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 as VERITAC-2 Data Conference Call. All lines will be placed on mute to prevent any background noise. After the speaker's remarks, there will be a question-and-answer session. If you would like to ask a question during this time, simply press star followed by the number one on your telephone keypad. If you would like to withdraw your question, again, press the star one. 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. Erica Hamilton in an early late-breaking session at the American Society of Clinical Oncology annual meeting and published in the New England Journal of Medicine on Saturday, May 31st. Full presentation and press release highlighting this information is available in the investor 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 two 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 two of the presentation and in the company's recent filing 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. 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. Today on this call, we will discuss the results from that VERITAC-2 trial that we believe support our view that vepdegestrant, or Befdeg, 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 needs, and our excitement around the opportunity for Befdeg in the ESR1 mutant setting continues to grow. As a reminder, as a PROTAC, Befdeg works by directly inducing degradation of the estrogen receptor via the proteasome. We believe this novel mechanism to block signaling is differentiated from other ER-targeting therapies in ER-positive HER2-negative breast cancer. Vepdegestrant is the first PROTAC degrader to enter and have a positive readout in a phase III trial, and we are on the verge of submitting the first-ever new drug application for a PROTAC. On slide five, 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 a 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 signaling. In contrast, as shown on the left side of the slide, tumors harboring an 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 signaling for tumor proliferation. Turning to slide six, 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 mutation. 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 III trial were previously treated with a CDK4/6 inhibitor. I'm excited to share that in VERITAC-2, vepdegestrant achieved a 2.9-months improvement in median PFS over fulvestrant in the ESR1 mutant population, with a statistically significant and clinically meaningful improvement in median PFS of five months versus 2.1 months for the fulvestrant arm. We believe data from the VERITAC-2 trial demonstrate that vepdegestrant's unique mechanism of action as a PROTAC degrader differentiates it 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 vepdegestrant 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 Pfizer teams for successfully completing the first phase III trials with a 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 vepdegestrant 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 eight, VERITAC-2 was a global phase III trial comparing the efficacy and safety of vepdegestrant 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 six 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 Befdeg at 200 mg orally once daily or fulvestrant 500 mg administered intramuscularly with loading doses on days one and 15 of the first cycle and then on day one 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 nine, a total of 624 patients were randomized to receive Befdeg or fulvestrant. Of these, 43% had tumors with ESR1 mutations, and in this population, 33% in the Befdeg 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 Befdeg 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 two 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 vepdegestrant demonstrated a statistically significant and clinically meaningful 2.9-months improvement in median PFS over fulvestrant, with a hazard ratio of 0.57 and two-sided p-value of 0.001. The group receiving vepdegestrant 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 vepdegestrant group and 6.0 months in the fulvestrant group. Notably, six-month landmark PFS was approximately doubled, with vepdegestrant at 45.2% versus fulvestrant at 22.7%. As seen on slide 12, we're looking at all patients. Befdeg did not meet the primary endpoint. Befdeg demonstrated a median PFS of 3.7 months versus 3.6 months for the fulvestrant arm, with a hazard ratio of 0.83 and two-sided p-value of 0.07. Investigators 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 Befdeg was 42.1% versus fulvestrant at 20.2%. For all evaluable patients, the CBR was approximately 34% for Befdeg and 29% for fulvestrant. In the ESR1 mutant population with measurable disease, the ORR was 18.6% with Befdeg and 4.0% with fulvestrant, and 10.9% with Befdeg and 3.6% with fulvestrant in the all-patient population. Of the responders with ESR1 mutant tumors, 11 of 18, or 61%, in the Befdeg 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, Befdeg demonstrated a consistent PFS benefit over fulvestrant across relevant pre-specified 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 Befdeg over fulvestrant. Overall, VERITAC-2 enrolled 22% pre or perimenopausal women, which is an important consideration because 15%-20% of new cases of invasive breast cancer are in pre or perimenopausal women. These data suggest Befdeg has the potential to provide clinically meaningful improvements as a monotherapy treatment option for the 40%-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 and efficacy, we are also very pleased with the safety and tolerability, which we believe is further evidence of a best-in-class profile. Befdeg 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 one or two 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 Befdeg. Grade one or two nausea was reported in 13% of patients. Notably, grade one or two vomiting and diarrhea were reported in less than 10% of patients receiving Befdeg and therefore are not included on the slide. The effect of Befdeg on the QT interval was explored in a sub-study of 88 patients in VERITAC-2, which showed a small QT prolonging effect of 11.1 milliseconds with Befdeg. No cases of torsade 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 Befdeg can address the unmet medical need with a best-in-class efficacy and tolerability profile. Our data from VERITAC-2 clearly demonstrate