Arvinas, Inc. (ARVN) Earnings Call Transcript & Summary

Ladies and gentlemen, thank you for standing by. My name is Desiree, and I will be your conference operator today. At this time, I would like to welcome everyone to the Arvinas ASCO Data Conference Call. [Operator Instructions] I would now like to turn the conference over to Jeff Boyle, Investor Relations. You may begin.

Thank you, and good morning, everyone. Thank you for joining us to review the results of the Phase III VERITAC-2 study of vepdegestrant as a monotherapy for ER-positive HER2-negative breast cancer. These data were presented by Dr. Erika Hamilton in an oral late-breaking session at the American Society of Clinical Oncology Annual Meeting and published in the New England Journal of Medicine on Saturday, May 31. Full presentation and press release highlighting this information is available on the Investors section of our website at arvinas.com. With me today are Arvinas' President and Chief Executive Officer, John Houston; and our President of Research and Development, Ian Taylor. Our Chief Financial Officer, Andrew Saik; and our Interim Chief Commercial Officer, Alex Santini, will join for the Q&A portion of the call. Our Chief Medical Officer, Noah Berkowitz, is unavailable this morning due to a religious observance. Before we begin, I want to remind you on Slide 2 of the presentation we posted this morning that today's discussion will contain certain forward-looking statements that involve risks and uncertainties. These risks and uncertainties are outlined on Page 2 of the presentation and in the company's recent filings with the Securities and Exchange Commission, which we urge you to read. Our actual results may differ materially from what is discussed on today's call. And with that, I'll turn the call over to our CEO, John Houston. John?

Thank you, Jeff, and welcome to everyone on the call. We were very excited to see our data presented at the ASCO oral late-breaking session yesterday and the publication in the New England Journal of Medicine, a truly significant first for Arvinas. And today, on this call, we will discuss the results from that VERITAC-2 trial that we believe support our view that vepdegestrant or vepdeg has the potential to become a best-in-class second-line therapy for ESR1 mutant breast cancer. This is an area where a novel treatment option can address high unmet need and our excitement around the opportunity for vepdeg in the ESR1 mutant setting continues to grow. As a reminder, as a PROTAC, vepdeg works by directly inducing degradation of the estrogen receptor via the proteasome. We believe this novel mechanism to block ER signaling is differentiated from other ER-targeting therapies in ER-positive HER2-negative breast cancer. Vepdeg is the first PROTAC degrader to enter and have a positive readout in a Phase III trial, and we are in the verge of submitting the first ever new drug application for a PROTAC. On Slide 5, this graphic shows that in the adjuvant and first-line metastatic treatment settings, most ER-positive breast tumors rely on estrogen signaling for growth and typically retain a wild-type ESR1-driven pathway. However, in later-line settings, particularly following treatment with endocrine therapy in combination with the CDK4/6 inhibitor, as shown on the right side of the slide, tumors often acquire resistance mechanisms that lead to estrogen receptor independent growth. As a result, many ESR1 wild-type tumors in the second line and beyond are no longer driven by ER signaling. In contrast, as shown on the left side of the slide, tumors harboring and activating ESR1 mutation present in up to 50% of tumors in the late-line setting remain responsive to ER-directed therapy, suggesting continued dependence on ER signaling for tumor proliferation. Turning to Slide 6. Currently, there is no established consensus for treatment of patients with advanced ER-positive HER2-negative breast cancer after disease progression on a CDK4/6 inhibitor and endocrine-based therapy. While sequential endocrine therapy is a well-established approach for patients with presumed endocrine sensitivity, current treatment options have limitations. In the second-line setting, approximately 20,000 patients are diagnosed each year in the U.S. with ESR1 mutant metastatic breast cancer. Treatment with fulvestrant, a current standard of care option in this setting, can be burdensome for patients as it is administered by painful intramuscular injection and has limited PFS benefit following disease progression on a CDK4/6 inhibitor and estrogen therapy. In the Phase III EMERALD trial, elacestrant, the most recently approved selective estrogen receptor degrader, or SERD, demonstrated a 1.9-month improvement in median progression-free survival or PFS over fulvestrant in patients with tumors harboring an ESR1 mutant mutation. And in the Phase III EMBER trial, imlunestrant showed a 1.7-month improvement in median PFS over fulvestrant in patients with tumors harboring an ESR1 mutation. It should be noted that only 67% of patients in the EMBER-3 trial were previously treated with a CDK4/6 inhibitor. I'm excited to share that in VERITAC-2, vepdeg achieved a 2.9-month improvement in median PFS over fulvestrant in the ESR1 mutant population with a statistically significant and clinically meaningful improvement in median PFS of 5 months versus 2.1 months for the fulvestrant arm. We believe data from the VERITAC-2 trial demonstrate that vepdeg's unique mechanism of action as a PROTAC ER degrader differentiated from other ER-targeting therapies in patients with tumors harboring an ESR1 mutation. I'll now turn the call over to Ian who will discuss the data in detail. I'll then outline how the data support our plans for the filing and potential approval of vepdeg in the second-line ESR1 mutant setting. Ian?

