Rain Therapeutics Inc.
Q2 2021 Earnings Call Transcript

Published: 10 Aug 2021

[Operator:]

Good afternoon and welcome to the Rain Therapeutics' Second Quarter 2021 Financial Results and Highlights of Recent Progress Conference Call. My name is Reese, and I will be your operator for today's call. At this time, all participants are in a listen-only mode. Later, we will conduct a question-and-answer session. I will now turn the call over to Glenn Garmont with LifeSci Advisors. Glenn, you may begin.

[Glenn Garmont:]

Senior Vice President of Finance. During today's call, Avanish will provide an overall business update, Richard will provide an update on Rain's clinical programs, Bob will provide an update on the research efforts, and Nelson will review the financials. Before we begin, I'd 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 quarterly report on Form 10-Q for the quarter ended March 31st, 2021 and subsequent filings with the SEC. All forward-looking statements made during this conference call are based on management's assumptions and estimates as of today, August 10th. Rain undertakes no obligation to update such statements to reflect events that occur or circumstances that exist after today, as - except as required by law. With that, I'd like to turn the call over to Avanish Vellanki, CEO of Rain Therapeutics. Avanish?

[Avanish Vellanki:]

Thanks, Glenn and thanks to everyone for joining us for our first earnings call as a public company, post our initial public offering this past April. As our first call, we'll be a bit more comprehensive about the overall clinical development strategy for our lead program, our MDM2 inhibitor called milademetan, also known as RAIN-32, we may refer to milademetan as mila for short. In this most recent quarter, we work towards putting our vision for milademetan in Action. We continue to view our program as a potential best-in-class MDM2 inhibitor. We're excited about the therapeutic window to mila, because we believe it lends an opportunity to pursue almost 50% of all cancers. As a reminder, MDM2 inhibition is a strategy to reactivate p53, called the guardian of the genome and MDM2 acts as a mechanism for cancer cells to circumvent the protective properties of p53. Now, p53 is mutated in approximately half of all cancers, and therefore, largely loses its relationship to MDM2 in those settings, so we do not expect MDM2 inhibition to be a relevant strategy in the half cancers with mutated p53. However, the other 50% of cancers are cancers with wild type p53. And where p53 might be inactivated by MDM2. We believe inhibiting MDM2 could be effective there. Our clinical strategy for mila will be a 1-2 punch and focused on the wild type p53 population. Step one will be to pursue clinical indications where we have confidence of tumor dependence on MDM2. The first three clinical trials that we have previously articulated and we'll review again shortly, are all MDM2-amplified p53 wild type cancers. All our clinical discussion today will be in this category. However, it's also possible to be MDM2-dependent without MDM2 gene amplification. And we're doing more work there. We hope to present non-clinical support for mila in those additional tumor types to support further investigation. Therefore, MDM2-dependent cancers, either through gene amp or other routes is step one of our clinical strategy and where we expect there to be the most sensitive patient population to MDM2 inhibition. Step two of this one-two punch will be in other p53 wild type tumors. In the second step, single agent MDM2 inhibition is not likely to be sufficient on its own and will require a combination with other agents. An example of this are indications like acute myeloid leukemia, we've seen many large biopharmas with MDM2 inhibitor programs historically jump straight into AML because of the patient opportunity, although we do not believe AML to be an MDM2-dependent cancer. It is however, predominantly p53 wild type. As such, MDM2 inhibition and AML will likely need synergistic combination agents. These other wild type p53 indications will be step two of our plan. And we think a well-tolerated MDM2 inhibitor program that is combinable with other agents can hold great promise. Today's call will largely be focused on step one, focusing on those patients we expect to be most sensitive to MDM2 - inhibition. Let me share what we've been up to. In the second quarter of this year, we work towards getting a pivotal Phase 3 trial started in patients with certain subtypes of liposarcoma or LPS. The first trial being planned for mila is in LPS patients with a histology type, called de-differentiated liposarcoma or DD LPS for short. Patients with DD LPS are eligible for the study with or without the presence of a related subtype called well-differentiated LPS or WD LPS. These two subtypes most often coexist. The reason for pursuing these two subtypes of LPS is that again, all patients with these subtypes exhibit MDM2 gene amplification. And because all patients have this gene amp, we don't need a companion diagnostic for this patient population. Post the second quarter in July, we've already announced that the Phase 3 trial now got the MANTRA study has now started the first patient having been randomized. With MANTRA now started, we expect to commence our second clinical study of Phase 2, tumor-agnostic Basket study in patients with advanced solid tumors in the second half of 2021. And that will be called the MANTRA-2 study. These patients will be prospectively selected based on a certain threshold of MDM2 gene amplification. For MANTRA-2, we will need a companion diagnostic strategy in the future as to biomarker selected population. We plan to follow-up that up with a second study with a third trial another Phase 3 trial and in patients with intimal sarcoma, and that study is anticipated to commence by early 2022. Intimal sarcoma like our strategy in liposarcoma is another largely MDM2 gene-amplified tumor type, and therefore no companion diagnostic strategy needed here either. Again, all three studies are in patients with MDM2 gene amplification. We continue to anticipate data timelines in line with what we stated in our recent S-1 filing. The very first data read from our milademetan program is anticipated to come from MANTRA-2, the Phase 2, tumor-agnostic basket trial with interim data in the second half of 2022. The second set of data is expected to come as interim data from the Phase 2 study in intimal sarcoma in late 2022. And then, third, topline final data from the pivotal MANTRA study in DD LPS in 2023. Therefore, we anticipate a steady stream of clinical news flow beginning in the second half of next year. Finally, we are very excited about working on a potential first-in-class strategy for DNA repair with the RAD52 research program. RAD52 inhibition is a strategy to address the limited therapeutic options in the DNA repair space, and especially the need in patients after relapse from PARP inhibitor. The program is early and we continue to expect selection of a lead candidate in 2022. We look forward to telling you more about our progress with this program when we can. With that, I'll turn it over to our Chief Medical Officer, Dr. Richard Bryce.