Befdeg 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. Befdeg also demonstrated a favorable safety and tolerability profile that resulted in few dose reductions or discontinuations. Importantly, treatment with Befdeg resulted in low rates and severity of GI adverse events that are commonly reported with oral SERDs and negatively impact 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 gives us confidence that Befdeg has the potential to offer a new treatment that does not 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, Befdeg 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 Befdeg 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. Befdeg showed a median PFS of five months versus 2.1 months for the group receiving fulvestrant, a 2.5 times improvement, and an objective response rate higher than any previous phase III trials with a 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 US, 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. 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 Befdeg 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 Befdeg, 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 Befdeg as soon as they are available. I'd like to conclude by thanking all of those involved in the Befdeg 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 needs. As you'll see on slide 19, we continue to work towards maximizing the potential of our PROTAC platform and deep pipeline. We have significant momentum across our development programs following this positive readout from our phase III evaluation of vepdegestrant. For our LRRK2 degrader, ERV-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 BCL-6 degrader, ERV-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 ERV-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. Operator, can you please open the queue? Thank you. We will now begin the question and answer session. If you have dialed in and would like to ask a question, please press star one on your telephone keypad to raise your hand and join the queue. If you would like to withdraw your question, simply press star one again. If you are called upon to ask your question and are listening via speakerphone in your device, please pick up your handset to ensure that your phone is not on mute when asking your question. Again, press star one to join the queue. Our first question comes from the line of Jonathan Miller with Evercore ISI. Your line is open. Hi, guys. Thanks so much for taking the question, and 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. 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 in 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 Befdeg into combination settings where maybe the markets would be more impactful? Thanks so much. Yes, thanks, Jonathan. Thanks for the question. Yeah, clearly, we are excited about the opportunity. The 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. Yes, certainly, we believe that Befdeg's profile is being a potential best-in-class degrader overall. In terms of the opportunity in the second line, we do think it's significant. 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 our second-line study combo with the CDK4/6. Clearly, the collaboration we have with Pfizer, which has been an excellent one, was set up in 2021 with a view that Befdeg would be second-line monotherapy, first-line combo with palbociclib, and maybe even an adjuvant study. The idea of having 50/50 development, 50/50 commercialization was a very attractive one. Now, as we stand today. Next question comes from the line of Derek Archila with Wells Fargo. Your line is open. Good morning. Thank you for the question. This is Hou calling in for Derek. First of all, just kind of asking the impact of SERENA-6, if patients move from AI to SERD in early line, how is it impacting its second-line plus market opportunity? Secondly, just seeing the New England Journal commentary, there was a commentary on the six-month kind of inclusion criteria before they have their most recent endocrine therapy progress. It did not seem to identify a more endocrine-sensitive population. Just wanting to ask, just based on the information you have, any additional color on that in terms of what may be some of the hypotheses? Yeah, thanks for the question. Certainly, it was intriguing to see the Serena 6 discussion yesterday at the session. Ian, any commentary? Yeah, I think, obviously, it's an interesting study, interesting result. If you're at the session and saw the discussion 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 PFS2 and overall survival before really understanding whether this early switch has a long-term benefit for patients. I think probably 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. 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. Yeah, in terms of the six-month inclusion criteria, yeah, we thought that by having patients be on for at least six months would eliminate or remove, I should say, patients that had primary endocrine resistance. 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 did not happen. We still had a drop-off. It was not 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 vepdegestrant or fulvestrant, and therefore, clearly endocrine resistance, whether it was secondary or otherwise, it is not clear. There is 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. That is something that we are going to continue to look at because clearly, unfortunately, having that inclusion criteria really did not do what we had hoped it would do. Awesome. Thank you so much. Our next question comes from the line of Jonathan Miller with Evercore ISI. Your line is open. Hi, guys. Thanks for coming back to my question. Same question, I just got cut off. I think the answer got cut off just at the second half when it was getting interesting. I’d love to hear about the current environment of the collaboration and plans. Yeah, 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 Befdeg would be a second-line monotherapy, first-line combo with palbociclib, and even an adjuvant study as well. The idea then of having a 50/50 commercialization scenario was very attractive, obviously, to both Pfizer and to Arvinas. As we stand today with the decisions not to go forward with the first-line study with the termocycline and a second-line combo study with the CDK4/6, we're left with second-line monotherapy. Even though we're excited