Kymera Therapeutics, Inc. Q2 FY2022 Earnings Call

Welcome to the Kymera Therapeutics Quarterly Conference Call. Leading the call from management are Nello Mainolfi, Founder and CEO; Jared Gollob, Chief Medical Officer; and Bruce Jacobs, Chief Financial Officer. After management's prepared remarks, we will open the call to your questions. Please note this event is being recorded. Before we get started, I would like to remind everyone that some of the comments that management may make on this call may include forward-looking statements, as outlined in the press release. Actual events and 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 Kymera's most recent filings with the SEC and any other future filings that the company may make with the SEC. You are cautioned not to place any undue reliance on these forward-looking statements and Kymera disclaims any obligation to update such statements. I will now hand the call to Nello Mainolfi, Founder and CEO. Please go ahead.

Thank you, operator, and thank you, everyone, for joining us on our second-quarter results conference call. We're excited to share with you today the continued progress we're making towards building Kymera into a best-in-class, fully integrated degrader medicine company. As we reach our two-year anniversary as a publicly listed company later this month, we can be really proud of a period of outstanding growth and achievement at Kymera. I want to start by saying that the second quarter has been significant for us, particularly in terms of substantial clinical progress we've made by advancing our three lead programs into important stages of their development. Specifically, we dosed the first patients in our three first-in-class clinical programs, including commencing patient dosing in Part C of our Phase I trial of KT-474. This achievement ushers in a new phase for the company as we look forward to demonstrating how targeted protein degradation and these molecules in particular can impact disease and patient lives. This is just the start of our journey towards treating patients in many disease areas such as hidradenitis suppurativa or atopic dermatitis through degradation of IRAK4 with KT-474, hematological malignancies and solid tumors with KT-333 or our selective STAT3 degraders, MYD88-mutant B cell lymphomas with our IRAKIMiD degrader KT-413, which has the potential to be the first precision medicine for this condition. At Kymera, as evidenced by our initial programs, we have the ambitions and capabilities to broadly apply our platform by expanding the druggable proteome to address inadequately drugged or undrugged targets, creating the potential for us to transform the lives of patients, which is really what the company was founded upon and is moving towards. We ended the second quarter in a solid financial position with approximately $482 million in cash. Three first-in-class TPD assets are in clinical studies. One program, KT-253, our MDM2 degrader, is close to IND filing, and we have multiple preclinical candidates expected to drive us to our goal of at least one new IND per year and productive collaborations with our partners Sanofi and Vertex. We have multiple patient data sets expected by year-end, including the Part C data for KT-474, our patient cohort. Our plan is to share this data later this year with the medical and investor communities as well as with our partner Sanofi to enable their decision around advancing KT-474 into Phase II studies. Now Jared will walk you through our recent progress and goals for 2022 for each of our disclosed programs. Before turning the call over to Bruce for a financial update, I will then finish with some concluding remarks before handing the call back to the operator for a Q&A session in which Jared, Bruce, and I would be available.