[Richard Bryce:]

Thank you, Avanish and good afternoon, everyone. So one of the key differentiators of milademetan is a late clinical-stage MDM2 inhibitor, as it's potentially favorable safety profile over that reported from others in this class. And in particular, we want to remind everyone of the low levels of severe cytopenias that is to say the hematological toxicities that were observed with milademetan from the larger prior study completed last year. Specifically, the rates of grade 3 and 4 thrombocytopenia, neutropenia and anemia were 15%, 5% and 0%, respectively in the preferred dosing schedule. In that study, milademetan was investigated in 4 different doses and schedules, with the optimal dose and schedule determined to be 260 milligrams given by mouth daily for three days, followed by a 11 days off on a repeating schedule. In other words, patients receiving the milademetan 6 days out of a nominal 28-day cycle. Our pivotal trial, the MANTRA trial mentioned by Avanish, is in the second-line setting, in de-differentiated liposarcoma, DD LPS. The current standard of care in liposarcoma today, after anthracycline-based chemotherapy is another type of chemotherapeutic agent called trabectedin, trade name Yondelis, which demonstrated the median progression-free survival or PFS of 2.2 months in DD LPS. In the previous milademetan study, there were a total of 53 patients with DD LPS enrolled. Now, we want to point out that some of our enthusiasm for milademetan stems from the prior data, in which, the cohort of patients treated with the dose and schedule with the worst PFS, still had a PFS of 6.3 months. That's still tripled that of trabectedin. And the cohort of patients that received 260 milligrams of milademetan in their preferred dosing schedule of 3 days on and a 11 days off, which demonstrated the most favorable tolerability, exhibited a median PFS of 7.4 months. Improved safety and better tolerability appear to actually lead to numerically-improved PFS, compared to those described in the literature and the syndication. Further, and it has been published earlier. Patients in that prior study exhibited some very long durations of treatment, extending and ongoing over several years in some instances. We believe the safety profile exhibited by milademetan from the prior study with the results of identifying an appropriate dosing schedule. The entirety of the MDM2 competitive landscape has been focused on trying to identify the right dose and schedule for a specific compounds of properties. Based on this prior trial, we believe milademetan is the first program with clinical evidence of a potentially successful efficacy and tolerability combination that is based on identifying the right dose and schedule. As Avanish mentioned, we recently announced the start of our pivotal Phase 3 MANTRA study for milademetan in patients with DD LPS. Last month, we announced the first patient randomized into the trial. This Phase 3 study of milademetan versus trabectedin is being conducted in patients with unresectable or metastatic, de-differentiated liposarcoma with or without a well-differentiated component, who have progressed on one or more prior systemic therapies, including at least one anthracycline-based therapy. This global study will randomize approximately 160 patients on a 1

[Bob Doebele:]

