Greetings, welcome to the Rain Oncology Inc. Q1 2023 earnings call. At this time, all participants are in a listen-only mode. A brief question and answer session will follow the formal presentation. If anyone should require operator assistance during the conference, please press star then zero on your telephone keypad. As a reminder, this conference is being recorded. It is now my pleasure to introduce your host, Dan Ferry. Thank you. Dan, you may begin. Thank you, operator, and good afternoon, everyone. With me today on the phone are Avanish Vellanki, Chief Executive Officer of Rain Oncology, Dr. Robert Doebele, Chief Scientific Officer, Dr. Richard Bryce, Chief Medical Officer, and Nelson Cabatuan, SVP of Finance. During today's call, Avanish will provide an update on the broader strategic vision for the milademetan franchise. Bob will review the biology and rationale of p53 reactivation and discuss possibilities for future clinical development of milademetan based on non-clinical research. Richard will provide an update on Rain's clinical strategy, and Nelson will review the financials. Before we begin, I would like to remind you that statements made during this conference call that are not historical facts are forward-looking statements within the meaning of the Private Securities Litigation Reform Act of 1995. These forward-looking statements are based upon Rain's current expectations and involve assumptions that may never materialize or may prove to be incorrect. Actual results could differ materially from those anticipated in such forward-looking statements as a result of various risks and uncertainties as described in Rain's most recent quarterly reports on Form 10-Q filed with the Securities and Exchange Commission and other SEC filings. All forward-looking statements made during this conference call are based on management's assumptions and estimates as of today, May 11, 2023. Rain undertakes no obligation to update such statements to reflect events that occur or circumstances that exist after today, except as required by law. With that, I'd like to turn the call over to Avanish Vellanki, CEO of Rain Oncology. Avanish. Thank you, Dan, and thanks to everyone for joining us for our Q1 2023 earnings highlights and corporate update. As Rain continues to drive forward with our late-stage clinical program, milademetan, or Mila, our oral small molecule inhibitor of the MDM2-p53 complex, we know this is a very important quarter for the company. I'm happy to report that we have achieved the required number of events to trigger the analysis of the primary endpoint in the global phase III registrational study for milademetan, or the MANTRA study. Therefore, we continue to expect the release of top-line data this quarter. We are very proud of the team at Rain, who showed a small company could take a phase I program, jump into a robust global registrational phase III trial, and aggressively enroll ahead of schedule. In building a capital-efficient business, these capabilities are prerequisites. We hope we get the results we're looking for to enable a potential solution for cancer patients with an unmet medical need. For me, this embodies the vision we had of being a biotech that exudes urgency and the financial prudence to innovate in this very challenging business of bringing forth new drugs to market. We hope the MANTRA study provides a new solution for patients with dedifferentiated liposarcoma or DDLPS. Further, we hope milademetan demonstrates how p53 reactivation could be impactful in treating a broad range of cancer patients. If the MANTRA top-line data are favorable, we believe it will signify that reactivation of p53 matters in cancer. This will be an important validation as we begin to think about our initiatives beyond DDLPS. We have already begun this work with ongoing and imminent planned studies to evaluate Mila across several tumor types in the MANTRA-2 and upcoming MANTRA-4 trials. Mechanistically, p53 is supposed to protect us from developing cancer. Today, there are no approved therapies in the treatment of cancer that are aimed at restoring or reactivating this innate anticancer agent. There are a multitude of potential indications to be considered with an effective strategy to restore p53, especially if the tolerability profile of Mila enables a wide-ranging set of combination partners. Bob and Richard will review some of our recent progress and plan next steps with the milademetan franchise. Our cash position at the end of the Q1 provides ample runway to complete all current ongoing and planned clinical trials of milademetan. This includes the completion of the ongoing phase II MANTRA-2 basket trial, which continues to enroll across tumor types, and the planned phase I/II MANTRA-4 basket trial, which is on track to start by mid-year, all on top of the pivotal MANTRA study. With that, I'd like to turn it over to our President and Chief Scientific Officer, Dr. Robert Doebele. Robert. Thanks, Avanish. Milademetan has been demonstrated to reactivate p53 in both non-clinical models and importantly in DDLPS patients treated in the phase I trial that was recently published in the Journal of Clinical Oncology or JCO. Furthermore, we have seen meaningful tumor reductions in several solid tumor types in the early data from the MANTRA-2 basket study. We eagerly anticipate top-line data from the MANTRA phase III study, which