Relay Therapeutics, Inc. (RLAY) Earnings Call Transcript & Summary

Good day, ladies and gentlemen, and welcome to the Relay Therapeutics Post-ESMO conference call. As a reminder, this conference call may be recorded. I would now like to introduce your host for today's conference, Mr. Pete Rahmer, Chief Corporate Development Officer at Relay Therapeutics. Sir, you may begin.

Thank you, operator, and good morning, everyone. You can access the press release from yesterday, the slides we are reviewing this morning and a replay of this call by going to the Investor Relations section of our website. Before we get started, I'd like to note that this presentation shall not constitute an offer to sell or the solicitation of an offer to buy securities of the company. Please note that we will not be addressing any questions regarding this morning's follow-on offering launch during the Q&A portion of this call. As a reminder, during this call, Relay Therapeutics will make certain statements that are considered forward-looking statements within the meaning of the Private Securities Litigation Reform Act of 1995, including expressed or implied statements regarding our strategy, business plans and objectives, the expected therapeutic and clinical benefits of our product candidates, the potential of our platform and our product candidates and progress and timing and execution of our clinical trials. Such forward-looking statements are not guarantees of future performance, and therefore, you should not put undue reliance upon them. These statements are subject to numerous risks and uncertainties that could cause actual results to differ materially from what we expect, and we refer you to our SEC filings available at www.sec.gov and on our website for a discussion of risk factors that could cause our actual results to differ materially from those discussed today. The forward-looking statements in this presentation speak only as of the original date of this presentation, and we undertake no obligation to update or revise any of these statements. Today on the call with me are Sanjiv Patel, our President and CEO; and Don Bergstrom, our President of R&D. So with that, I'll turn the call over to Sanjiv.

Moving to Slide 3. Thank you, Pete, for that introduction and thank you for those of you on the line. To remind you, Relay Therapeutics is an emerging breed of biotech sitting at the intersection of leading-edge computational and experimental techniques. Moving to Slide 4. Over the last 6 years, we've gone a long way towards validating our approach by building an extensive precision medicine pipeline with now 3 molecules in clinical trials. All of this speaks to the productivity of our platform. Moving to Slide 5. We started this year out in January of 2022 with a set of challenging objectives. In our June 27th disclosure, we showed we've gone a long way towards meeting or exceeding each one of those goals. And additionally, that day, we laid out a catalyst-rich further 24 months to come. Today, we continue to demonstrate our execution focus by reviewing the exciting data presented at ESMO yesterday where we showed additional interim data for RLY-4008's efficacy. Today, we'll also add an additional catalyst in that we guide towards fully enrolling the pivotal RLY-4008 cohort in the second half of 2023. Moving to Slide 6. To give some background on the RLY-4008 program, we believe that fibroblast growth factor receptor 2, FGFR2, has all the hallmarks of a cancer driver oncogene, which makes it an attractive precision oncology target. We estimate a highly selective FGFR2 inhibitor could address between 8,000 and 20,000 advanced cancer patients with FGFR2 alterations annually in the U.S. Moving to Slide 7. We believe the current generation of nonselective inhibitors are limited by off-target toxicities, including hyperphosphatemia and diarrhea. So while the 2 inhibitors with accelerated approval for FGFR2-altered cholangiocarcinoma achieved 23% to 36% objective rate of response in FGFR2 inhibitor-naive patients, we believe the dose of these agents is actually limited by the toxicity related to the off-target inhibition. Our therapeutic hypothesis was that a highly selective inhibitor of FGFR2 can be optimized for the inhibition of FGFR2, potentially leading to high response rates and better durability of response. Moving to Slide 8. We believe RLY-4008 is the first known highly selective irreversible FGFR2 inhibitor designed to avoid engagement of other FGFR family members, which, as I mentioned, can lead to clinical toxicities. RLY-4008 has demonstrated also a greater selectivity not only within the FGFR family, but across the kinome more generally. Moving to Slide 9. At the ESMO Congress this past weekend, interim clinical data were presented on RLY-4008 that we believe further validate our translational hypothesis that selective inhibition of FGFR2 has the potential to transform the treatment of patients with FGFR2-driven tumors. Our safety database now includes 195 patients treated with RLY-4008, including 89 patients treated at the 70 milligrams once-daily pivotal dose and shows RLY has shown a generally favorable initial safety and tolerability profile, reflecting largely Grade 1 Or grade 2 toxicities related to the inhibition of FGFR2. RLY-4008 is highly selective for the inhibition of FGFR2 with no clinically significant off-target toxicities, including hyperphosphatemia and diarrhea. The benefit of all of this is we're able to optimize the dose of FGFR2 inhibition, and this is manifested in clinical activity that we have observed in FGFR2-driven tumors. Among 17 patients with FGFR2-fusion cholangiocarcinoma naive to prior FGFR inhibitors, eligible for efficacy evaluation and treated at the 70-milligram pivotal once-daily dose, 15 of the 17 achieved a tumor response for an objective rate of response that's interim 88%. 14 of these patients have a confirmed partial response and 1 has an unconfirmed partial response. This compares favorably to the 23% to 36% objective rate of response reported in the 2 pan-FGFR inhibitors with accelerated approval in this population. While the duration of response data are not yet mature, 15 patients remain on treatment. These interim data in FGFR2-driven cholangiocarcinoma, along with the early efficacy data outside of cholangiocarcinoma we shared last year, give us confidence that we'll be able to develop RLY-4008 across the spectrum of FGFR2-driven tumors with the opportunity to address between 8,000 and 20,000 patients annually in the U.S. Moving to Slide 10, where I'll now turn the call over to our President of R&D, Don Bergstrom, to walk through the details of the data.

