Greetings, and welcome to the Rain Oncology, Inc. First Quarter 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. 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 first quarter 2023 earnings highlights and corporate update. As Rain continues to drive forward with our late-stage clinical program milademetan, our oral small molecule inhibitor of the MDM2-p53 complex, we note 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 3 registrational study for milademetan, the MANTRA study, and 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 1 program, jump into a robust global registrational Phase 3 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 have of being a biotech that exudes urgency and the financial prudence to innovate in this challenging business of bringing new drugs to market. We hope the MANTRA study provides a new solution for patients with dedifferentiated liposarcoma or DDLPS, but 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've already begun this work with ongoing and imminent planned studies to evaluate milademetan 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 anti-cancer agent. There are a multitude of potential indications to consider with an effective strategy to restore p53, especially if the tolerability profile of milademetan 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 first quarter provides ample runway to complete all current, ongoing, and planned clinical trials of milademetan. This includes the completion of the ongoing Phase 2 MANTRA-2 basket trial, which continues to enroll across tumor types, and the planned Phase 1/2 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. Bob Doebele. Bob?

Thanks, Avanish. Milademetan has been demonstrated to reactivate p53 in both non-clinical models and, importantly, in DDLPS patients treated in the Phase 1 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 3 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 TP53. 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 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 the 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 on all models tested, including those with EGFR, MET, ALK, RET, and KRAS oncogenes, but the addition of a MEK inhibitor substantially enhanced anti-tumor 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 explore 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, and good afternoon, everyone. As stated earlier, we recently published in the JCO the results of the U101 Phase 1 first-in-human study of milademetan. Those data demonstrated encouraging single-agent activity in DDLPS, which prompted our randomized Phase 3 MANTRA trial from which we expect top-line data as previously advised by the end of this quarter. To recap our Phase 3 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. And 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 is designed to observe the effects of milademetan monotherapy across a range of solid tumors exhibiting a certain degree of MDM2 amplification. Currently, with a central lab confirmed MDM2 gene copy number of eight or greater, and 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. And to reiterate, this is a Phase 1/2 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, and 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. So with the imminent MANTRA trial readouts and the additional 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 for 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 on financial results for the first quarter ended March 31, 2023. I would also like to invite you to review our quarterly report on 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 $0.56 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 milademetan, higher payroll-related costs for our R&D personnel, and various other R&D costs for milademetan. General and administrative expenses were $5.1 million for the three 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, legal costs, and higher payroll-related costs. Total non-cash stock-based compensation expenses were approximately $1.6 million for the three months ended March 31, 2023, as compared to $1.2 million for the same period in 2022. As of the first quarter ended March 31, 2023, Rain had $109.8 million in cash, cash equivalents, and short-term investments. Consistent with the prior earnings call, Rain will not provide guidance on cash runway at this time. At quarter-end March 31, 2023, our cash position provides a runway to complete all ongoing and planned clinical trials of milademetan, including the Phase 3 MANTRA trial in liposarcoma, Phase 2 MANTRA-2 basket trial, and the planned Phase 1/2 MANTRA-4 basket trial. We will continue to assess our cash runway and provide further guidance if appropriate after the release of our MANTRA top-line results this quarter. For the first quarter 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. The first question is from Yigal Nochomovitz of Citigroup. Please go ahead.

Yes. 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, and were these all the wild-type p53 patients? Thanks.

Thanks for the question, Yigal. Bob?

Yes. We have nothing new to report from what we reported in 2022. But 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 and 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 reached the number of events now for the primary endpoint. Will the study have enough follow-up to also have a view on mature OS at this point, or is it too early? And then assuming success, 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. So, regarding OS, there will be an interim look at the OS data. It will be immature as written into the SAP. So I think it will be meaningless. So the primary analysis is obviously based on PFS.

And 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 gastronomy 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, CRO is another comp we'd look to. So those represent some pretty good comps for potential pricing.

The next question is from Joe 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. And then Bob on the MEK inhibitor combination and pre-clinically, 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?

Yes. Thanks for the question. In terms of the MEK inhibitor combination, there are 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-Risk downstream mediator of MEK kinase signaling specifically ARC can phosphorylate and stabilize MDM2, increasing its activity. So inhibition of that pathway may further help reduce MDM's inhibition on p53. The other one is that phosphorylated ARC 2, active ARC 2 can inhibit p53 directly. And so both of those I think provide additional reasons why we're interested in this. And the second part of your question was about extrapolating to TKIs and other targeted therapies. The answer would likely be yes; for example, drugs that target upstream receptor tyrosine kinases would also inhibit the downstream MEK kinase pathway. Therefore, we suspect that the same mechanism might be at play.

Next question is from Soumit Roy of Jones Trading. Please go ahead.

Hello everyone, and congratulations on all the progress. Are you planning to publish any scientific publication on the MANTRA trial concurrent with the data, or is it going to be something later in the year?

Hi Soumit, I'll take that one. We believe that ultimately a publication is worthwhile. We can’t comment on when that might occur, but if we find compelling evidence, it could certainly lead to a treatment-changing regimen, which we would hope to publish. I’m sorry, but I can't provide more details about the timing.

Got it. So should we expect a fair amount of detail when you present the MANTRA data, it's beyond just the top-line like sarcoma subtype or copy number or stratification by lines of therapy, those kind of details will be there.

So again, we can't comment too much on the level of disclosure, 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. So we have to be somewhat thoughtful in terms of the extent of the data that we present top-line, but 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. Two from me, on the MANTRA study, assuming a positive readout, please 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. So did you ask for the stats assumptions or did you ask for the timeline for the NDA? I'm sorry, I didn't hear that correctly.

Yes, it was the stats. So 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. and what do those timelines kind of look like typically?