about that market opportunity, that then would be split 50/50 between Pfizer and Arvinas. That becomes less attractive, certainly less attractive to Pfizer and not very attractive to us. We're 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. That's the type of discussion we're having with Pfizer right now. Yeah, thanks so much. Our next question comes from the line of Evan Siegelman with BMO. Your line is open. Hi there. This is Connor on for Evan. Thanks for taking our question. As you mentioned, right, you previously discontinued some of the combination trials with the CDK4/6 evaluating vepdegestrant in earlier lines. I guess we're just wondering, what are your latest thoughts on sort of the path for Befdeg clinical development beyond what we've seen in VERITAC-2, sort of opportunities for combo? I believe Pfizer is included in combination with their CDK4/6. Love to get your thoughts there. Thank you. Yes, thanks. So yeah, 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, one B study with abemaciclib in the second line. Also, Pfizer have added vepdegestrant into their ongoing CAT6 study. We will see how that data pans out over the coming months. That could be an interesting next step. The reality is that the current state of the collaboration is no further development of vepdegestrant is planned. 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, it was with one set of parameters, and now we are in a different setting. Our focus is to make sure that the value of vepdegestrant 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 ERV-102, ERV-393, ERV-806, and 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. Got it. Thank you. Our next question comes from the line of Eliana Merle with UBS. Your line is open. Hi, this is Tiju Thom for Eli. Thanks for taking my question. 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. There are a lot of phase one or phase three trials of SERD in one L. What would be a scenario that would potentially start a phase three trial for Befdeg in first line? To the class, I mean, what we're doing right now is focused on, along with Pfizer, focused on 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. 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. We would, at that point, if we had that compound back, be looking to partner or write license. We are very well aware of the costs needed to launch a product. We want to make sure that everyone knows that our focus is on getting value for Befdeg, but really focusing on the rest of our pipeline where we think the future of the company is. Yeah, I think just really quick follow-up. How much do you expect in milestones, maybe as the agreement still stands today, from filing approval in second-l ine? Yeah, there's certainly milestones for approvals in the current plan. Obviously, they've been moved fairly quickly into the profit share component. That was the major part of the agreement, was actually the profit share, the 50/50 aspect of that. Yeah, the reasonable milestone that we come up with approval. Thanks for that. Our next question comes from the line of Paul Choi with Goldman Sachs. Your line is open. Hi. Thank you. And good morning, everyone. Thanks for taking the question. 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. Thank you. Ian, do you want to start with that, and then maybe Alex? Yeah. I mean, I think label discussions with the FDA are not something that we're going to comment on. As you said, we've had good productive discussions with them. As with all submissions, there's going to be lots that's a review issue. How things end up looking in the label will be part of that review issue and backward discussion we continue to have as part of the process. Yeah. 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. That refers to the significance in the GI tox and the advantages over the current standard of care. We certainly will be able to point to patient-reported outcomes once that data becomes available as well. 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. Okay. Great. Thanks for taking the question. Our next question comes from the line of Sudan Loganathan with Stephens. Your line is open. Hello. Good morning. This is Felix Poma 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 ESR1 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 lines of treatment. Can you have a breakdown in those guidelines of treatment? That would be very helpful as well. Thanks for the question. Alex, do you want to talk? Yeah. 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. Of that patient population, approximately 40-50% of those patients will express an ESR1 mutation. That's the addressable market. 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. Yeah. Regarding the breakdown. Yeah. Regarding the breakdown, second and third line, it's in the forest plot. Obviously, we only had 20% of the patients, as I mentioned in the presentation, who were at two prior lines, so far fewer patients. In both cases, the hazard ratio is below one in favor of Befdeg. Obviously, the confidence intervals overlap, but as you said there in the presentation, every subgroup that we looked at, and Erica Hamilton made this point strongly too in her presentation, were in favor of Befdeg, including third-line and second-line. No big difference there, but differences in patient numbers. Okay. Thank you. Our last question comes from the line of Tyler Van Buren with TD Securities. Your line is open. Hi. This is Frances on for Tyler Van Buren. Just one question. Can you elaborate on the frequency of QT prolongation? Has this been observed with other SERD? How do HCPs weigh the QT risk versus other factors that you demonstrated here, such as favorable GI tolerability? Yeah. I mean, I think in talking to the investigators of the study, because it was very mild, I think that's how Erica Hamilton characterized it yesterday, keeps the 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. Particularly in the monotherapy setting, it's really a non-issue in the investigators' opinion. Thank you. That concludes our question-and-answer session. I would like to turn the call back over to John Houston for closing remarks. Thanks, everybody. Thanks to everyone for joining us this morning. We certainly look forward to providing additional updates throughout the year. Thank you very much. This concludes today's conference call. You may now disconnect.