Thank you, Sanjiv. The ongoing trial of RLY-4008, the ReFocus trial, has now been amended to achieve 3 objectives: first, generate registrational data in our pivotal population of FGFR2 fusion-positive cholangiocarcinoma without prior FGFR inhibitor treatment; second, generate supportive data for the pivotal population in 3 other cohorts of cholangiocarcinoma patients; and lastly, establish robust proof of concept outside of cholangiocarcinoma with additional expansion cohorts. Moving to Slide 11. This is a reminder that the patients we are discussing today represents our pivotal population treated across RLY-4008 doses in the Part 1 dose escalation and the initial disclosure of data from the pivotal expansion cohort, all treated at the pivotal dose of 70 milligrams once daily. Moving to Slide 12. This slide highlights the baseline characteristics for the efficacy and safety population. Most patients had cholangiocarcinoma with FGFR2 fusion and ECOG performance status 0 or 1. Most patients had high disease burden as indicated by large baseline tumor size and most have been previously treated with 2 or more systemic therapies, predominantly chemotherapy. The efficacy population includes all FGFR inhibitor-naive, FGFR2 fusion or rearranged patients with the opportunity for at least tumor assess -- 2 tumor assessments to confirm response or who discontinued prior to 2 assessments. Data are presented across all dose levels and at the pivotal dose of 70 milligrams once daily. The overall safety population includes all patients that received at least 1 dose of RLY-4008 as of the data cutoff date of August 1. Moving to Slide 13. Here, we focus on interim efficacy for patients treated at the 70-milligram once-daily pivotal dose. We observed remarkable activity in these patients with all patients having radiographic tumor regression and 15 of 17 patients experiencing partial response, resulting in an interim ORR of 88.2%. And a confirmed ORR of 82.4% with the 1 unconfirmed response patient continuing therapy with 4008. This includes 1 patient who had a near complete response who then went to surgery with curative intent. That's the patient highlighted by the star in the chart. Of note, the 2 patients with stable disease as best response remain on therapy. Moving to Slide 14. Here, we show the radiographic tumor regression and response per RECIST across all dose levels with the dark blue bars highlighting patients treated at the registrational dose. Nearly all patients had tumor regression, and the majority had response per RECIST with ORR at 63.2% across all dose levels and a confirmed ORR of 57.9%. Moving to Slide 15. This slide summarizes response for RECIST and duration of treatment. Dark blue bars again represent the patients treated at the pivotal dose of 70 milligrams once daily. Median duration of response has not been reached, but we believe initial durability is encouraging with 5.5 months median duration of exposure. Most responders remain on treatment with the longest duration of response observed exceeding 1 year. Moving to Slide 16. the CT scans show confirmed partial response in the female patients treated at the 70-milligram once-daily pivotal dose. Note marked regression of both the intrahepatic lesions as well as the bone metastasis. She remains on treatment with 68% tumor regression. Moving to Slide 17. The safety database for the ESMO disclosure included all patients who received at least 1 dose of RLY-4008 in both the dose escalation and dose expansion parts of the trial. As the expansion cohorts only initiated enrollment in December 2021, interim efficacy data for the majority of patients enrolled in the dose expansion remained immature as of the August 1, 2022, data cutoff, but these patients are included in the safety database. Moving to Slide 18. As of the data cutoff, most adverse events were expected FGFR2 on-target, low-grade, monitorable, manageable and largely reversible. The most common AEs are indicative of selective FGFR2 inhibition. The low rate of hyperphosphatemia and diarrhea reflect the FGFR2 selective mechanism of RLY-4008. All reported instances of these 2 AEs were Grade 1 or Grade 2. We believe the lack of off-target toxicity has allowed for optimized inhibition of FGFR2 and more complete inhibition of FGFR2 than can be achieved with nonselective FGFR inhibitors. And this has enabled the interim response rates that were reported at the ESMO Congress. Moving to Slide 19. We anticipate making additional data updates for RLY-4008 in 2023, including disclosure of the full data set from the Part 1 dose escalation expected in the first half of 2023, an initial disclosure of RLY-4008 activity in other dose expansion cohorts, including patients with FGFR2-driven tumors outside of cholangiocarcinoma. Moving to Slide 20. We disclosed preliminary efficacy data for patients with FGFR2-driven tumors outside of cholangiocarcinoma and