Thanks, Richard and good afternoon, everyone. The Rain team has been working to evaluate the opportunity for milademetan across the broad range of tumors in line with the opportunity afforded by a safe inhibitor of MBM2 and wild type p53 cancers. As Avanish mentioned previously, our initial strategy is to evaluate potential MDM2-dependent tumor types. Since we acquired the program less than a year ago, we've moved quickly to commence numerous non-clinical studies alongside our clinical efforts, and we believe this will lead to an exciting frequency of milademetan data. On the non-clinical side, I will describe some of our recent and exploratory work. We've had several datasets based on this recent work accepted for presentation at upcoming conferences. We plan to issue a separate press release with the details behind these presentations shortly. First, we plan to present non-clinical data to further support the evaluation of milademetan and MDM2-amplified p53 wild type tumors including in vitro, organoid, PDX models, as well as bioinformatics analysis to identify predictive biomarkers for milademetan. We believe that MDM2 amplification when properly accounting for mutual exclusivity with TP53 mutations, represents an opportunity to target MDM2-dependent tumors in a tumor-agnostic manner. This work has been submitted and accepted to the EORTC-NCI-AACR Virtual Conference with a triple meeting in October of 2021. Second, we have also previously articulated our interest in a novel application for MDM2 inhibition in breast cancer. GATA3 frameshift mutations represent approximately 15% of hormone positive breast cancer cases. We are evaluating a synthetic lethal interaction in tumors harboring GATA3 frameshift mutations and loss of MDM2. We have extended these findings to include inhibition of MDM2 with milademetan and we'll present these data at the triple meeting as well. Third, Merkel cell carcinoma represents another potential clinical opportunity for milademetan and another unique manner to lead to MDM2 dependence. The majority of Merkel cell carcinomas are induced by the polyomavirus, which drives expression and activity of MDM2 thereby abrogating the need for TP53 mutations. Further, data from competitors in Merkel cell carcinoma have helped to validate MBM2 as a target with other programs exhibiting single agent activity, thereby moderating risk in this setting. Thus Merkel cell carcinoma represents a further opportunity for what we believe is an enhanced therapeutic window for milademetan. Dr. James DeCaprio of the Dana-Farber Cancer Institute is one of the world's preeminent researchers in Merkel cell and has tested milademetan and multiple Merkel cell models, both in vitro and in vivo, and Dr. DeCaprio's group will be presenting this work also at the upcoming triple meeting. Our fourth presentation will be on mesothelioma. Mesothelioma remains an attractive cancer type for MDM2 inhibition and this is based both on the low TP53 mutation rate as well as the high rate of CDK into a loss coupled with the unmet need and lack of targeted therapies in this tumor type. We've collaborated with Dr. Lynn Heasley at the University of Colorado to test milademetan and multiple mesothelioma cancer models. And this work will be presented at the upcoming World Conference on lung cancer in September 2021. In summary, we anticipate at least 4 abstracts at upcoming conferences relating to clinical opportunities for milademetan. And we are continuing to explore opportunities in other potential clinical indications, including combinatorial approaches. Finally, Rain's internal research program developing inhibitors of RAD52 continues to make progress and we note the recent addition of Dr. Simon Powell from Memorial Sloan Kettering, who discovered the synthetic lethal interaction between RAD52 and BRCA deficiency to Rain's Scientific Advisory Board. And with that, let me now turn it over to Nelson to review our financial results. Nelson?

[Nelson Cabatuan:]

Thank you, Bob and good afternoon, everyone. I'm pleased to provide a brief overview of our financial results for the second quarter of 2021 and also would like to invite you to review our Form 10-Q filed today for more details. With the second quarter of 2021, we reported a net loss of $8.2 million or $0.39 per share, compared to net loss of $2.6 million or $0.78 per share in the second quarter of 2020. Research and development expenses were $5.5 million in the second quarter of 2021, as compared to $1.5 million in the second quarter of 2020. This was primarily driven by the clinical cost for a lead product candidate, milademetan as we're preparing to launch our Phase 3 pivotal trial in DD LPS in July 2021, as well as personnel costs. General and administrative expenses were $2.7 million for the second quarter of 2021, compared to $1.1 million for the second quarter of 2020. The increase was primarily due to increases in various third-party G&A costs, including legal, outside consulting, as well as accounting and audit fees. As of June 30, 2021, Rain had $164.6 million in cash, cash equivalents and short-term investments, which provides funding for advanced research and development pipeline. This included $121.5 million in net proceeds from our initial public offering in April 2021. Furthermore, as of June 30, 2021, Rain had approximately 26.5 million shares of common stock outstanding. We continue to expect our full year 2021 operating spend to be approximately $50 million and $60 million, and a projected year-end balance of approximately $137 million to $147 million in cash, cash equivalents and short-term investments. With that, I'll now turn the call over back to Avanish.