we believe will solidify the role for milademetan in cancer by formally demonstrating that this targeted approach of restoring p53 activity by disrupting the MDM2-p53 complex is meaningful in cancer. Based on its mechanism of action, milademetan should not be limited to liposarcoma, as it may become part of a broader strategy to reactivate p53 in numerous tumor types that harbor wild-type T p53. Ultimately, up to 50% of all cancers may be addressable by disrupting the MDM2-p53 interaction. Given the critical importance of p53 and the large number of patients potentially affected by MDM2-mediated p53 loss, there's a great interest in targeting the MDM2-p53 complex to restore p53 activity. We continue to believe there exists a large market opportunity for novel therapies such as milademetan in cancer patients, particularly as part of combination therapies in patients whose tumors harbor wild-type p53. Combination therapies could prolong time on targeted or immune therapy by targeting this critical pathway in cancer cells. In a recent collaboration with Memorial Sloan Kettering Cancer Center, we sought to determine efficacy of combination therapy in patient-derived lung adenocarcinoma models harboring an oncogenic driver and MDM2 amplification. The data showed that MDM2 inhibition with milademetan and MEK inhibition is synergistic in vitro, as evidenced by increased apoptosis compared to either agent alone. Milademetan demonstrated monotherapy in vivo activity in all models tested, including those with EGFR, MET, ALK, RET, and KRAS oncogenes. The addition of a MEK inhibitor substantially enhanced antitumor activity in the majority of models. We view these data as compelling, given the broad activity across different oncogene-driven models, and highlight the potential for combination strategies in oncogene-driven non-small cell lung cancer with MDM2 amplification. These results also strengthen the argument for broader milademetan plus MEK inhibitor combinations across solid tumors with wild-type p53 based on non-clinical data that Rain previously presented at the 2022 EORTC-NCI-AACR meeting. We continue to evaluate additional avenues to innovate with biomarker-driven precision therapeutic strategies and the additional potential for milademetan across new indications. At this point, I'll hand it over to our Chief Medical Officer, Richard Bryce, to discuss additional updates around Rain's clinical trial pipeline. Richard? Thank you, Bob. Good afternoon, everyone. As stated earlier, we recently published in the JCO the results of the U101 Phase I first in human study of milademetan. Those data demonstrated encouraging single-agent activity in DDLPS, which prompted our randomized Phase III MANTRA trial from which we expect top-line data, as previously advised, by the end of this quarter. To recap, our Phase III MANTRA study rapidly accrued 175 patients, and we believe the accelerated enrollment speaks to the tremendous unmet need in this patient population. As a reminder, this is an event-driven trial requiring at least 105 progression events to trigger the primary PFS analysis. As Avanish noted, we have crossed this threshold of the required number of events, giving us confidence we will have the top-line results this quarter. We anticipate that should the MANTRA data be supportive, we will submit an NDA for milademetan in DDLPS in the United States with similar submissions in Europe and possibly other regions as well. Moving on to the MANTRA-2 basket study, this was designed to observe the effects of milademetan monotherapy across a range of solid tumors exhibiting a certain degree of MDM2 amplification. Currently, with the central lab confirmed MDM2 gene copy number of eight or greater. Per our initial protocol, we are continuing to enroll up to 65 patients, and the study is being opened in additional sites throughout the U.S., Europe, and the Asia Pacific region. If the data from this study support meaningful, confirmed, and durable responses across a range of cancers, we intend to pursue a discussion with the FDA to better understand the requirements for a tumor-agnostic registrational filing. Alternative strategies were previously discussed in the event that our expectations do not hold up to the initial protocol-specified assumptions. Now on to MANTRA-4, our second tumor-agnostic basket study, which is a combination study with Roche's atezolizumab. To reiterate, this is a phase I/II trial designed to enroll 30 patients with wild type p53 advanced solid tumors that also exhibit loss of function of the CDKN2A gene. This strategy, targeting tumors with CDKN2A loss, could potentially target over 40,000 patients per year in the United States. We remain on track to start the MANTRA-4 trial in mid 2023. We hope to rapidly progress the initial dose escalation portion of this trial into the efficacy signal-seeking phase, supporting our strategy to expand the potential use of milademetan beyond DDLPS. With the imminent MANTRA trial readout, additionally, the opportunities that may arise from the two basket studies in patients with tumors that are either MDM2 gene amplified or with CDKN2A loss, together with our first combination data with a checkpoint inhibitor in the latter, we are excited by the potential benefits to patients and the future commercial opportunities across a wide range of cancers and patient populations. With that, let me