Thank you, John. First, I'd like to begin by thanking the patients and physicians who participated in the trial and congratulating the Arvinas and Pfizer teams for successfully completing the first Phase III trial with the PROTAC and earning a podium presentation at the ASCO Annual Meeting as well as the publication in the New England Journal. The efficacy and tolerability from the trial support our conviction that vepdeg has the potential to be a best-in-class monotherapy treatment for patients in the second-line ESR1 mutant setting. Turning to the trial design on Slide 8. VERITAC-2 was a global Phase III trial comparing the efficacy and safety of vepdeg versus fulvestrant in patients with ER-positive, HER2-negative advanced breast cancer who were previously treated with endocrine therapy and a CDK4/6 inhibitor and may have received up to one additional line of endocrine therapy. Patients eligible for the study must have received their most recent endocrine therapy for at least 6 months before disease progression, which must have occurred since the last line of therapy administered. Patients were stratified by ESR1 mutation status and the presence or absence of visceral disease and randomized to receive vepdeg at 200 mg orally once daily or fulvestrant 500 mg administered intramuscularly with loading doses on days 1 and 15 of the first cycle and then on day 1 of each subsequent 28-day cycle. The primary endpoint was progression-free survival or PFS by blinded independent central review or BICR in two populations, patients with ESR1 mutations and in all patients. Select secondary endpoints included overall survival, clinical benefit rate, or CBR, objective response rate, or ORR, and safety and tolerability. As shown on Slide 9, a total of 624 patients were randomized to receive vepdeg or fulvestrant. Of these, 43% had tumors with ESR1 mutations. And in this population, 33% in the vepdeg group and 12% in the fulvestrant group remained on treatment at the time of data cutoff. The median treatment duration in the ESR1 mutant population was 5.1 months in the vepdeg group and 2.8 months in the fulvestrant group. The most common reason for discontinuation in both groups was disease progression. On Slide 10, you'll see that baseline patient characteristics were generally well balanced between treatment arms and all patients had received a prior CDK4/6 inhibitor. All patients had received prior therapy in the advanced or metastatic setting and approximately 20% had received 2 prior lines of therapy for advanced or metastatic disease. Therefore, the patient population in VERITAC-2 is representative of the real-world second-line setting in the U.S. and its clear and rational design allows for meaningful interpretation of benefit compared to the standard of care. Turning to the results of the study on Slide 11. We'll first look at the primary endpoint of PFS among the ESR1 mutation population, where vepdeg demonstrated a statistically significant and clinically meaningful 2.9-month improvement in median PFS over fulvestrant with a hazard ratio of 0.57 and 2-sided p-value of 0.001. The group receiving vepdeg showed a median PFS of 5.0 months versus 2.1 months for the group receiving fulvestrant, more than doubling the amount of time to disease progression. The median follow-up was 7.4 months in the vepdeg group and 6.0 months in the fulvestrant group. Notably, 6-month landmark PFS was approximately doubled with vepdeg at 45.2% versus fulvestrant at 22.7%. As seen on Slide 12, when looking at all patients, vepdeg did not meet the primary endpoint. Vepdeg demonstrated a median PFS of 3.7 months versus 3.6 months for the fulvestrant arm with a hazard ratio of 0.83 and 2-sided p-value of 0.07. Investigator-assessed PFS was consistent with the BICR-assessed PFS, demonstrating the robustness of the Phase III study results. Additional secondary endpoints shown on Slide 13 included clinical benefit rate or CBR and objective response rate or ORR. Among evaluable patients with ESR1 mutant tumors, the CBR with vepdeg was 42.1% versus fulvestrant at 20.2%. For all evaluable patients, the CBR was approximately 34% for vepdeg and 29% for fulvestrant. In the ESR1 mutant population with measurable disease, the ORR was 18.6% with vepdeg and 4.0% with fulvestrant and 10.9% with vepdeg and 3.6% with fulvestrant in the all population -- all patient population. Of the responders with ESR1 mutant tumors, 11 of 18 or 61% in the vepdeg group compared to 1 of 4 or 25% in the fulvestrant group remained on treatment without progression. The median duration of response was not reached. Overall survival data at key secondary endpoint were immature at the time of data cutoff and median OS has not been reached in either treatment group. As seen on the forest plot on Slide 14, in the ESR1 mutant population, vepdeg demonstrated a consistent PFS benefit over fulvestrant across relevant prespecified prognostic demographic and baseline disease characteristic subgroups, including in patients with more difficult-to-treat visceral disease. Notably, treatment in both pre, peri and postmenopausal settings favored vepdeg over fulvestrant. Overall, VERITAC-2 enrolled 22% pre or perimenopausal women, which is an important consideration because 15% to 20% of new cases in invasive breast cancer are in pre or perimenopausal women. These data suggest vepdeg has the potential to provide clinically meaningful improvements as a monotherapy treatment option for the 40% to 50% of patients in the second-line plus setting with ESR1 mutant advanced breast cancer. Turning to Slide 15. In addition to clinically meaningful improvement in efficacy, we are also very pleased with the safety and tolerability, which we believe is further evidence of a best-in-class profile. Vepdeg was generally well tolerated with a manageable safety profile as demonstrated by low rates of discontinuations and dose reductions due to treatment-emergent adverse events. Most treatment-emergent adverse events were grade 1 or 2 in severity. Rates and severity of gastrointestinal AEs, which are burdensome and commonly reported adverse events with oral SERDs that can negatively affect patients' daily lives were low with vepdeg. Grade 1 or 2 nausea was reported in 13% of patients. Notably, Grade 1 or 2 vomiting and diarrhea reported in less than 10% of patients receiving vepdeg and therefore, are not included on the slide. The effect of vepdeg on the QT interval was explored in the sub-study of 88 patients in VERITAC-2, which showed a small QT prolonging effect of 11.1 milliseconds with vepdeg. No cases of Torsades de Pointes were reported and no patients discontinued study treatment due to prolonged QT. Moving to Slide 16. In the second-line ESR1 mutant setting, our market research indicates clinicians remain underwhelmed by the available monotherapy treatment options that aren't fulfilling the efficacy and/or tolerability needs of an estimated 20,000 new patients in this setting each year who have previously received CDK4/6 inhibitors and may include patients who are pre or perimenopausal. Slide 17 summarizes why we believe vepdeg can address the unmet medical need with a best-in-class efficacy and tolerability profile. Our data from VERITAC-2 clearly demonstrate vepdeg provides a statistically significant and clinically meaningful improvement of 2.9 months in median PFS over fulvestrant in previously treated patients with ESR1 mutated ER-positive HER2-negative advanced breast cancer. Vepdeg also demonstrated a favorable safety and tolerability profile that resulted in a few dose reductions or discontinuations. Importantly, treatment with vepdeg resulted in low rates and severity of GI adverse events that are commonly reported with oral SERDs and negatively impacts patients' daily lives. VERITAC-2 enrolled a broad real-world patient population representative of those previously treated for breast cancer with all patients having received prior CDK4/6 inhibitors. The totality of these data give us confidence that vepdeg has the potential to offer a new treatment that doesn't require a trade-off between efficacy and tolerability. Our recent discussions with the FDA have been productive, and we are on track to submit a new drug application to the FDA in the coming weeks. I'm also happy to share that in patient-reported outcome data, which will be submitted for presentation at a medical conference later this year, vepdeg showed statistically significant improvement in time to deterioration across several indices, including overall quality of life and pain interference. These data further support our belief that vepdeg can be a best-in-class treatment option for patients with ESR1 mutant advanced breast cancer. I'll now turn the call back to John.