cholangiocarcinoma with prior FGFR inhibitor treatment at the Triple Meeting in late 2021. Note that these patients were treated in the Part 1 dose escalation and only a small number were treated at the 70-milligram once-daily pivotal dose, especially in cholangiocarcinoma patients previously treated with an FGFR inhibitor, where none of the patients in the 2021 disclosure were treated at the pivotal dose. We anticipate disclosing updated data on these patient populations from the Part 2 dose escalation where all patients are treated at the 70-milligram once daily dose in 2023. Moving to Slide 21. To recap this weekend's ESMO disclosure and our anticipated RLY-4008 disclosures in 2023, we have now generated what we believe is a robust safety database supporting the FGFR2 selectivity of RLY-4008 and the ability to achieve optimized levels of FGFR2 inhibition, which we expect to report in a full disclosure of the dose escalation experience in the first half of 2023. The ESMO disclosure from this weekend demonstrated the potential benefit of FGFR2 selectivity on radiographic tumor regression with an interim 88% ORR for patients dosed at the pivotal dose. We anticipate fully enrolling the pivotal cohort in the second half of 2023. Also this morning, we were excited to announce the collaboration with Foundation Medicine to develop the FoundationOne CDx as a companion diagnostic for RLY-4008. And we continue to enroll patients with FGFR2-driven tumors outside of cholangiocarcinoma, where we anticipate reporting initial efficacy data in these patients at the 70-milligram once-daily dose in 2023. Moving to Slide 22. In June 2022, we showed for the first time our growing breast cancer franchise, anchored by the franchise of the PI3K-alpha mutant-selective molecules that have emerged from our unrivaled knowledge of this target. PI3K-alpha mutations occur in approximately 40% of hormone receptor-positive HER2-negative tumors, making it one of the largest validated precision oncology opportunities. We are developing a franchise of PI3K-alpha mutant-selective agents. RLY-2608, a pan-mutant selective inhibitor of PI3K-alpha initiated monotherapy dose escalation in December 2021, and combination dose escalation with fulvestrant in April 2022. Given the magnitude of the PI3K-alpha opportunity and our commitment to generate the definitive therapies for patients with PI3K-alpha mutant tumors, we have continued our investment in research and early development for this target with a second pan-mutant selective inhibitor, RLY-5836, anticipated to be ready to enter the clinic in 2023, and a research focused on other mechanisms for addressing this patient population, including PI3K-alpha mutant-specific inhibitors. Clinical experience will help inform the best approaches for addressing the breadth of the PI3K-alpha opportunity. And we believe we have deep target insight and drug discovery output to be able to nimbly adapt to any clinical experience. We have also added 2 new targets to our breast cancer franchise, a selective CDK2 inhibitor; and a bifunctional degrader of the estrogen receptor alpha, which continue to progress towards the clinic. Moving to Slide 23. The first-in-human trial for RLY-2608 is designed to evaluate the safety, tolerability, pharmacokinetics, pharmacodynamics and preliminary antitumor activity and consists of 2 separate arms. The first arm will assess RLY-2608 as a single agent for patients with unresectable or metastatic solid tumors with a PI3K-alpha mutation. The second arm will evaluate RLY-2608 in combination with fulvestrant for patients with PI3K-alpha mutant hormone receptor-positive, HER2-negative locally advanced or metastatic breast cancer. Each arm will have 2 parts. First the dose escalation part to determine the maximum tolerated dose and/or recommended Phase II dose, followed by a dose expansion part to evaluate RLY-2608 in genomically defined populations. We anticipate disclosing initial clinical data from this study in the first half of 2023. Moving to Slide 24. In December 2020, we partnered our SHP2 inhibitor, GDC-1971, with Genentech, given the broad range of rational combination opportunities in their portfolio. Last summer, Genentech initiated a combination trial of 1971 with their KRAS G12C inhibitor, GDC-6036. And they have recently initiated a combination trial of 1971 with atezolizumab. Last month, Genentech made the first disclosure of clinical data from the GDC-6036 program at the world lung congress. And while early, we believe the data suggests a potentially differentiated profile for GDC-6036 and validate our decision to partner 1971, which we feel could have a differentiated SHP2 profile with Genentech. The economics of this collaboration have been meaningful for Relay Therapeutics to date, and we retain the opportunity for substantial downstream participation in 1971. Moving to Slide 25. I'll now hand it over to Pete to wrap up.