now turn it over to Nelson to review our financial results. Nelson? Thank you, Richard. I am pleased to provide an update for financial results for the Q1 ended March 31, 2023. I would also like to invite you to review our quarterly report and Form 10-Q filed today for more details. For the three months ended March 31, 2023, Rain reported a net loss of $20.5 million, as compared to a net loss of $17.4 million for the same period in 2022. Net loss per share for the three months ended March 31, 2023 was $0.66, as compared to a net loss per share of $0.66 for the same period in 2022. Research and development expenses were $16.7 million for the three months ended March 31, 2023, as compared to $13.6 million for the same period in 2022. The increase was primarily related to clinical trial costs for Mila, higher payroll aid costs for our R&D personnel, and various other R&D costs for Mila. General administrative expenses were $5.1 million for the 3 months ended March 31, 2023, as compared to $3.9 million for the same period in 2022. The increase was primarily due to higher professional services and legal costs, as well as higher payroll related costs. Total non-cash stock-based compensation expenses were approximately $1.6 million for the 3 months ended March 31, 2023, as compared to $1.2 million for the same period in 2022. As of the Q1 ended March 31, 2023, Rain had $109.8 million in cash equivalents and short-term investments. Consistent with the prior earnings call, Rain will not provide guidance in cash runway at this time. At quarter ended March 31, 2023, our cash position provides runway to complete all ongoing and planned clinical trials of milademetan, including the phase III MANTRA trial in liposarcoma, phase II MANTRA-2 basket trial, and the planned phase I/II MANTRA-4 basket trial. We will continue to assess our cash runway and provide product guidance, if appropriate, after the release of our MANTRA top line results this quarter. As of the Q1 ended March 31, 2023, Rain had approximately 36.4 million shares of common stock outstanding. With that, I'll turn the call back over to Avanish. Thanks, Nelson. With that, we'll be happy to answer any questions. Operator? Thank you. We will now be conducting a question-and-answer session. If you would like to ask a question, please press star and then one on your telephone keypad. A confirmation tone will indicate your line is in the question queue. You may press star and then two if you would like to remove your question from the queue. For participants using the speaker equipment, it may be necessary to pick up your handset before pressing the star keys. One moment please while we poll for questions. The first question is from Yigal Nochomovitz of Citigroup. Please go ahead. Yeah. Hi, thanks for taking the questions. I think, Bob, you mentioned that you saw some early signs of tumor reductions in several solid tumors, if I heard you correctly, in the MDM2 amp, basket trial. Could you expand a little bit on that? What solid tumors, and did you see a correlation with MDM2 copy number? Were these all the wild-type T p53 patients? Thanks. Thanks for the question, Yigal. Bob? Yeah. you know, we have nothing new to report from what we reported in 2022. You'll recall that we saw tumor reductions in patients with lung cancer, pancreatic cancer, breast cancer, and biliary cancer. At that time, there was no correlation with copy number other than the fact that they were all amplified. Yes, all the patients were p53 wild type. The next question is from Michael Schmidt of Guggenheim. Please go ahead. Hey, guys. Thanks for taking my question. On the MANTRA trial, great to see that you've reached a number of events now for the primary endpoint. You know, will the study have enough follow-up to also have a view on mature OS at this point, or is it too early? You know, assuming success, you know what are good pricing analogs as we sort of model this out? Anything that comes to mind? Thanks. Thanks for the question, Michael. I'll turn over to you, Richard, for the first part of that, and I'll take the second pricing question. Richard? Sure. Thanks, Michael. Regarding OS, there will be an interim look at the OS data. It will be immature, as written into the SAP. I think, it will be, you know, meaningless. The primary analysis is obviously based on PFS. Michael, to answer the second question regarding pricing analogs, I think the comps that we use, broadly speaking for pricing assumptions, potential pricing assumptions if we were to go to the next step, we look at programs in the GIST space, ripretinib is one analog we would look to. We could also look at other subpopulations in the sarcoma space, in more rare indications like PEComa. FYARRO is another comp that we'd look to. Those represent some pretty good comps for potential pricing. The next question is from Joseph Catanzaro of Piper Sandler. Please go ahead. Hey guys, thanks so much for taking my questions here. Maybe first one, I know you guys have spoken on this a little bit in the past, but wondering if you have any sort of updated thoughts on the level of disclosure that we should expect in a top-line release as it relates to PFS and median hazard ratio p-values. Bob, on the MEK inhibitor combination, and preclinically, I'm wondering if we understand sort of the mechanism of cooperativity there and whether it can be extrapolated to other