Thanks, Nello. We've made substantial progress with our clinical programs this quarter, which I am excited to share. I'll start with our IRAK4 program and a lead candidate KT-474, an orally available potential first-in-class degrader of IRAK4, a key protein involved in inflammation mediated by the activation of toll-like receptors and IL-1 receptors. A barren activation of these pathways is the underlying cause of multiple immune inflammatory conditions. KT-474 is being developed for the treatment of TLR, IL-1R driven immune inflammatory diseases with high unmet medical need such as hidradenitis suppurativa, atopic dermatitis, rheumatoid arthritis, lupus, GI inflammation, and potentially others. KT-474 is designed to block TLR/IL-1R mediated inflammation more broadly compared to monoclonal antibodies targeting single cytokines and to enable pathway inhibition that is superior to IRAK4 kinase inhibitors by abolishing both the kinase and scaffolding functions of IRAK4. We are collaborating with Sanofi on the development of degrader candidates targeting IRAK4 including KT-474, outside of the oncology and immuno-oncology fields. Late last year, we completed dose escalation in over 100 healthy volunteers in the single ascending dose and multiple ascending dose portions of the KT-474 Phase I trial. This was the first randomized placebo-controlled trial for a heterobifunctional degrader. The data demonstrated near complete IRAK4 degradation in peripheral blood mononuclear cells and skin, robust inhibition of multiple ex vivo stimulated disease relevant cytokines, and a favorable safety profile. At the SID Annual Meeting in May, we disclosed that KT-474 degrades IRAK4 and inhibits cytokine production in different immune and skin cell types, highlighting the broad impact of KT-474 across multiple disease relevant cell types and supporting the continued development of IRAK4 degraders in patients with HS, AD, and other IL-1R/TLR driven autoimmune diseases of the skin, where IRAK4 plays a central role in the pathogenesis of inflammation. You can find that poster along with all our other publications in the Scientific Resources section of our website. Most recently, as Nello just mentioned, we are excited to share that we commenced dosing patients in the patient cohort Part C of the Phase I clinical trial. Part C is an open-label study of KT-474 that is expected to enroll up to 20 patients with moderate to severe hidradenitis suppurativa or atopic dermatitis to examine the safety, PK/PD, exploratory biomarker, and clinical activity of this first-in-class degrader therapeutic. While we are in the early stages of the patient cohort, we expect enrollment to progress as planned so we can disclose the data before year-end. KT-474 is being administered daily on an outpatient basis for 28 days, with patients followed through day 42. Patients will receive a daily dose of 75 milligrams of KT-474 with food. This dose is expected to provide a plasma exposure that is approximately equal to that achieved with the 100 milligram per day dose in the fasting state in healthy volunteers in the MAD portion of the trial, which showed maximal or close to maximal degradation in blood and skin and broad disease relevant cytokine inhibition ex vivo. The goal for this study is to confirm that our PD and safety profile in patients aligns with what we have seen in healthy volunteers. EPDM points include the impact of KT-474 on IRAK4 levels in PBMC and in active HS and AD skin lesions as well as on the expression of proinflammatory gene transcripts in skin lesions and on both whole blood ex vivo cytokine induction and plasma biomarkers of inflammation.

Thanks, Jared. I'll keep my comments brief. For the quarter, we recognized $11.5 million of revenue; this total reflects revenue recognized pursuant to our Sanofi and Vertex collaborations. At the end of the quarter, our deferred revenue total on the balance sheet was approximately $84 million, reflecting partnership revenue we expect to recognize over the next several years, excluding the receipt of any potential future milestones. On operating expenses, R&D for the quarter was $41.3 million, of which $4.8 million represented non-cash stock-based compensation. The adjusted cash R&D spend of $36.5 million, which excludes this stock-based compensation, reflects a 14% increase from the comparable amount in the March quarter. On the G&A side, our spending was $11 million, of which $4.9 million was non-cash stock-based comp. The adjusted cash G&A spend was $6.1 million, reflecting an 8% decrease from the comparable amount in the March quarter. Finally, we exited the second quarter with a cash and equivalents balance of approximately $482 million, which provides a runway based on our current anticipated spending levels into 2025. Recall that it’s our policy not to include in our cash runway any payments from milestones that we have not yet received.

Thanks, Bruce and Jared. In conclusion, we're clearly very excited about all that we've accomplished this year at Kymera as well as by all that is in front of us. We're in a strong position with an exciting first-in-class pipeline that is progressing through the clinic; the best-in-class platform in the discovery engine about which you will continue to hear as we disclose more programs and data; productive partnerships with Vertex and Sanofi that allow us to extend across multiple disease areas; and a very strong position that you just heard from Bruce that enables us to continue to invest in high-value programs and generate several important data sets in the next few years. We're poised to deliver key clinical insights in the second half of this year and continue to demonstrate the potential of our approach to targeted protein degradation to improve the lives of patients. The second half of the year's impact, as you've already heard; we look forward to generating, for the first time, key patient data in HS and AD from our KT-474 IRAK4 degrader program, as well as key proof of mechanism data in two oncology clinical programs, KT-413 IRAKIMiD degrader and KT-333 as STAT3 degrader. We mentioned earlier our key goals for this data set that, to summarize briefly for KT-474, we're looking to confirm that the healthy volunteer PD and safety profile in this patient cohort, which we believe could be a game-changing profile towards a small molecule or anti-inflammatory drug. In oncology, we want to demonstrate that these molecules are behaving as predicted based on our preclinical studies and that the translation of degradation and safety is occurring in a predictable way. If we can do this well, which we have confidence in, then we can set clear expectations of clinical activities starting from 2023 and beyond once we would be focusing on our responders population. We're also very excited by the prospect of adding our fourth clinical program later in the year with our MDM2 degrader KT-253, which we believe will have significant clinical potential. We have also several earlier programs with clear degrader rationale and large commercial opportunities that we're advancing towards the clinic and will be disclosing as we approach clinical investigation. We did tremendous progress this year, and I want to thank the Kymera team, our collaborators, our partners, and importantly, all the healthy volunteers and patients, which allow us to advance the development of our potentially transformative therapies. Finally, I would like to thank all of you who have taken time this morning for our call. I look forward to a great Q&A discussion. And for that, I will hand the microphone back to the operator so we can take your questions. Thank you again.