[Avanish Vellanki:]

Thanks, Nelson. We'd like to reiterate again that we believe milademetan's unique therapeutic window will be able to provide a benefit for patients across a multitude of cancers, including up to an estimated 50% of all cancers with wild type p53. The team at Rain Therapeutics will do everything we can to move the forward - through our arm program forward for patients as quickly as we can. Let me turn the call back to the operator for a Q&A session.

[Operator:]

Thank you. We will now begin the question-and-answer session. And our first question is from Yigal Nochomovitz from - I'm sorry, our first question is from Michael Schmidt from Guggenheim Securities. Please go ahead. And now, this is Graig Suvannavejh from Goldman Sachs. Please go ahead.

[Graig Suvannavejh:]

Hey, good afternoon. Can you hear me, okay?

[Avanish Vellanki:]

Perfect, Graig -

[Graig Suvannavejh:]

Hello?

[Avanish Vellanki:]

[Graig Suvannavejh:]

Okay, great.

[Nelson Cabatuan:]

Yeah, we can hear you, Graig.

[Graig Suvannavejh:]

Thanks so much. Thanks for providing the update, lot of details in the call. So it's appreciated. I'm just going to keep my questions a bit high level at this point. But on the Caris collaboration, I think it's an interesting one. Can you just remind us how to think about what that will do in terms of being able to whether accelerate, you know, enrollment timelines? And what could you expect that you would have gotten out of this versus not having it? And then just on enrollment? I know it's hard to predict, given where we are with COVID. But because you're a new company, and we've seen many companies trying to navigate through kind of any COVID-related impacts. But as it relates to your particular indication and the patient population, do you anticipate any potential delays just due to COVID? Thanks.

[Avanish Vellanki:]

Thanks for the question, Graig. Let me ask Bob to answer the question about Caris and Richard address the enrollment question. Bob?

[Bob Doebele:]

Yeah, thanks for attending, Graig and thanks for your question. So what we hope to get out of the collaboration with Caris is, of course, access to more patient tested, right. So we know that a large number of patients are increasingly using next-generation sequencing to help identify patients either for clinically approved therapeutics or for clinical trials. And so by collaborating with Caris, that allows us to identify additional patients for the basket study to enroll.

[Richard Bryce:]

Yeah. So this is Richard Bryce here just to add to that also. So what Caris have the ability to do is, really look back at the database, identify patients with these pre-identified or predetermined criteria, in other words, wild type TP53 and MDM2 copy - amplification copy number 12 or more and have already begun that sort of process. So, coupled with, you know, identify - identification of patients, if you like, that are in the system currently under treatment together with their just-in-time sites as well as a referral to, the option of referral to our regular sites, if you like, that we hope to be able to effectively frontload enrollment into this study as soon as it's open and ready to go. That's essentially how it's going to work with Caris. You had - sorry, you had a question about COVID too?

[Graig Suvannavejh:]

I did, yes. Just wondering if there's a way that you can anticipate whether or provide any direction for us if in this patient population, whether COVID could have an impact on your trial and all the timelines just generally speaking?

[Richard Bryce:]

Well, sure. I mean, generally, it absolutely could and really just depends the way that the pandemic is sort of fluctuating up and down. I mean, what we've seen, not within our organization here, because the trials haven't been running that long, but with other trials and sponsors that we're beginning to see the sites are opening up, they're a little bit more receptive to in-patient visits, there's a lot of still online telemedicine going on. But for clinical trial purposes, you do need that sort of phase to phase element and component. And we have noticed that, you know, our sites are now more receptive and opening up to that. So, as long as we don't sort of go into another sort of deep and long sort of shutdown, prolonged shutdown, as we experienced a year or so ago, I think we're over the worst of that and it shouldn't have a major impact as things stand currently on our enrollment timelines.

[Graig Suvannavejh:]

And then if I could just follow-up just now that MANTRA is kind of up and running. Could you sort of remind us of how the trial design is different and/or similar versus the initial prior experience you had? And how much of that prior experience are you able to replicate in the Phase 3 trial design here?

[Avanish Vellanki:]

Let me ask Bob to take that one.