Thanks, Ian. There's still a high unmet need for improved monotherapy treatment options for the approximately 20,000 patients treated each year in the second-line ESR1 mutant setting. Vepdeg showed a median PFS of 5 months versus 2.1 months for the group receiving fulvestrant, a 2.5x improvement and an objective response rate higher than any previous Phase III trials with an ER monotherapy in the second-line ESR1 mutant population. Additionally, VERITAC-2 enrolled patients who are representative of the real-world second-line population in the U.S. with all patients previously treated for ER-positive HER2-negative breast cancer with a CDK4/6 inhibitor and endocrine therapy. We've heard from physicians how important this consideration is when evaluating the right treatment option for their patients. And when we think about the patients we intend to help, the potential to offer an efficacious treatment with very low rates of the adverse events that negatively impact patients' lives, nausea, diarrhea, vomiting, is something we believe clearly differentiates vepdeg from currently available treatments. Turning to next steps. We're excited about the potential to improve the lives of patients in the second-line ESR1 mutant setting with vepdeg, and we are on track to submit a new drug application to the FDA in the coming weeks. We and Pfizer are working to ensure this potentially best-in-class treatment option, if approved, is available for patients as quickly as possible. We will provide any material updates to the commercialization plan for vepdeg as soon as they are available. I'd like to conclude by thanking all of those involved in the vepdeg development program, most importantly the patients themselves. These data are a tremendous win for patients and further validate PROTAC degraders in therapeutically relevant diseases with high unmet need. As you'll see on Slide 19, we continue to work towards maximizing the potential of our PROTAC platform and deep pipeline. We have a significant momentum across our development programs following this positive readout from our Phase III evaluation of vepdeg. For our LRRK2 degrader, ARV-102, we plan to share the initial data from the single ascending dose cohorts of the Phase I study in Parkinson's disease in the second half of 2025. We also recently shared exciting preclinical data at the AACR Annual Meeting for our BCL6 degrader, ARV-393, and plan to share additional preclinical and preliminary Phase I clinical data in the second half of this year. We're also excited by a recent IND clearance from the FDA, allowing us to proceed with clinical evaluation of ARV-806, our KRAS G12D degrader and anticipate initiating a Phase I study in the near future. Together, these updates and upcoming catalysts continue to showcase the potential of our PROTAC degraders to address difficult-to-treat diseases, and we're excited for what's ahead across our pipeline. So with that, operator, can you please open the queue?