Sure. So we're not going to comment on NDA timelines just yet. Let's cross the first bridge before we get to that next step. But 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 and the study was powered on has addressed 0.5 and 94% power to achieve that, hence the 105 events that we were looking for.

Did that answer your question, Sam?

Yes. Regarding MANTRA-2, can you share any information about enrollment rates after the copy number change from 12 to 8 and what that looks like?

Yes. I'll turn it over to Bob to talk a little bit about it.

I think all we can say at this point is enrollment has picked up substantially due to a number of factors. We think lowering the copy number may be one of them, but 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 2? Obviously, it goes to burn rate as well, but 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. So we're absolutely on track to start the MANTRA-4 trial in the mid-year timeframe.

And in terms of the timelines for enrolling the first part of the safety part before the second part, the other part of Jeff's question.

So to answer that, it's somewhat difficult to determine. It really depends on whether we need to deescalate. The study will begin at a limited number of sites for the safety portion. It's challenging to speculate. If deescalation is not necessary, then three patients might be sufficient before we proceed. It ultimately relies on what we observe with that initial cohort.

And just to remind everyone in terms of what we've 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. So we do expect that finding patients is readily achievable. As Richard just mentioned, the first three patients may be all it takes before we move on to the second phase for the signal-finding part of the study. So it could be rather rapid, but we can't really put a timeline on it just yet.

The next question is from Faisal Khurshid of SVB Securities. Please go ahead.

Hey guys, thanks for taking the question. Two from me. One on MANTRA. Can you discuss what evidence supports the three-month assumption for the control arm, especially if there's any evidence beyond the commonly cited J&J Phase 3 study? And then on MANTRA-2, could you discuss what gives you confidence in the copy number cutoff that you're using and why you think it shouldn't be any higher or any lower?

Sure. Thanks for the question, Faisal. Let me turn both of those questions over to Bob on both the MANTRA assumptions for the control arm as well as the copy number.

Yes. So in terms of the first question, the MANTRA study was based primarily on the observational data from the registrational trial of trabectedin. So that median PFS was 2.2 months. We built in some additional cushion—almost a 50% improvement in that, to three months. That remains the only perspective quality data set that we are 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 differentiated or non-well differentiated dedifferentiated liposarcoma subtypes. In terms of the second question, confidence around the copy number, early on we saw activity below copy number 12 in patients who are still amplified. So 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 suggest that we have a very reasonable biomarker cutoff for this patient population.

Did I answer the question, Faisal?

Yes, 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 about 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. I'm just wondering, even if you're showing 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. So let me start that and I'll ask Richard to follow-up in case I'm missing anything. You're absolutely right. We did articulate previously three potential avenues to achieve success in the MANTRA-2 and 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 and confirmed across tumor types, obviously there are quite a few permutations as to how this could proceed to look at the potential range of options. We might see some responses without durability in some tumors, or durable responses in some tumors, but maybe we don't see durability across the board. I think we want to certainly ensure that we pick the route that has the best regulatory chance of success, and we'll need to review the totality of the data before making that decision. 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; this is all we could say today with the information that's currently available. Richard, anything to add there?

No, I think you covered it from a strategic level. I think the only thing to add here is that there is a lot of interest in academic centers and elsewhere in potential combination partners in this specific population with patients who, as we know, have multiple other 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. So there are many opportunities to look at this moving forward and we just need to identify what makes sense and what the priorities are for addressing these.

Okay. Great. Thanks. And then 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?

Sure. So I'll address that. We're not going to say too much here; apologies for that, because we do want to cross the key inflection point for this 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 to 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 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. 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? And then 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 or presentations at this current time; so there's nothing new we can share there. With regard to the first part of your question, I'll turn that over to Richard regarding the ex-U.S. site expansion plan. Richard?

Yes, I may not directly answer the question because I’m not entirely clear on what you asked. Our challenge is identifying sites that already have a molecular genomic screening program established. This determines the countries and individual centers we'll approach. While we do have these sites, I cannot specify which countries or sites we will target, but we are on track to introduce up to 20 additional sites in the next two to three months.

Got it. Thank you. And then, just one question; this is more of a scenario question, but hopefully this doesn't happen. But assuming MANTRA doesn't read out positively, can you share if you've thought about it, your implications for continuing or even discontinuing MANTRA-2 and MANTRA-4?

Yes, 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 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. But one of the things that I wanted to explore is that I don't know is that I think you all had 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 notion of growth arrest is really important, especially in maybe part of the tumor, maybe another part of the tumor where 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.

Yes, I'll address several points. In terms of growth arrest, it's important to note that p53 reactivation can lead to either growth arrest or cell death. Specifically regarding liposarcoma, most tumors do not shrink significantly with any therapies, including aggressive chemotherapies that are currently considered the standard of care, not necessarily due to a lack of cancer cell death. These tumors often contain substantial amounts of fatty and stromal tissue, which may not diminish even when cancer cells die. We know that milademetan can indeed promote tumor shrinkage, sometimes quite rapidly, and our MANTRA-2 data provides evidence for this in other tumor types. As for heterogeneity, in dedifferentiated liposarcoma patients, there are often well-differentiated components that may respond differently, but we lack reliable measures to assess this. Furthermore, cancer patients exhibit heterogeneity; even with our most effective therapies, there are still non-responders. So while there is variability, I'm not certain if this fully addresses your question. I'm happy to provide more detail if needed.

I appreciate the explanation about the tumor heterogeneity, particularly regarding the well-differentiated component of a desmoid patient and its potential relationship with 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 3 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 second quarter earnings call. Thank you.

Ladies and gentlemen, that concludes today's conference. Thank you for joining us. You may now disconnect your lines. Goodbye.