We will now begin the question-and-answer session. Our first question comes from Brad Canino with Stifel. Please go ahead.

Good morning. On KT-474, can you share any additional findings from your preclinical investigations of the potential mechanism behind the QT effect and why it becomes saturated as you've observed in Phase 1? I think you previously discussed the cardiomyocytes assay around the 1Q call, but is there anything else to add that you've done? And then on KT-413, the IRAKIMiD, some of your peers have had recent difficulty finding a therapeutic window for these given the on-target IKZF1 neutropenia. Can you talk about your confidence in achieving the required IRAK4 degradation within a feasible window? And then maybe discuss the likelihood of observing any anecdotal clinical activity in MYD88 mutated patients that might be enrolled within that all-comer group? Thank you.

Thank you, Brad. While you asked two questions, I’ll address them both. Starting with the second question, our strategy with the IRAKIMiD degrader aims to create a synergistic effect that is cell-autonomous, meaning that the degradation of IRAK4 interacts with the degradation of Ikaros and Aiolos in MYD88 mutant lymphoma, resulting in a significant antitumor effect both in laboratory settings and in live models. We manage this combination in a single molecule by thoroughly understanding the degradation kinetics and the impact on the specific cell types, as well as the management of the established pharmacology, which includes both the expected and unforeseen effects. We have two key differences compared to previous efforts. First, we anticipate no adverse pharmacology from IRAK4 degradation, as it is generally well tolerated. Therefore, the only pharmacological effects we need to monitor will come from the IMiD component. Our drug behaves uniquely compared to other tested drugs in this mechanism; we administer it once every three weeks and it has a pharmacokinetic/pharmacodynamic profile that ensures strong degradation for the initial two to three days, after which we see a recovery of targets and some blood cell types known to be affected by IMiD biology. This combination of pharmacokinetics and dosing frequency allows us to induce significant apoptosis early on, which means we do not need to administer doses continuously, contributing to a manageable safety profile. We have conducted extensive studies in non-human primates and believe this profile will translate well into clinical settings. Additionally, we focus on translating pharmacokinetics and pharmacodynamics, which are integral to our technology, as we monitor protein levels. Our starting doses in trials are chosen with a specific PK/PD profile in mind, enabling us to understand and mitigate risks during translation. Regarding KT-474, I do not have any new updates to share. What we’ve discussed before is that the QT finding is non-adverse. We’re pleased to talk about it, as it is non-dose responsive and self-limiting. We believe it is saturated given our mild affinity for the HERG channel, which is likely fully engaged based on the molecule's tissue distribution. The key factor is that this finding does not respond to dosage or concentration changes, which significantly reduces the risk profile of the molecule moving forward. This helps us avoid excluding QT in scenarios where the risk of arrhythmia could be heightened, which we have not encountered so far. Jared, do you want to add context regarding the mechanism?

In terms of the mechanism from the in vitro work with the iPSC cardiomyocytes, we have been encouraged by how our in vitro findings align with what we've observed in vivo in healthy volunteers. The effect we see on current in these cardiomyocytes is attributed to a mild and delayed effect on HERG, which corresponds with the delayed effect observed in vivo. It also seems to be specific to the compound and not related to any on-target effects. We have clearly demonstrated that the impact on HERG is not caused by the degradation of IRAK4, as shown by our use of another IRAK4 degrader in this in vitro system that degrades IRAK4 effectively without affecting HERG. Returning to your question, Brad, regarding the activity of MYD88 mutant lymphoma during dose escalation, we are currently enrolling a diverse group of B-cell lymphoma patients in Phase 1a to expedite the dose escalation process. From our preclinical studies, we know that achieving a 60% to 80% knockdown of IRAK4 in the IMiD substrate Ikaros and Aiolos is necessary for antitumor effectiveness in MYD88 mutant lymphoma. While we are enrolling a wide array of B-cell lymphoma patients in Phase 1a, we will start focusing more on DLBCL patients and possibly a few MYD88 mutant patients once we reach doses that provide that 60% to 80% knockdown. Therefore, it’s possible that towards the end of Phase 1a, we may see some antitumor activity in the MYD88 mutant group. Our primary aim is to concentrate on antitumor activity in Phase 1b, where we will specifically enroll MYD88 mutant wild-type DLBCL patients, which will take place next year. What we aim to report later this year is focused on obtaining the desired knockdown of the three targets associated with antitumor activity in preclinical models, ensuring we can achieve this at doses that are safe and well tolerated.