[Operator Instructions] And our first question comes from the line of Jonathan Miller with Evercore ISI.

Congrats on the oral presentation. I guess I'm thinking back to your earnings call a couple of weeks ago and to some conversations that we've all had with you recently. And I'm recalling you say that the second-line monotherapy opportunity is meaningful, but maybe less attractive to your partner, split 50-50, less attractive to you, split 50-50. I'm hearing a lot of enthusiasm for that market and your voice today. Should I take this call as a sign that we can expect news soon about the future of that partnership, the future of the commercialization potential, the future of the ability to move vepdeg into combination settings where maybe the markets would be more impactful?

Yes. Thanks, Jonathan. Thanks for the question. Yes, clearly, we are excited about the opportunity. Last several weeks has been difficult not to be able to talk about our data. And now we've got the chance to do that. And yes, we believe that has shown its profile as being a potential best-in-class degrader overall. In terms of the opportunity in the second line, we do think it's significant. And what you're alluding to, I think, is also a reality. We also made announcements that we would not go forward with our first-line Phase III study and a second-line study combo with a CDK4/6. And clearly, the collaboration we have with Pfizer, which has been an excellent one, was set up in 2021 with a view that vepdeg would be a second-line monotherapy, second line -- first-line combo with palbociclib and maybe even an adjuvant study. So the idea of having 50-50 development, 50-50 commercialization was a very attractive one. Now as we stand today [Audio Gap].

Next question comes from the line of Derek Archila with Wells Fargo.

This is [ Hal ] calling in for Derek. So I guess first of all is just kind of asking the impact of SERENA-6 if patients move from AI to SERD in early lines, how is it impacting its second-line plus market opportunity? And then secondly, just in the New England Journal commentary, there was a commentary on the 6 months kind of inclusion criteria before they have the most recent endocrine therapy progress. It did not seem to identify a more endocrine sensitive population. So just wanted to ask just based on the information you have, any additional color on that in terms of what may be some of the hypothesis?

Yes. Thanks for the question. And certainly, it was intriguing to see the SERENA-6 discussion yesterday at the session. Ian, any commentary?