[Bob Doebele:]

Yeah, thanks again for the question, Graig. So, in terms of replicating the data, you know, we are focused again, on a very unique population of patients of de-differentiated liposarcoma. We had 53 of those patients that were enrolled on the Phase 1 trial. So we actually have what we believe is a large experience with this somewhat rare tumor type. And we've tried to replicate as many of those aspects of that initial clinical trial as possible going forward in terms of the randomized Phase 3.

[Avanish Vellanki:]

Yeah, I'll just add to that, Graig. So, of course, what's different about this trial is still the second-line study, the prior study did not restrict for just refractory patients, there were some naive patients as part of that overall study from the Phase 1, which was predominantly a safety study to identify the dose and schedule. So and there was no active comparator with any sort of control agent in the prior study. So the biggest differences going forward here is that, this is the second-line and later study with a standard of care as to comparator agent.

[Graig Suvannavejh:]

All right, thanks so much. I'll jump back in the queue.

[Operator:]

And our next question is from Yigal Nochomovitz with Citi. Please go ahead.

[Yigal Nochomovitz:]

Yeah, hi. This is -

[Avanish Vellanki:]

Hey, Yigal -

[Yigal Nochomovitz:]

Yigal Nochomovitz - hi, how are you doing?

[Avanish Vellanki:]

Great.

[Yigal Nochomovitz:]

I just have two questions - just had two questions here. On the MANTRA-2, is that study set up in such a way that it could be a pivotal trial, which would lead to a tumor-agnostic label? Or the idea that you would, you know, run, enroll a bunch of different solid tumors and then run Phase 3 as an individual solid tumors for registration purposes?

[Avanish Vellanki:]

Bob?

[Bob Doebele:]

Yeah. Thanks for attending, Yigal and thanks for the question. So the intention of this study is obviously to explore across a broad set of tumors and you know, we know that there have been successes in other tumor types with oncogenic drivers across multiple different tumor types as long as there's a uniform genetic definition. So, the goal here really is to run a seamless Phase 2 trial across multiple different tumor types with the intention of evaluating efficacy. And if that efficacy is sufficient across these tumor types, then to go for an agnostic indication, rather than breaking this into individual tumor types with MDM2 amplification and wild type p53. That would remain as a potential backup strategy, of course, if we see significant activity in some tumor types, but not others, but really the primary intent is an agnostic approach.

[Yigal Nochomovitz:]

Okay. And then just one operational question. I know that this is a solid tumor trial, the basket trial. What happens if a de-differentiated liposarcoma patient is screened in the - for the basket trial? Or can that just not happen? I'm just wondering if they'll get shuttled to the Phase 3 MANTRA trial?

[Bob Doebele:]

Yeah, that's a great question. So as part of the inclusion-exclusion criteria, we've actually excluded both de-differentiated liposarcoma and intimal sarcoma patients, because we have specific trials for those indications. And so, yes, we went after those patients be enrolled on another trial, but they're excluded from the basket.

[Yigal Nochomovitz:]

Okay, thank you.

[Operator:]

And our next question is from Joe Catanzaro with Piper Sandler. Please go ahead.

[Joe Catanzaro:]

Hey, guys. Thanks so much for taking my questions here. Two for me, maybe want to follow-up on the biomarker collaborations. I'm just wondering if you could elaborate a bit more, I would presume that patients that are identified via Caris would need to be referred to active participating clinical sites. I'm just wondering how efficient that process is? And does the collaboration function of local assessment that would then need to be centrally confirmed? Thanks.

[Bob Doebele:]

Yeah, thanks again, Joe for the question. So to answer that. So there's two ways that patients who would be tested by Caris could be enrolled in our study. One, they could be referred to one of our, you know, established sites that will be open across the US. But the second possibility is through a just-in-time mechanism. So to open the site where that patient is being seen. And so that is a second option. So we think obviously, if, you know, just-in-time site is obviously, probably far closer to home than a referral site. In terms of local testing, yes, we have, I think what is a novel and very flexible approach to enrolling patients. So patients are enrolled and dosed based on local testing, however, every patient that is enrolled in the study will have central testing through Tempus's next-generation sequencing so that we'll have uniform genomic data on a single platform for every single patient. And so the data will be analyzed both by those that are positive according to central testing via Tempus or just positive via their local testing, but negative via Tempus.

