that question. So the trial, as you know, is now enrolling, and we're anticipating initial data in 2022. We're starting with a safety lead-in, and that will likely be the focus of the initial data, which would include safety and tolerability, and may also include clinical activity. So that's what you can look forward to.
spk02: Perfect. That's helpful. And then on the 2101 dose confirmation study, Looking at the entering clinicaltrials.gov, I guess there's a couple things that are confusing to me. It looks like there's two PK sequences that, at least according to clinicaltrials.gov, are exactly the same. What is the difference between PK module sequence one and PK module sequence two? Are those two different doses of 21-01, or is there some other difference that's not obvious from the clinicaltrials.gov entry?
spk03: Yeah, so again, that's another good question. So one of the objectives of the study is to evaluate the PK profile of 21-1 after it's administered orally. And we're going to be doing a single dose of 21-1 in the fasted state as well as in the fed state. And that will enable us to compare the PK effects of absorption of the drug. We're also going to do a PK following IV And that will enable us to compare the PK of the oral to the IV directly in the same patient. So it's a very important experiment. The other module is going to allow patients to take the drug, 21-on-1, in multiple doses over the course of their consolidation cycles. And that will enable us to repeat the PK later on during the cycle so we can get steady-state PK assessments to see what the steady-state levels are during dosing. And that will also give us an opportunity to evaluate the safety with multiple doses. So one is a single-dose module and one is a multiple-dose module.
spk02: It looks like there's actually two single-dose modules. Maybe I'm reading this incorrectly, but there's sequence one and sequence two. Are you testing two different doses of 2101 or –
spk03: Well, I have to go back to look at how it's written in the clinical trials, but I believe the sequences refer to whether someone gets the oral or the IV first or second.
spk02: I got it, okay. And then, in terms of the multiple dose that you mentioned, it looks like patients will only get 2101 during the first cycle. Is that correct? They won't be able to go on and receive 2101 in subsequent cycles. they'll basically have to go back to IV ATO?
spk03: Yeah, so the patients are undergoing induction and consolidation with standard of care, IV and ATRA. And they'll be participating during their consolidation phases, during the time when they wouldn't be getting the IV arsenic. So we'll be able to include them in the study along the course of their normal standard of care treatment. And when they finish their study procedures, they can go back to continue getting their standard of care treatment with the IV. Perfect. Thanks again for taking my questions.
spk06: Thanks, Phil. Thank you. Our next question comes from the line of Jason Butler from JMP Securities. Your line is now open.
spk10: Hi. Hi. Thanks for taking the questions, and I appreciate all the updates. Just to follow up on 2101, can you just – Review for us the most important parameters of the PK profile that you're focused on here. Obviously, you mentioned steady state, AUC. Did TMAX and CMAX also matter here? And then I have a follow-up. Thanks.
spk03: Sure. So the PK parameters, and just to remind you, this drug has already been evaluated in a Phase I study in non-APL patients, patients who had MDS, AML, and CMML. And the PK was assessed using the standard parameters with CMAX and AUC, and it's already been shown that the drug can be administered and achieve equivalent exposures relative to IV arsenic. We're basically repeating many of those procedures in APL patients using a direct crossover comparisons just to firm up our understanding of what the go-forward dose is using similar types of analyses. And then we'll be able to start the registration trial in 2022. Got it.
spk10: Okay. And then can you give us an update on progress with the select MDS trial? Is everything ramping there the way you'd expect it?
spk05: Yeah, so the SelectAML and MDS trial are both remaining on track. We're pleased with the progress, and we remain, you know, on target to our guidance.
spk10: Great. Thanks for taking the questions.
spk06: Thanks, Jason. Thank you. Our next question comes from the line of Mark Bradenback from Oppenheimer. Your line is now open.
spk11: Hey, good morning, and thanks for taking the questions. I'm just wondering, with respect to the 5609 expansion in PDAC, if there's any specific reason for initially going after patients who received fulfurinox in the first line and then doing your combinations with gemcitabine in the second line versus the other way around. And another question I had is just with respect to the nomination of your next development candidate in 2022, is that potentially going to be associated with a milestone payment under your collaboration with GBT? Thanks for taking the questions.
spk05: Yeah, so to answer the first question around our pancreatic cancer expansion, so we're starting focused in the second line. This is an area of tremendous unmet need. If you think about the only approved second line therapy has a PFS of approximately three months. In addition, you know, we have preclinical data that supports synergy with gemcitabine. And so this is a place in which we really are leveraging what we know about the underlying biology. and the mechanistic data, as well as the clinical data and preclinical data that we've generated. And so this gives us an opportunity for a data readout that we think will have very clear next steps. So that's a little bit of the rationale. And, you know, as that continues to progress, we could consider moving into the front line, but our first focus will be in the second line, where there's the area greatest on that need. In terms of partnering, I'll, sorry, DC, I'll turn that back to Nancy.
spk01: Thanks, Mark. So we are continuing to guide to having our next development candidate next year in 2022. You know, we have multiple programs in preclinical development. We said our most advanced is our CDK-12 program. And at this point in time, we haven't yet sort of communicated what the development candidate will be. But by having a portfolio of programs in preclinical, it allows us to, you know, be able to select the one that we think is, you know, best to move forward at that point in time. So stay tuned for that.