Yes. And I think, obviously, it's an interesting study, interesting results. If you're at the session and saw the discussions and the discussion afterwards, I think it's relatively clear that there's certainly no strong consensus that this is going to become common practice really anytime soon. I think people feel like they need to see more data in terms of PFS 2 and overall survival before really understanding whether this early switch has a long-term benefit for patients. So I think probably more -- certainly more data from that study will be required, maybe even more studies will be required before it really changes practice and then changes the first-line and second-line opportunity overall. So I think there's still great opportunity for monotherapy for the foreseeable future. I think that was really the consensus from sitting in the audience. Yes, in terms of the 6-month inclusion criteria, yes, we thought that by having patients be on for at least 6 months would eliminate or remove, I should say, patients that had primary endocrine resistance. And we've all seen that from the curves from EMERALD and other studies where you get that quick drop off at the first scan. We also thought that restricting no prior chemo and no prior fulvestrant would also fortify and do the same thing. It seems like that didn't happen. We still had a drop-off. It wasn't quite as steep as the other studies, but we still had a drop off at the first scan of patients that were not responding to either vepdeg or fulvestrant and therefore, clearly endocrine resistance, whether it was secondary or otherwise, it's not clear. There's our hypotheses. One could be just that having 100% prior pretreatment with CDK4/6 inhibitor is really a driver of not having endocrine resistance for a lot of patients based on whatever alternate mutations they have in their tumors. But that's something that we're going to continue to look at because clearly, unfortunately, it really -- having that inclusion criteria really didn't do what we had hoped it would do.

Our next question comes from the line of Jonathan Miller with Evercore ISI.

Same question. I just got cut off. I think the answer got cut off just at the second half when it was getting interesting. So I'd love to hear about the current environment and the collaboration plans.

Yes. I hope I can give the same answer I was giving. I think I started off by saying that, obviously, the collaboration we had with Pfizer, which has been excellent, was set up with the predicate that vepdeg would be a second-line monotherapy, first-line combo with palbociclib and then even an adjuvant study as well. And the idea then of having a 50-50 commercialization scenario is very attractive, obviously, to both Pfizer and to Arvinas. But as we stand today, with the decisions not to go forward with a first-line study with atirmociclib and a second-line combo study with the CDK4/6, we're left with second-line monotherapy, and even though we're excited about that market opportunity, that then would be split 50-50 between Pfizer and Arvinas and that becomes less attractive, certainly less attractive to Pfizer and not very attractive to us. So we are currently in discussion with Pfizer about how we can resolve that. Clearly, it's more attractive if one of the companies has all of the benefit here in moving into that market, and that's the type of discussion we're having with Pfizer right now.

Our next question comes from the line of Evan Seigerman with BMO.

This is [ Connor ] on for Evan. As you mentioned, right, you previously discontinued some of the combination trials with the CDK4/6s evaluating vepdeg in earlier lines. I guess we're just wondering what are your latest thoughts on sort of the path for vepdeg clinical development beyond what we've seen in VERITAC-2, sort of opportunities for combo. I believe Pfizer is included in combination with their KAT6. I'd love to get your thoughts there.

Yes. Thanks. So yes, as I just said, the first-line study was canceled and the second-line study we had with CDK4/6 was also canceled. The ongoing studies we have is a second-line study, Ib study with atirmociclib in second line. And also Pfizer have added vepdegestrant into their ongoing KAT6 study. So we'll see how that data pans out over the coming months, and that could be an interesting next step. But the reality is that the current state of the collaboration is no further development of vepdeg is planned. So that goes back to the previous answer, which involves looking at the collaboration and coming up with a resolution that recognizes the fact that when we signed the deal in 2021, there was with one set of parameters and now we're in a different setting. Our focus is to make sure that the value of vepdeg is recognized and that we then get focused on the rest of our pipeline because the rest of the pipeline we have is incredibly attractive with our LRRK2, BCL6, KRAS G12D and two other -- at least two other programs moving into the clinic shortly. That's where we think the biggest driver of value is going to be for Arvinas over the very short term.

Our next question comes from the line of Eliana Merle with UBS.

This is Tejas on for Ellie. I guess if you could just provide any color at this time on how much commercial spend you expect will be needed from you guys to support the launch in second line? And then there are a lot of Phase I -- or Phase III trials of SERDs in 1L. And what would be a scenario that would potentially start a Phase III trial for vepdeg in first line?