Thanks, Don. We have a robust precision medicine pipeline with over 13 active programs that continue to progress as planned with the potential to address hundreds of thousands of patients annually in the U.S. alone. And we believe the data presented today continue to validate our approach. The more we do, the better we get. Moving to Slide 26. As we look forward, we have laid out a clear robust set of milestones over the next 24 months for RLY-4008 and across our breast cancer portfolio that we intend to deliver upon. These anticipated milestones include the initial clinical data disclosure for RLY-2608 expected in the first half of next year, a clinical data disclosure on RLY-4008 outside of cholangiocarcinoma also expected next year and an anticipated clinical start of our selective CDK2 inhibitor, which is expected in Q4 2023 or Q1 2024. Our ER alpha degrader development candidate nomination is expected in 2023 also. And today, we're happy to report that the combination trial of RLY-1971, now GDC-1971 with atezolizumab, has been initiated. As of the end of Q2 2022, we had cash of approximately $838 million, which we believe is sufficient to take us into at least 2025. And so with that, we would now like to open it up to Q&A. And as a reminder, please note that we will not be addressing any questions regarding this morning's follow-on offering launch during the Q&A portion of this call. If we don't have time to answer your questions during the live webcast, please follow up and we'll try to answer them off-line. Now I'll turn it over to the operator.