Yeah. And then really derisking the molecule, right? As I said in the remarks earlier, it's about ensuring that the molecule has the profile that aligns with what we seem to be really active preclinically. If we can show that, basically the degradation and safety, then we derisk the molecule, and the biological and clinical question will be asked once we focus more on MYD88 mutant patients, which will be as soon as we can, likely in 2023 and beyond. Thanks, Brad.

The next question is from Michael Schmidt with Guggenheim. Please go ahead.

Hey, guys. Thanks for taking my questions. I had a couple on KT-474 as well. On the QT signal, assuming that this non-adverse level of QT prolongation is being confirmed in the patient study, what is your expectation how that might potentially affect the longer-term clinical potential of the drug? Is there any expectation, for example, that that would preclude certain patients down the road from using the drug or certain combinations that might be affected by that? The other question I had is just on Part C on the exploratory clinical endpoints. Understanding that it is non-placebo controlled and that, as you said, the steady-state knockdown is only reached in the second half of this four-week period, is there a certain level of efficacy based on these outcomes in AD & HS that one would expect or hope to see based on the PK/PD of the drug? Thanks so much.

Thanks. To address a couple of questions here from Michael. The first one, then I'll pass it to Jared for the second one. We've done, as you can imagine, extensive work on trying to contextualize these non-adverse QT findings for advancing this drug towards clinical and commercial success. Our view is this: if the findings remain within the range we have observed thus far, we expect that there would be no impact on clinical, regulatory, or commercial success of this drug. I'll explain a bit where we're coming from. For a 10 to 20 millisecond change, especially in the absence of concentration dependency and large excursions, what we're discussing is something that slightly modifies the baseline of subjects that doesn't really reach a high-risk level for arrhythmia. From our early explorations with our experts and interactions with the FDA, we expect that we can advance this molecule in a broad variety of disease indications regardless of the background. Jared will comment on which specific small number of patients may not be suited for this particular drug with this profile.

We feel as though this should affect very few patients in the target indications. Patients who have prolonged QT at baseline and those with hereditary syndromes resulting in QT prolongation, as well as patients who are on other drugs that they cannot come off of that are clearly shown to prolong the QT interval, would be the patients that would not be able to go on to our study and might be excluded from use of the drug if approved and commercially available. However, we expect that to be a very small fraction of the total patients eligible for this type of treatment.

Going back to the Part C, just to reiterate, the goal of the study has always been to demonstrate that transitioning this technology from healthy volunteers to patients is possible. It's important to note that this is the first drug to go into patients outside of oncology from heterobifunctional degrader machines. So we wanted to see that going from healthy volunteers to patients, where there are many cell types contributing to pharmacology. We want to ensure that the degradation profile is maintained. The initial study design was 14 days. Based on the learnings from the healthy volunteer study, we've extended it to 28 days. The goal is to confirm both PD and safety. Now given the extension to 28 days and based on data with other molecules, there may be early signs of clinical efficacy. We have added exploratory clinical endpoints but remain committed to sharing data on PD and safety. We also remain aware that we expect to reach maximum pharmacology only in the latter part of the study.

The next question is from Chris Shibutani with Goldman Sachs. Please go ahead.

Can you hear me now?

Yes.

With the Part C study for KT-474, on dosing and patient selection, you made the modification to do the 75 milligrams in the fed state. Can you ensure that we all understand the basis for that selection of the change? Secondly, with the two types of patients, HS and AD, should we expect it to be differential in terms of the kinds of exploratory responses that you might see from this Part C group based on your understanding of the kinetics of degradation as well as kind of the kinetics of the pathophysiology of the different disease states? I realize that we're only going out to 28 days, but if there's any basis for thinking that there might be a difference between those two patient types, that would be helpful to know and will you share and break out that data based on those patient types? Thanks.