targeted kinase inhibitors. Thanks. Thanks for the question, Joe. Let me take the first one in terms of the level of disclosure, and then I'll hand it over to Bob. The comment we'll share there is we don't know yet. That'll be a decision ultimately when we see the data, so we can't comment on what that level of disclosure will currently be. Bob? Yeah, thanks for the question. In terms of the MEK inhibitor combination, there's multiple mechanisms to implicate why there may be synergy. I think I'll highlight two recent publications that are of great interest. One that phospho- RSK, a downstream mediator of MAP kinase signaling, specifically ERK, can phosphorylate and stabilize MDM2, increasing its activity. Inhibition of that pathway may further help reduce MDM2's inhibition on p53. The other one is that ERK2, phosphorylated ERK2, so active ERK2 can inhibit p53 directly. Both of those, I think, provide additional reasons why we're interested in this. The second part of your question was about extrapolating to TKIs and I, or other targeted therapies, and the answer would likely be yes. You know, for example, drugs that target upstream receptor tyrosine kinases would also inhibit the downstream MAP kinase pathway and therefore, we would suspect that that same mechanism might be at play. The next question is from Soumit Roy of JonesTrading. Please go ahead. Hello, everyone, and congratulations on all the progress. Are you planning to publish any scientific publication on MANTRA trial concurrent with the data, or it's gonna be something later in the year? Hi, Soumit. I'll take that one. We think that ultimately a publication does make sense. We can't comment on the timing of when that would be. If there's compelling evidence, certainly there could be a treatment-changing regimen, a paradigm-shifting regimen. We would ultimately hope to publish that. Sorry, I can't give any more color on timing. Got it. Should we expect a fair amount of detail when you present the MANTRA data? It's beyond just the top line, like subtype or copy number or stratification by lines of therapy. Those kind of details will be there? Again, we can't comment too much on what the level of disclosure will be, but what we have said in the past is, if the results are favorable, we certainly would hope to garner the support of a future medical conference for a presentation. We have to be somewhat thoughtful in terms of the extent of the data that we present at the top line. Again, the extent of the top line level of disclosure will be determined at the time of reviewing the data. The next question is from Sam Slutsky of LifeSci Capital. Please go ahead. Hey, everyone. Good afternoon. Thanks for the questions. 2 from me. Just on the MANTRA study, assuming a positive readout, can you just remind us what the steps and timelines look like post-top line data to filing the NDA as well as just ex-U.S. filings? Hi, Sam. I'm sorry. Did you ask for the stats assumptions, or did you ask for the timeline? Yes. for the NDA? I'm sorry. I didn't hear that correctly. Yeah, it was the steps. Kind of what goes into place post-top line data to get the NDA filing ready for both U.S. submission as well as ex-U.S., what do those timelines kind of look like typically? Sure. We're not gonna comment on NDA timelines just yet. Let's cross the first bridge, I think, before we get to that next step. I'll pass it over to Richard to review the stats assumptions for the MANTRA study as they were initially designed. Richard? Sure. Very simply, I think we've disclosed this several times before. The stats assumptions in the study was powered on a hazard ratio 0.5 and 94% power to achieve that, hence the 105 events that we were looking for. Does that answer your question, Sam? Yeah. This This second one just on MANTRA-2, anything you're able to say in terms of enrollment rates post the copy number change from 12 to 8 and kinda what that looks like? Yeah. I'll turn it over to Bob to talk a little bit about it. you know, I think all we can say at this point is enrollment has picked up substantially, you know, due to a number of factors. We think lowering the copy number may be one of them. We're very pleased with enrollment rates right now. The next question is from Jeff Jones of Oppenheimer. Please go ahead. Thanks, guys, and congratulations on reaching the required number of events. I think what I've got left, how should we be thinking about timelines for MANTRA-4, given the dose de-escalation design before moving into that phase II? you know, obviously, it goes to burn rate as well. just ballpark, how should we be thinking about timing there? Sure. Thanks for the question, Jeff. Let me turn that one over to Richard. Richard? Sure, Jeff. We're absolutely on track to start the MANTRA-4 trial in the midyear timeframe. In terms of the timelines for enrolling the first part of the safety part before the second part, you know, the other part of Jeff's question. Sorry, yeah, to answer that's, that's kind of a little bit difficult. It's, it's how long is a piece of string in a way. The, based on whether we need to deescalate or not. The study will open at a small number of sites for the safety portion. It's really hard to speculate, Jeff. If we don't have to deescalate, you know, 3 patients and we kinda move on. It really depends on what we see with that initial cohort. Just to remind everyone in terms of what