[Operator Instructions] Out first question comes from Salveen Richter with Goldman Sachs.

This is Tommie on for Salveen. Congratulations on the data. Could you just walk us through how we should think about the read-through from this update to how 4008 might perform in mutant and amplified CCA and also outside of CCA as well as the implications that you see to the Dynamo platform more broadly.

Thanks, Tommie. Maybe I'll start with the second part of that question and then hand it over to Don for the first part. I mean obviously, as we put together the platform of leading-edge computational and experimental techniques, the hope is to try and change the way that we can discover medicines to make it more efficiently done and more effective. And so as we've seen multiple times, we've selected a target. We've put together a modulation hypothesis. We've created a comprehensive preclinical package. We've made an IND. We put out with 3 molecules in the clinic. And I think this data that we showed last year at the Triple Meeting as well as this year shows that we can translate preclinical data into clinical data. And so I think each time we do it, we gain more experience and we believe that we become more effective. And so I think the quality of the data that we showed, I think, gives us more confidence that the platform will continue to get better at what it does. In terms of the read-through from the activity at these levels, infusions and what that points to do in amplifications and mutations, let me hand it over to Don.

Sure. Thanks, Sanjiv. When we think about how to translate what we've seen in cholangiocarcinoma more broadly across FGFR2-altered patient populations, I think it's really 2 questions: so one is a chemical question, do you have the right drug for being able to target these patients; and the second is the biology question, is FGFR2 a driver mutation in these patients. I think the data that we've disclosed over the course of this weekend have shown quite strongly that RLY-4008 is the right drug to be able to ask this question. In a patient population in cholangiocarcinoma where we know FGFR2 is a driver oncogene, we've been able to show now that with RLY-4008, we're able to achieve a high level of FGFR2 inhibition. We see manageable AE profile largely related to inhibition of FGFR2 and that's translated into an 88% response rate again in a patient population that's a positive control, if you will, where you know that FGFR2 is a driver. So that gives us confidence that RLY-4008 is the right drug to then be able to answer the question in other patient populations. I think the thing that gives us confidence about the biology of FGFR2 in other tumors in that FGFR2 is potentially a driver that could be RLY-4008 sensitive in other tumor types is our preclinical data, where we've been able to show across different mutations and amplifications that RLY-4008 is potent and active against the spectrum of oncogenic FGFR2 mutations and shows robust preclinical activity. And then our initial clinical experience with 4008 that we disclosed last year, where we showed that we had been able to achieve a confirmed partial response in a breast cancer patient with an oncogenic FGFR2 mutation and we showed tumor shrinkage in patients with FGFR2 amplification. So we're continuing to enroll these patient populations outside of cholangiocarcinoma. We look forward to disclosing the data next year.

Our next question comes from Yaron Werber with Cowen.

Congrats on the data. I have a couple of questions. Maybe, Don, maybe just for you, they're sort of interrelated. What we're increasingly learning about the biology is FGFR2 mutations are a driver, but they're really oncogenic in conjunction with other mutations. And the data now in FGFR-naive patients is very compelling because so far you're looking patients really are not progressing once they are responding. How long do you think, based on preclinical data, do you think you might be able to show a response for? Or does it really mean that to fail, you really need to have a mutation outside of FGFR2 tree? And then secondly, there was a paper in Nature about a month ago, talking about the lesion 18 or E18 truncation that is a sensitive driver mutations in the absence of other concomitant mutations, and as a result, recommending FGFR2 inhibitors. Have you tested that preclinically? And I think it also talks about in the Foundation Medicine database potentially a doubling of that incidence of FGFR2 now that are sensitive to inhibitors. Can you address that?

Yaron, thanks for the question. Maybe given the 2 questions, maybe we'll take them one at a time. So maybe we'll take the second one first, which is there was an interesting Nature paper that came out over the last few weeks that's drawn our attention to a potentially much broader patient population. So maybe I'll hand it over to Don just to talk through our thoughts on that paper.

Yes, Yaron, we definitely read that paper with great interest. When we look at the patient population where we have shown the data this weekend at ESMO and the FGFR2 fusion patients, obviously, we've shown a very high response rate. These are patients with clear FGFR driver. And the way fusions have conventionally been defined is that you have a fusion partner in frame with FGFR2. And that's in that Nature paper, that was the conventional definition that was used in the FMI algorithm to call a productive gene fusion. What was interesting to us about the Nature paper is that it suggested you can have other gene rearrangement events that just truncate the FGFR2 protein after exon 17. There's no gene fusion partner that's expressed downstream of exon 17, and that itself is the oncogenic event. The reason why that's of significance is because in that publication, it was shown that those alterations are highly sensitive to FGFR inhibition. And as you pointed out, Yaron, those represent potentially a doubling of the rearrangement population because you're now introducing patients that haven't conventionally been defined as being FGFR2 -- oncogenic FGFR2 fusion. But these data would suggest that, that's a population with FGFR2 genomic rearrangements that could be highly sensitive to treatment with an FGFR inhibitor. And given the 88% response rate we've shown in the fusion this weekend, I think that would give us confidence that we potentially could have high activity in this expanded FGFR2-altered population as well.

And maybe Don, maybe just point back to the first of Yaron's questions around how we think about potential duration of action in on-target versus off-target mutations.

Right. Obviously, Yaron, the durability data at this point remain early. But as we were designing 4008, I think we've learned from the experience of the pan-FGFR inhibitors and we've learned from the experience of precision oncology more generally. For the pan-FGFR inhibitors, you see at least half of the patients who progress with new on-target mutations in FGFR2. We designed 4008 to be potent against all of those mutations with the hope that we'd be able to suppress that as an acquired resistance mechanism. It's still too early to say definitively whether we've been able to do that. But again, by design, we would hope that we would manage to successfully suppress any major acquired resistance mechanism for FGFR2 inhibition. The second lesson is just the lesson that we've learned from precision oncology more generally. When you look at other driver oncogene targets, including, for example, ALK or EGFR, as we've seen successive generations of therapies that show improved potency, improved mutant coverage and improved selectivity compared to earlier generation agents, what that frequently has translated into is higher response rates and significantly greater durability of response for the more potent, more selective agents. For RLY-4008, we showed this weekend that with our design, we've been able to achieve the markedly higher response rate. I think time will tell whether that translates into markedly longer duration of response as well. But again, with the precedent, I think we are confident that, that could translate into significantly longer durability.