Starting with your first question, why the 75 milligram dose: our aim all along has been to bring in what we call the sort of minimally efficacious dose into Part C, meaning the smallest dose that gives us maximum pharmacology that we think would be associated down the road with clinical activity. From the Part B MAD, we determined that the 100 milligram dose, when administered in the fasting state, gave us maximum knockdown in the blood and near-maximal knockdown in the skin, also significantly impacting ex vivo cytokine induction. So we saw that as our minimally effective dose. In the healthy volunteer study, subjects were treated on an inpatient basis. In Part C in patients, this will be done on an outpatient basis for 28 days of dosing. It's not practical to dose those subjects in the fasting state. We wanted to ensure we could dose them in the fed state. We observed a modest food effect that led to a modest increase in plasma exposure in the presence of food. Therefore, we conducted an additional SAD food effect cohort to determine what dose in the fed state would give us the same plasma exposure of the 100 milligrams in the fasting state, and we found that the 75 milligrams was appropriate. Regarding your question about AD versus HS and the ability to detect a clinical signal, studies using active agents where subjects are treated for extended periods, up to 12 weeks, may see signs of clinical response as early as 28 days in either AD or HS. Therefore, we don't expect any clinical signal advantage for either AD or HS, which is why we're planning on accruing an approximate equal number of patients for both conditions in Part C, restricting the enrollment to patients with moderate disease.

We expect the 75 mg dose to have the same activity in terms of PD as the 100 mg dose in the MAD cohort. The other point is that the pathophysiology is very different. The kinetics of IRAK4 degradation's impact on the pathophysiology of these two diseases could be different. We actually don't know. The goal of this study is to ensure that the molecule performs as expected: to demonstrate degradation and tolerance since we plan to leave the more complex questions of efficacy for future studies.

The key aspect is to observe IRAK4 knockdown in the skin. We aim for at least 85% or greater knockdown, which should help us assess the expression of pro-inflammatory gene transcripts. These transcripts may differ in AD versus HS. Nevertheless, downregulating those transcripts in conjunction with IRAK4 protein expression is a goal for both conditions. If confirmed, this will give us confidence moving forward that we can impact the disease's natural history.

Hello, good morning. Can you talk more about the type of patients you're recruiting for the Phase I Part C study regarding prior treatment? Any additional information would be great. Also, you mentioned earlier the 10 to 20 millisecond QT prolongation with no need for monitoring. Is there a threshold for QTc prolongation that would trigger monitoring from the FDA? Thank you.

In terms of your first question about the patient population for Part C, these will be HS and AD patients with moderate to severe disease. They could be treatment-naive patients or those who have had prior treatments, including prior biologic therapies. If patients are on biologic therapies at screening, they will need to come off those treatments with appropriate washout periods specified in the protocol.

The other question concerned QT. We have had extensive discussions with our cardiology consultants, and they believe that a 10 to 20 millisecond change does not necessitate cardiac monitoring. Probably, an excursion exceeding about 40 milliseconds could require some degree of cardiac monitoring, but this is ultimately determined by the FDA based on the context of the QT interval and arrhythmia risks.

Good morning. Thanks for taking my question. Regarding your earlier-stage pipeline beyond 474, could you comment on the intended development plan for KT-253 once the IND is filed later this year? What do you expect the news flow for the MDM2 program to look like in 2023? Secondly, can you provide any updates on your efforts with the molecular glue programs you’ve mentioned previously, and when do you anticipate having a development candidate to discuss? Thanks.

The reason we started the MDM2 program is that we felt it was an area of clinical investigation and commercial opportunities that has been untapped. The biology of p53 as a key tumor suppressor gene and the potential to stabilize p53 in various tumors has been a focus but perhaps not using the appropriate technology. We have a compelling case for degrading MDM2 in AML given existing data and some preclinical evidence that supports targeting MDM2 in this scenario. However, we aim to expand our investigation into other tumors, both liquid and solid. Our first-in-human study will commence towards the end of the year or early the next year, likely focusing on both solid tumors and AML approaches. We expect news flow to be centered on proof of mechanism early next year as we conduct these studies. Regarding molecular glue programs, it's fair to say these projects are still in discovery stage, and if we are close to the clinic, we will disclose details then.

Hi. Thanks for taking my questions. Starting off on KT-474, given the degradation dynamics and the need for maximal degradation in skin by two weeks, should we be comparing the four-week data to other programs in AD and HS or more like two to three week endpoints for those trials? Thanks.