[Joe Catanzaro:]

Okay, got it. Thanks. That's helpful. If I could just ask the follow-up about the potential combination strategies in the broader sort of basket of p53 wild type tumors. Are you thinking chemotherapy, I guess, which makes a lot of biological sense? But are there other targeted approaches that you think would be combinable? And I guess it would sort of be driven potentially, in part by the tumor types you would think to pursue? I know, you mentioned AML. Just curious if there are any others? Thanks.

[Bob Doebele:]

Yeah, thanks for that question as well. So, we are obviously thinking about combinatorial approaches. So now that we've, you know, set about launching our monotherapy trials that we've just described, I think our focus is really shifting to these combinatorial approaches in the remainder of the wild type - p53 population. Although chemotherapy might make sense mechanistically, safety-wise, it is a bit more challenging given the overlapping toxicities between milademetan in chemotherapy. So I think our focus is much more on targeted therapies and immunotherapy which is not anticipated to have as much overlapping toxicity and where there's still a good mechanistic rationale for those combinations. And again, that may end up being more tumor-specific, but could also be genetically-driven.

[Joe Catanzaro:]

Okay, got it. Thanks so much for taking my questions.

[Operator:]

And our next question comes from Michael Schmidt with Guggenheim Securities. Please go ahead.

[Charles Zhu:]

Good afternoon, everybody. This is Charles Zhu on for Michael Schmidt. Thanks for taking the questions. Your selection of copy number 12 for the MDM2-amplified basket trial. Could you elaborate on how much of that was driven by patient demographics given almost all patients are p53 wild type at that cut off and maybe to what extent might wild type p53 but MDM2-amplified tumors with copy number less than 12 could potentially benefit from your approach? Thanks.

[Avanish Vellanki:]

Thanks, Charles. So I'll hand over to Bob to outline as well.

[Bob Doebele:]

Yeah, thanks for your question, Charles. So the way that we think about setting a cut point for MDM2 amplification is based on the biology. So, p53 mutations and MDM2 amplification really functionally have the same effect, which is loss of p53 function. So based on that assumption, we performed a mutual exclusivity analysis to determine the MDM2 copy number at which p53 mutations became exceedingly rare. Again, given this assumption about mutual exclusivity, if they're really performing the same function, they shouldn't coexist at a significant threshold. And so we think that this copy number 12 represents you know, a biologically meaningful, but also stringent cut off for patients' tumors who are MDM2-dependent. Now, the second part of your question is, are there patients with lower levels of MDM2 copy number that may have benefit. I think that's possible. And we may be able to get a small glimpse into that based on our trial design, you'll remember that I said that, all patients will be enrolled based on local testing, some of them may not qualify based on or may not meet the central testing standard. And if we see activity that's meaningful in the non-centrally confirmed patients, that may be a hint that we should look or explore lower copy numbers as well.

[Charles Zhu:]

Got it. That makes sense and thanks for the color. The other potential milademetan studies in Merkel cell, GATA3 breast or mesothelioma. I may have missed it. But what's your thinking in terms of timelines to initiating those studies? And, is this something where you'd want to see some emerging clinical data from currently planned or ongoing studies before mapping out those new trials? Or I guess, is the near-term of preclinical data a sufficient launch point? Thanks.

[Avanish Vellanki:]

Hi, Charles, I'll take that one. So we haven't publicly articulated timelines for the studies in dose indications yet. Now, of course, we did talk about some upcoming non-clinical presentations to add further support to that strategy. And we look forward to presenting that in the very near future. But I think we'll leave it there in terms of timing, we're not ready to talk about timing yet. Now, we will point you to a lot of information from peers in those indications that does defend this approach. Specifically, we talked about other MDM2 program is being evaluated in Merkel cell carcinoma, refer you back to some of the MDM2 inhibitor data from 2020 to talk to that point, we do think that MDM2 has been validated in that specific setting. And some of the other settings we talked about. We haven't seen any information from other MDM2 inhibitor programs where we could be a little bit more novel of an approach. But please stay tuned as we continue to explore additional tumor types and we'll articulate plans once they're fortified.

[Charles Zhu:]

Understood. Thanks for taking the questions.

[Avanish Vellanki:]

Thanks, Charles.

[Operator:]

Seeing none, I will now turn the call back over to Avanish Vellanki, CEO of Rain Therapeutics.

[Avanish Vellanki:]

Thank you, everyone for taking the time to join today's call and we look forward to providing another update next quarter. Thank you.

[Operator:]

And thank you, ladies and gentlemen. This concludes today's conference. Thank you for participating. You may now disconnect.