we previously said publicly, this is a very large patient population in the U.S., and this overall is planned to be a 30-patient study. We do expect that finding these patients is readily achievable. As Richard just mentioned, the first 3 patients may be all it takes before we move on to the second phase for the signal finding part of the study. It could be rather rapid, but we can't really put a timeline on it just yet. Okay. Appreciate that, guys. Thanks. Thank you. The next question is from Faisal Khurshid of Leerink Partners. Please go ahead. Hey, guys. Thanks for taking the question. Two from me, one on MANTRA. Can you discuss what evidence supports the 3-month assumption for the control arm, especially if there's any evidence beyond the commonly cited Johnson & Johnson Phase III study? Then on MANTRA-2, could you discuss what gives you confidence in the copy number cutoff that you're using and, you know, why you think it shouldn't be any higher or any lower? Sure, sure. Thanks for the question, Faisal. Let me turn both those questions over to Bob on both the MANTRA assumptions for the control arm as well as the copy number. Yeah. In terms of the first question, the MANTRA study, of course, was based on primarily the observational data from the registrational trial of trabectedin. That median PFS was 2.2 months. Of course, we built in some additional cushion, almost a 50% improvement in that 2.2 months to 3 months. That remains the only perspective quality data set that we're aware of. Most other publications are either retrospective, which are subject to enormous bias, as well as intermingling of patients that may have either well diff or non, well diff, D diff liposarcoma subtypes. In terms of the second question, you know, confidence around the copy number, early on, we saw activity below copy number 12 in patients who are still amplified. We're relatively confident that our copy number is a reasonable cutoff for inclusion in the trial. You'll remember also that we've done mutual exclusivity analysis and that patients at this copy number are very unlikely to have inactivating p53 mutations. Several lines of evidence suggesting that we're at a very reasonable biomarker cutoff for this population of patients. Did I answer the question, Faisal? Yep. That was great. Thank you. Thank you. The next question is from Mitchell Kapoor of H.C. Wainwright. Please go ahead. Hey, everyone. Thanks for taking the questions. Just wanted to ask a little bit on the solid tumor plans. You've mentioned previously that you have three different plans you could pursue with MANTRA-2, the tumor-agnostic strategy, the expansion strategy, and then combinations as a last resort. Just wondering, even if you're showing, you know, good data as a monotherapy, would you still have plans to follow up with a combination strategy in these MDM2 amplified patients beyond the combinations that you would be pursuing with MANTRA-4? Sure. Let me start that, and I'll ask Richard to follow up in case I missed anything. You're absolutely right. We did articulate previously three potential avenues to achieve success in the MANTRA-2 MDM2 amp basket study. If we see monotherapy activity with durable confirmed responses across a variety of tumor types, and as we mentioned, we're continuing to enroll across all tumor types, then the expectation would be to have a conversation with the agency and pursue that strategy. Again, that is if the responses are durable, confirmed across tumor types. Obviously, there's quite a few permutations as to how this could proceed, and to look at the potential range of options, we could see potentially responses without durability in some tumors, durable in some tumors. Maybe we don't see durability across the board. I think we wanna certainly ensure that we pick the route that has the best regulatory shot of success, and we'll need to review the totality of the data before we make that decision. That certainly is to say that we could see some monotherapy activity, but perhaps we might need to go down an additional avenue in order to achieve a level of efficacy that we think would get registrational support. I think that's all we can say today, with the information that's currently available. Richard, anything to add there? No, I think you covered it from the strategic level. I think, you know, the only thing to sort of add into the mix here is that there is a lot of interest in academic centers and elsewhere, and potential combination partners in this specific population with patients who, as we know, because I think we shared the data at the time of the interim analysis, who have multiple other sort of co-mutations. It makes sense to explore all possibilities to look at those, whether they be in the context of company-sponsored trials or ISTs. You know, there's many opportunities to look at this moving forward, and we just need to figure out, you know, what makes sense and what the priorities are for addressing these. Okay, great. Thanks. Just on the liposarcoma launch strategy, could you just kind of remind us what that would look like for a rollout, potentially, how many reps you would need in the U.S. for a launch? I'll address that. We're not gonna say too much here, apologies for that, because we do wanna cross the key inflection point for the company of the data. But in terms of previously made public comments around what the sizing