Well, to the cost, I mean what we're doing right now is focused on -- along with Pfizer, focused on the submission to the FDA, which will happen fairly shortly and also submissions in other regions ex U.S. That's our immediate focus. We have a fairly small but mighty commercial team that is doing all the planning to be launch ready, relatively minimal cost, to be quite honest. And the plan would be to get to kind of an agreement with Pfizer about what that launch would look like and who would do it. If it's Pfizer, then that's fine. They go ahead and they have the infrastructure. If they do not want to do that for whatever reason, then I could guarantee that we would not be in a position to do that launch on our own. So we would -- at that point, if we had that compound back, we'd be looking to partner or out-license. We're very well aware of the costs needed to launch a product. And we want to make sure that everyone knows that our focus is on getting value for vepdeg, but really focusing on the rest of our pipeline where we think the future of the company is.

Yes. I think just a really quick follow-up. How much do you expect in milestones maybe as the agreement still stands today from approval -- filing approval in second line?

Yes. There's certainly milestones for approvals in the current plan. And obviously, they moved fairly quickly into the profit share component. So that was the major part of the agreement. It was actually the profit share, the 50-50 aspect of that. So yes, the reasonable milestone that we come up with approval.

Our next question comes from the line of Paul Choi with Goldman Sachs.

I want to ask how you're thinking about potential inclusion and recommendations within guidelines and how that might evolve and also specific label claims that you and your partner, Pfizer, might be seeking in order to help best position vepdegestrant in this particular population.

Ian, do you want to start with that and then maybe Alex.

Yes. I mean I think label discussions with the FDA are not something that we're going to comment on. As we said, we've had good productive discussions with them. And, yes, as with all submissions, there's going to be lots that's a review issue. And so how things end up looking in the label will be part of that review and back for discussion we continue to have as part of the process.

Yes. And I think from a commercial standpoint, highlighting what Ian and John had referenced earlier, I mean we'll have a fair amount of opportunity to talk about the efficacy profile, the median PFS improvement, the absolute improvement, the delta improvement. We'll have an opportunity to talk about the tolerability profile, which is actually quite good. And that refers to the significance in the GI tox and the advantages over the current standard of care. And we certainly will be able to point to patient-reported outcomes once that data becomes available as well. So we'll have a fair amount of very, very positive messages to be able to convey that will align with our label once that submission process is complete, reviewed and ultimately approved.

Our next question comes from the line of Sudan Loganathan with Stephens.

This is [indiscernible] for Sudan Loganathan. Congrats on the data. I have a couple of questions. I believe on Slide 16, you had indicated that the epidemiology for ESR-mutant patients is around 20,000 for second line plus. Is it only second line or third line? If you can help us understand the breakdown. Secondly, the PFS breakdown -- for those who have had one prior line of treatment versus two prior line of treatment, can you have a breakdown in those prior lines of treatment, that would be very helpful as well.

Thanks for the question. Alex, do you want to talk about?

Yes. The 20,000 patients is a combination of both the second-line setting and the third-line setting. Approximately 40,000 patients is the addressable market in the second-line setting. And of that patient population, approximately 40% to 50% of those patients will express an ESR1 mutation. So that's the addressable market. And a number of those patients will be captured in the second-line setting and a number of those patients will be captured in the third-line setting.

Regarding breakdown second and third line, as in the forest plot, obviously, we only had 20% of the patients, as I mentioned in the presentation, who are -- had two prior lines, so far fewer patients. But in both cases, the hazard ratio is below 1 in favor of vepdegestrant. Obviously, the conference intervals overlap. But as we said in the presentation, every subgroup that we looked at, and Dr. Hamilton made this point strongly too in her presentation, were in favor of vepdeg, including third line and second line. So no big difference there, but differences in patient numbers.

Our last question comes from the line of Tyler Van Buren with TD Securities.

This is [ Francis ] on for Tyler Van Buren. Just one question. Can you elaborate on the frequency of QT prolongation? Has this been observed with other SERDs? And then how do HCPs weigh the QT risk versus other factors that you demonstrated here such as favorable GI tolerability?

Yes. I mean I think in talking to the investigators in the study because it was very mild, I think that's how Erika Hamilton characterized it yesterday, QT effect of 11.1 milliseconds and the confidence interval stays below 20 milliseconds. That's a really important point. They have not been worried about it at all. Patients have no symptoms as a result of it. There was no Torsades de Pointes. There was no discontinuations for QT. So particularly in the monotherapy setting, it's really a nonissue in the investigator's opinion.

And that concludes our question-and-answer session. I would like to turn the call back over to John Houston for closing remarks.

Thanks, operator, and thanks to everyone for joining us this morning, and we certainly look forward to providing additional updates throughout the year. So thank you very much.

This concludes today's conference call. You may now disconnect.