That's a great question. We don't know yet. We're in the early trial stages, so it's hard to tell how that will turn out. As noted, we expect to maximize skin pharmacology by the end of the study’s second part, which is around week three or four. The study is small and non-placebo controlled, so setting benchmarks for efficacy will be challenging. Instead, we intend to focus on demonstrable expectations, particularly around PD and safety—those are our priorities.

Great. Good morning. Thanks for taking my questions. First, regarding QT prolongation, have you identified any concerning structures within the compound? It’s crucial to understand if other compounds in your pipeline have this issue. For IRAK4, could you provide some context on efficacy expectations for AD and HS? Other companies have mentioned they aren't aiming for specific outcomes, but they see significant potential in part of the therapy. Thank you.

We understand well what drives the weak affinity for the HERG channel. To reiterate, we do not degrade HERG nor show significant effects on cardiomyocyte functions. We have no concerns about other programs in our pipeline. Regarding efficacy, the IL-1/TLR pathway has shown a wide impact by blocking single cytokines. Our offering is a molecule that can potentially comprehensively block this pathway, possibly leading to greater efficacy compared to existing agents. The question isn’t if it’s going to be active, but rather how and where it will be most active in relation to various diseases. Ultimately, clinical investigation will validate these expectations.

Thanks so much for taking the question. For STAT3, can you describe what you expect to see in terms of PD and proof of mechanism, such as the percent degradation anticipated at the upcoming update, bearing in mind that this is still in dose escalation? Additionally, it's vital to understand what we have learned from other STAT3 clinical programs in the oncology setting, particularly in why degradation versus inhibition may be useful.

Preclinically, we've observed that achieving around 90% degradation of STAT3 in a patient population dependent on that target can yield favorable responses for a few days. Reaching that level or similar with a good safety profile would be a substantial derisking event. In terms of external landscape, though inhibitors and anti-sense programs have emerged, none have exhibited excellent engagement. Despite various attempts, it hasn't been effective enough to gauge efficacy versus our degradation approach. We believe that our method holds more promise.

Hey, good morning. Given the recent demonstration of clinical activity in liver cancer by a peer using a STAT3 inhibitor, should we expect you to enrich that solid tumor arm with liver cancer patients, or are other solid tumors being prioritized within this program?

We are exploring multiple solid tumor types preclinically, and those data will guide us on whether to enrich specific patient populations in future studies. This decision will rely heavily on what we observe in our preclinical research while keeping in mind the driver of effectiveness within the solid tumors treated with our agents.

Hi, good morning, everyone. Just a follow-up about STAT3. Can you discuss the anticipated therapeutic index? Do you have any expectations regarding myelosuppression or neutropenia, and have you seen anything in the preclinical tox package that hints at potential side effects? Additionally, can you clarify if you will be taking serial biopsies to look at target degradation, distribution, and activity impacted in tumor samples?

We have options for biopsies during the dose escalation. This isn't mandated, and we’re relying on the patient's cooperation. So we can't guarantee that we'll have the data, but we'll certainly make efforts to collect tumor data. Regarding safety, at pharmacologically active doses, our compounds have shown to be well-tolerated preclinically, and we’ll monitor this closely once we start dosing in the clinic.

Hi, everyone. Thanks for squeezing me in here. Regarding the previously disclosed QT finding, is there any plan to run a thorough QTc study? Additionally, can you clarify whether you'll be reporting mean reductions in EASI at day 28, and if you might report other metrics like EASI-50 or EASI-75 or EASI-90 in the atopic dermatitis patients?

Within our Phase I trial, we've had extensive ECG monitoring during the healthy volunteer portion. We identified this subclinical modest QT finding; this diminishes the necessity of running a thorough QT study in the future. We know what to expect, and routine ECG monitoring will track this finding. Regarding the endpoints, we will analyze them in several ways, including EASI metrics, but we haven't finalized how to look at these as we scale the data.

Thank you, Jared. In closing, I want to express my gratitude to everyone for being present during our call and thank you for the insightful questions. We are excited about our advancements this year, treating patients with our various programs. We remain focused on improving patient outcomes through impactful therapies that we developed within Kymera. I look forward to further discussions and results as we move towards our goals in the upcoming year. Thank you.

The conference has now concluded. Thank you for attending today's presentation. You may now disconnect.