could look like, we've said in the range of 25-35 domestic sales reps to launch for this market size. We've also said that Rain would pursue a commercial effort with our internal capabilities, but that we would look to partner ex-U.S. That's the extent of the prior public comments we've made so far. The next question is from Graig Suvannavejh of Mizuho Securities. Please go ahead. Hi, guys. This is Avantika on for Graig Suvannavejh. I just had a quick question about MANTRA-2. I know you had previously said that you were planning on opening clinical sites outside of the U.S. Has this happened yet? A second question is, are you thinking about providing any more timeline guidelines for another readout for MANTRA-2? Hi, Avantika, thanks for the question. I will talk to the second part of that in terms of guidance for the MANTRA-2 study. We're not providing any additional guidance for additional presentations at this current time, so there's nothing new we can share there. With regards to the first part of your question, I'll turn that over to Richard with regards to the ex-U.S. site expansion plan. Richard? Yeah. Forgive me if I don't answer the question directly because I wasn't sure I sort of picked it up right entirely. You know, our challenge here is finding sites that have a molecular or genomic screening program in place, already in place. That's drives the countries and individual centers that we will move to and approach. We do have those. We haven't. I don't think we're in a position to disclose exactly which countries and obviously which sites we're gonna go to. We are on track to introduce those additional up to 20 sites in the next 2 to 3 months. Got it. Thank you. Just one question. This is more of a scenario question, but hopefully this doesn't happen. Assuming MANTRA doesn't read out positively, can you share, if you've thought about it, your any implications for continuing or even discontinuing MANTRA-2 and MANTRA-4? Yeah, I'll take that question, Avantika. It's a great question, and of course, internally, we've gone through certainly scenario planning efforts. I don't think we're in a position yet to talk about those scenarios today. I think we want to let the data, the quality of the data will certainly dictate what those scenarios will look like. Therefore, I think it'd be premature and probably inappropriate to comment on those scenarios today. Apologies for that. The next question is from Tony Butler of EF Hutton. Please go ahead. Avanish and Bob, maybe this question probably pretty simple. I recall in Gounder, I think in JCO, the phrase growth arrest. Obviously the phrase is obvious to what may be going on at the tumor site. One of the things that I wanted to explore is that I don't know is that I think you all have evaluated tumor growth kinetics before. The question is in DDLPS, is tumor heterogeneity sufficiently high that tumor growth kinetics can actually vary by individual cells within that overall tumor per patient? The reason I ask is because the again, the notion of growth arrest is really important, especially in maybe part of the tumor, maybe another part of the tumor where, you know, it may not have an effect because the kinetics change. Is that true or false? Thanks for the time. Well, thanks for the question, Tony. I'll turn that one over to Bob. Yeah. I'll try and tackle that. There are a lot in there. In terms of growth arrest, remember, p53 reactivation can induce growth arrest or apoptosis. When we're dealing with liposarcoma specifically, you'll recall that tumors don't shrink in most cases with any therapies, even current standard of care, aggressive chemotherapies. That may not necessarily be to lack of cancer cell death. Remember, these cells are high, or these tumors contain a very large amount of fatty tissue, stromal tissue, and other things that may not go away with cancer cell apoptosis or death. That's part of it. We do know that milademetan can induce tumor shrinkage and even in some cases very rapidly and you know, refer back to our MANTRA-2 data for evidence of that in other tumor types. In terms of the heterogeneity, we know that there are both in dedifferentiated liposarcoma patients, there is often well-diff components, and they may respond differently, but there's not a good handle on that nor validated measures to measure that. Of course, within any cancer patients, there's heterogeneity from patient to patient. Even with our best therapies that have remarkable response rates, there are always non-responders. There's always heterogeneity. I don't know if that completely answers your question or not. Happy to elaborate further if necessary. I think you got. I appreciate the color around the exact tumor heterogeneity, and especially in the sort of WD component of a DD patient and how that might actually be affected by growth arrest. Thank you. Thank you, Tony. There are no further questions at this time. I would like to turn the floor back over to Avanish Vellanki for closing comments. Please go ahead, sir. Thank you, operator. As a reminder for everyone, we do expect top-line phase III data from the registrational MANTRA study this quarter, and we look forward to reporting that data soon and providing a full company update on our next Q2 earnings call. Thank you. Ladies and gentlemen, that concludes today's conference. Thank you for joining us. You may now disconnect your lines.