Our next question comes from Jason Gerberry with Bank of America.

Two for me, just 1 regulatory and then 1 question about something from the presentation. So just on the regulatory front, based on these data, do you believe sort of maintaining ORR in this sort of 80%-plus range could be sufficient to drive a line-agnostic approval? Or how important is it to the subgroups that will be front-line patients or the durability of response ultimately to driving that line-agnostic label that you seek? And then the other question, the discussion commented to some biomarkers that may be impacting the response rates on 4008. Just curious, versus other FGFR inhibitor studies, do you see response rates at all being skewed to any certain biomarkers or co-mutations and when we might get some more data on that front?

Thanks, Jason. Maybe we'll split them again. Maybe, Pete, you can take the regulatory question around response rates.

Yes. So unsatisfactory answer a little bit, Jason, it's going to depend on the totality of the data. Fortunately, when we amended the protocol to add in the pivotal cohort, we did open up additional pivotal cohorts to help address this question. And so we expanded our FGFR pretreated patient population to 50. We have an FGFR completely treatment-naive so a front-line cohort with 20 patients in it. And then we've also been enrolling other alterations, other FGFR2 alterations, in that setting to mutations amplifications. And it will really just come down to the totality of that data and how it matures over time.

And then the second question around the biomarker question raised by the discussions in the presentation.

Yes, yes. So certainly, we have a robust translational medicine program for RLY-4008, where we're looking at ctDNA serially over the course of treatment. We're also doing robust characterization of baseline of other co-recurring mutations with FGFR2. I think it was an interesting question, an open question, that was posed by the discussion, obviously one that we're following up on. Although I think with the level of clinical activity we're seeing, it would be unlikely that the 88% response rate would be solely due to having some sort of population imbalance. We anticipate in a future disclosure that we will share more complete molecular characterization of our patients, both baseline and serial characterization.

Our next question comes from Bradley Canino with Stifel.

Congrats on the data. Two questions from me. First, can you tell us the average dose intensity in the 17 RP2D patients? And has everyone remained above 40 milligrams? And then second, given the strong efficacy you're showing in second line, how important is the frontline cholangio opportunity for you now? I know all 3 pan-FGFRs have trials ongoing, but the primary outcome dates are like 5 years away or more despite the aggressive nature of the disease.

Thanks. Maybe I'll hand both of those over to Pete.

Yes. So I think the -- on your first question -- sorry, remind me again the first question? Dose intensity?

The average dose intensity, yes.

So we haven't gotten to exact detail on the nature of the interruptions and reductions and to what dose levels. But as a reminder, in the June 27 disclosure, we said the average dose intensity across the patients was approximately 90% of the initial dose. And I think we continue to see that dose intensity is not an issue for this -- for our patients on this study. And remind you that all the way down to 40 milligrams once daily, we maintained dose coverage of 90-plus percent receptor occupancy through the dosing interval.

And the second question, Bradley, again, if you could just remind us of that?

The frontline...

Just on the importance of the front-line study, yes.

I think the importance is really for patients here. And in the front-line setting, unfortunately, this is an aggressive disease and the front-line patients with standard of care being chemo doublet are still poorly controlled with not great median OS. So we would hope to try to demonstrate a benefit across all patients with FGFR2-driven cholangiocarcinoma. And I would think this data today gives us confidence that we may be able to continue to mature 4008 to be the best option for patients not only in cholangiocarcinoma, FGFR2-driven disease, but all patients with FGFR2-driven disease.

I'm sorry, we're out of time. I'd like to turn the call back over to Sanjiv Patel for any closing remarks.

Thank you to all of you who joined us today. We're excited about the potential of our programs and appreciate your continued support of our company and our mission to transform the drug discovery process with the goal of bringing life-changing therapies to patients. Thanks, again.

This concludes the program. You may now disconnect. Everyone, have a great day.