spk11: Okay. Super helpful. Thank you.
spk06: Okay. Thank you. As a reminder, to ask a question, you will need to press star 1 on your telephone. To withdraw your question, press the brown key. Our next question comes from the line of Zegbe Jala. I'm Roth Capital Partners. Your line is now open.
spk07: Good morning. Thanks for taking my questions. The first one I have here is on 1425. A follow-up to Phil's question, just trying to understand how much data we're going to see or is it something where we're just going to be looking at initial safety and maybe some biomarker or we're going to have substantial patient numbers to really kind of understand. I just know people get excited when you have any kind of combo study with venetoclax. I just kind of want to help set expectations for that.
spk01: Yes, as David said earlier, you know, we initiated the trial this last quarter. We're very excited about the opportunity for combining Tammy Baratine with Ben Aza. We think that based on the sort of biology and the data that we have with Tammy and Aza, we have the real potential in being an oral targeted drug, a real potential to add benefit to those patients. And at this point in time, we're guiding to initial data next year. We're starting the trial with a safety lead-in, but both of the drugs are given at their sort of full doses during that safety lead-in. And we'll present, you know, the data that we have next year, which will include safety and clinical activity from the patients that we've enrolled at the time.
spk07: Thanks. And then the next one here is about the APL program. I've been kind of thinking that, you know, this is going to be a pretty big deal getting that dose confirmation data because I think it could help set expectations really well for the actual study. So I was just wondering, you know, how are you guys thinking about interpretation of the results from the dose confirmation study and how that may influence the outcome of the actual study, full study?
spk01: Yeah, I think as David said earlier, we already have data with 2101 that it is orally bioavailable and that it shows sort of comparable PK parameters to IV, the historic IV data. And so in some ways, this next data set is really to hone in on the exact dose that we want to take into the Phase III trial that we expect to start next year. So we think that it's not a question of, you know, will we be able to find something to move into phase three in terms of just what is the best dose to take forward. And so we're, you know, very excited about the fact we started that trial. We're already gathering data and that we're on track to initiate the phase three next year. And, you know, a lot of enthusiasm for the opportunity for this to make a big difference for patients.
spk07: Thanks, Nancy. And I'm just going to merge my last two questions here to save time. For 5609, I know that's a bit tricky question, but we're just curious as to how you're viewing the probability of success of this program in solid versus liquid tumors. And then the last bit is just about your pipeline, any comment on indications for the candidate that could be nominated, and then also try to understand if there's any update on on efforts with DBT. I know you guys noted the milestone payments. I was just wondering how things are going there. And then I think that my iconic district fee program is no longer ongoing. So I think the first two are probably the focus.
spk01: Okay. Let me make sure I'll get those. So I think your first question was on how do we think about probability of technical success for 5609 in the solid versus the heme space? Here I would say one of the things that we've known, we've been working on CDK7 inhibition from the time that we started the company. We've explored CDK7 inhibition preclinically in both hematologic cancers as well as solid tumors, and we've seen a high degree of activity both in heme tumors and in solid tumors, and we've always had an interest in both. And so I think if we looked at sort of the biology, the mechanism, the preclinical data, we think that there's a very good possibility for making a difference in both heme tumors and in solid tumors. When we initiated the program, we decided to focus on one, which was in solid tumors. But now that we have that data and see sort of encouraging biologic activity in and clinical activity and a good biomarker and a better sense of where might be the best place to take it in heme tumors related to the RB pathway alteration, that really has opened up the door for us to now sort of simultaneously explore it in the clinic. So I guess I'd say we like both opportunities, and we think that they are just also the starting out points for, you know, a greater exploration in a variety of solid and heme tumors. So thank you. I'd answer, we'd like both a lot. Eric, maybe you want to take the question on GBT and also talk a little bit about the myotonic dystrophy program, which is continuing ongoing. But Eric?
spk04: Yeah, thanks, Zegba, for the question. Of course, our sickle cell program and type 1 myotonic dystrophy programs are really built around our expertise in kind of understanding the levers, the molecular levers that control kind of the expression of specific genes. And these are both diseases where we know exactly what gene we need to modulate the expression of in order to hopefully have a therapeutic benefit. So both of those programs, as you know, are preclinical in the discovery stage, and very active very active chemistry programs, and, you know, stay tuned for further updates. In terms of the sickle cell program, you know, it's a collaboration with GBT, and, of course, they will be primarily responsible for communicating and updating progress on that program. But we're quite pleased with the kind of platform we've built for each of those diseases and the chemistry approaches we're taking.
spk07: Thanks for taking my questions and looking forward to the updates in 2022.
spk06: Thanks, Siga. Thank you. At this time, I'm showing no further questions. I would like to turn the call back over to Nancy Simonian for closing remarks.
spk01: Thank you, Operator, and thank you, everyone, for joining us today. We appreciate your continued support. This is a very exciting period for Cirrus, and we look forward to providing further updates on our progress as we continue to advance to a fully integrated biopharmaceutical company with a portfolio of targeted medicines in cancer and monogenic diseases. Please reach out to us if you have any additional questions, and have a wonderful day.
spk06: This concludes today's conference call. Thank you for participating. You may now disconnect.
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